WorldWideScience

Sample records for brain tissue injury

  1. Injury Response of Resected Human Brain Tissue In Vitro.

    Science.gov (United States)

    Verwer, Ronald W H; Sluiter, Arja A; Balesar, Rawien A; Baaijen, Johannes C; de Witt Hamer, Philip C; Speijer, Dave; Li, Yichen; Swaab, Dick F

    2015-07-01

    Brain injury affects a significant number of people each year. Organotypic cultures from resected normal neocortical tissue provide unique opportunities to study the cellular and neuropathological consequences of severe injury of adult human brain tissue in vitro. The in vitro injuries caused by resection (interruption of the circulation) and aggravated by the preparation of slices (severed neuronal and glial processes and blood vessels) reflect the reaction of human brain tissue to severe injury. We investigated this process using immunocytochemical markers, reverse transcriptase quantitative polymerase chain reaction and Western blot analysis. Essential features were rapid shrinkage of neurons, loss of neuronal marker expression and proliferation of reactive cells that expressed Nestin and Vimentin. Also, microglia generally responded strongly, whereas the response of glial fibrillary acidic protein-positive astrocytes appeared to be more variable. Importantly, some reactive cells also expressed both microglia and astrocytic markers, thus confounding their origin. Comparison with post-mortem human brain tissue obtained at rapid autopsies suggested that the reactive process is not a consequence of epilepsy.

  2. Facilitated assessment of tissue loss following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Anders eHånell

    2012-03-01

    Full Text Available All experimental models of traumatic brain injury (TBI result in a progressive loss of brain tissue. The extent of tissue loss reflects the injury severity and can be measured to evaluate the potential neuroprotective effect of experimental treatments. Quantitation of tissue volumes is commonly performed using evenly spaced brain sections stained using routine histochemical methods and digitally captured. The brain tissue areas are then measured and the corresponding volumes are calculated using the distance between the sections. Measurements of areas are usually performed using a general purpose image analysis software and the results are then transferred to another program for volume calculations. To facilitate the measurement of brain tissue loss we developed novel algorithms which automatically separate the areas of brain tissue from the surrounding image background and identify the ventricles. We implemented these new algorithms by creating a new computer program (SectionToVolume which also has functions for image organization, image adjustments and volume calculations. We analyzed brain sections from mice subjected to severe focal TBI using both SectionToVolume and ImageJ, a commonly used image analysis program. The volume measurements made by the two programs were highly correlated and analysis using SectionToVolume required considerably less time. The inter-rater reliability was high. Given the extensive use of brain tissue loss measurements in TBI research, SectionToVolume will likely be a useful tool for TBI research. We therefore provide both the source code and the program as attachments to this article.

  3. Investigation of elemental changes in brain tissues following excitotoxic injury

    Science.gov (United States)

    Siegele, Rainer; Howell, Nicholas R.; Callaghan, Paul D.; Pastuovic, Zeljko

    2013-07-01

    Recently the ANSTO heavy ion microprobe has been used for elemental mapping of thin brain tissue sections. The fact that a very small portion of the proton energy is used for X-ray excitation combined with small variations of the major element concentrations makes μ-PIXE imaging and GeoPIXE analysis a challenging task. Excitotoxic brain injury underlies the pathology of stroke and various neurodegenerative disorders. Large fluxes in Ca+2 cytosolic concentrations are a key feature of the initiation of this pathophysiological process. In order to understand if these modifications are associated with changes in the elemental composition, several brain sections have been mapped with μ-PIXE. Increases in Ca+2 cytosolic concentrations were indicative of the pathophysiological process continuing 1 week after an initiating neural insult. We were able to measure significant variations in K and Ca concentration distribution across investigated brain tissue. These variations correlate very well with physiological changes visible in the brain tissue. Moreover, the obtained μ-PIXE results clearly demonstrate that the elemental composition changes significantly correlate with brain drauma.

  4. Investigation of elemental changes in brain tissues following excitotoxic injury

    Energy Technology Data Exchange (ETDEWEB)

    Siegele, Rainer, E-mail: rns@ansto.gov.au [Institute for Environmental Research, ANSTO, Locked Bag 2001, Kirrawee DC, NSW 2232 (Australia); Howell, Nicholas R.; Callaghan, Paul D. [Life Sciences, ANSTO, Locked Bag 2001, Kirrawee DC, NSW 2232 (Australia); Pastuovic, Zeljko [Institute for Environmental Research, ANSTO, Locked Bag 2001, Kirrawee DC, NSW 2232 (Australia)

    2013-07-01

    Recently the ANSTO heavy ion microprobe has been used for elemental mapping of thin brain tissue sections. The fact that a very small portion of the proton energy is used for X-ray excitation combined with small variations of the major element concentrations makes μ-PIXE imaging and GeoPIXE analysis a challenging task. Excitotoxic brain injury underlies the pathology of stroke and various neurodegenerative disorders. Large fluxes in Ca{sup +2} cytosolic concentrations are a key feature of the initiation of this pathophysiological process. In order to understand if these modifications are associated with changes in the elemental composition, several brain sections have been mapped with μ-PIXE. Increases in Ca{sup +2} cytosolic concentrations were indicative of the pathophysiological process continuing 1 week after an initiating neural insult. We were able to measure significant variations in K and Ca concentration distribution across investigated brain tissue. These variations correlate very well with physiological changes visible in the brain tissue. Moreover, the obtained μ-PIXE results clearly demonstrate that the elemental composition changes significantly correlate with brain drauma.

  5. Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury.

    Science.gov (United States)

    Graham, D I; Raghupathi, R; Saatman, K E; Meaney, D; McIntosh, T K

    2000-02-01

    A characteristic feature of severe diffuse axonal injury in man is radiological evidence of the "shearing injury triad" represented by lesions, sometimes haemorrhagic, in the corpus callosum, deep white matter and the rostral brain stem. With the exception of studies carried out on the non-human primate, such lesions have not been replicated to date in the multiple and diverse rodent laboratory models of traumatic brain injury. The present report describes tissue tears in the white matter, particularly in the fimbria of Sprague-Dawley rats killed 12, 24, and 48 h and 7 days after lateral fluid percussion brain injury of moderate severity (2.1-2.4 atm). The lesions were most easily seen at 24 h when they appeared as foci of tissue rarefaction in which there were a few polymorphonuclear leucocytes. At the margins of these lesions, large amounts of accumulated amyloid precursor protein (APP) were found in axonal swellings and bulbs. By 1 week post-injury, there was macrophage infiltration with marked astrocytosis and early scar formation. This lesion is considered to be due to severe deformation of white matter and this is the first time that it has been identified reproducibly in a rodent model of head injury under controlled conditions.

  6. Effect of mild hypothermia on glucose metabolism and glycerol of brain tissue in patients with severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    WANG Qiong; LI Ai-lin; ZHI Da-shi; HUANG Hui-ling

    2007-01-01

    Objective:To study the effect of mild hypothermia on glucose metabolism and glycerol of brain tissue in patients with severe traumatic brain injury (STBI) using clinical microdialysis.Methods: Thirty-one patients with STBI ( GCS ≤8) were randomly divided into hypothermic group (Group A) and control group (Group B). Microdialysis catheters were inserted into the cerebral cortex of perilesional and normal brain tissue. All samples were analyzed using CMA microdialysis analyzer.Results: In comparison with the control group, lactate/glucose ratio ( L/G) , lactate/pyruvate ratio ( L/P) and glycerol (Gly) in perilensional tissue were significantly decreased; L/P in normal brain tissue was significantly decreased. In control group, L/G, L/P and Gly in perilensional tissue were higher than that in normal brain tissue. In the hypothermic group, L/P in perilensional tissue was higher than that in relative normal brain.Conclusions: Mild hypothermia protects brain tissues by decreasing L/G, L/P and Gly in perilensional tissue and L/P in "normal brain" tissues. The energy crisis and membrane phospholipid degradation in perilensional tissue are easier to happen after traumatic brain injury, and mild hypothermia protects brain better in perilensional tissue than in normal brain tissue.

  7. Protective effects of acupuncture on brain tissue following ischemia/reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Mingshan Wang; Fuguo Ma; Huailong Chen

    2008-01-01

    BACKGROUND: In patients with cerebrovascular disease, by means of the neuroendocrine system, acupuncture supports the transformation of a local pathological status into a physiological status. Recently, great progress has been made in studying the protective effects of acupuncture on brain ischemia/reperfusion injury. OBJECTIVE: To summarize research advances in the protective effects of acupuncture on brain ischemia/reperfusion injury. RETRIEVAL STRATEGY: Using the terms "acupuncture, transcutaneous electrical acupoint stimulation, cerebral ischemia/reperfusion injury, and cerebral protection", we retrieved articles from the PubMed database published between January 1991 and June 1994. Meanwhile, we searched the China National Knowledge Infrastructure with the same terms. Altogether, 114 articles and their results were analyzed. Inclusive criteria: studies that were closely related to the protective effects of acupuncture on brain ischemia/reperfusion injury, or studies, whose contents were in the same study field and were published recently, or in the authorized journals. Exclusive criteria: repetitive studies. LITERATURE EVALUATION: Thirty articles that related to the protective effects of acupuncture on brain ischemia/reperfusion injury were included. Among them, 7 were clinical studies, and the remaining 23 articles were animal experimental studies. DATA SYNTHESIS: ① Animal experimental studies have demonstrated that acupuncture improves brain blood perfusion and brain electrical activity, influences pathomorphological and ultramicrostructural changes in ischemic brain tissue, is beneficial in maintaining the stability of intracellular and extracellular ions, resists free radical injury and lipid peroxidation, and influences cytokine, neurotransmitter, brain cell signal transduction, and apoptosis-regulating genes. ② Clinical studies have demonstrated that acupuncture not only promotes nutritional supply to local brain tissue in patients with cerebral

  8. Effect of ketamine on aquaporin-4 expression and neuronal apoptosis in brain tissues following brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    Zangong Zhou; Xiangyu Ji; Li Song; Jianfang Song; Shiduan Wang; Yanwei Yin

    2006-01-01

    BACKGROUND: Aquaporin-4 (AQP-4) is closely related to the formation of brain edema. Neuronal apoptosis plays an important part in the conversion of swelled neuron following traumatic brain injury. At present, the studies on the protective effect of ketamine on brain have involved in its effect on aquaporin-4 expression and neuronal apoptosis in the brain tissues following brain injury in rats.OBJECTIVE: To observe the effect of ketamine on AQP-4 expression and neuronal apoptosis in the brain tissue following rat brain injury, and analyze the time-dependence of ketamine in the treatment of brain injury.DESIGN: Randomized grouping design, controlled animal trial.SETTING: Department of Anesthesiology, the Medical School Hospital of Qingdao University.MATERIALS: Totally 150 rats of clean grade, aged 3 months, were involved and randomized into control group and ketamine-treated group, with 75 rats in each. Each group was divided into 5 subgroups separately at 6,12, 24, 48 and 72 hours after injury, with 15 rats at each time point. Main instruments and reagents:homemade beat machine, ketamine hydrochloride (Hengrui Pharmaceutical Factory, Jiangsu), rabbit anti-rat AQP-4 polyclonal antibody, SABC immunohistochemical reagent kit and TUNEL reagent kit (Boster Co.,Ltd.,Wuhan).METHODS: This trial was carried out in the Institute of Cerebrovascular Disease, Medical College of Qingdao University during March 2005 to February 2006. A weight-dropping rat model of brain injury was created with Feeney method. The rats in the ketamine-treated group were intraperitoneally administered with 50 g/L ketamine (120 mg/kg) one hour after injury, but ketamine was replaced by normal saline in the control group. In each subgroup, the water content of cerebral hemisphere was measured in 5 rats chosen randomly. The left 10 rats in each subgroup were transcardiacally perfused with ketamine, then the brain tissue was made into paraffin sections and stained by haematoxylin and eosin. Neuronal

  9. Brain tissue oxygen tension and its response to physiological manipulations: influence of distance from injury site in a swine model of traumatic brain injury.

    Science.gov (United States)

    Hawryluk, Gregory W J; Phan, Nicolas; Ferguson, Adam R; Morabito, Diane; Derugin, Nikita; Stewart, Campbell L; Knudson, M Margaret; Manley, Geoffrey; Rosenthal, Guy

    2016-11-01

    OBJECTIVE The optimal site for placement of tissue oxygen probes following traumatic brain injury (TBI) remains unresolved. The authors used a previously described swine model of focal TBI and studied brain tissue oxygen tension (PbtO2) at the sites of contusion, proximal and distal to contusion, and in the contralateral hemisphere to determine the effect of probe location on PbtO2 and to assess the effects of physiological interventions on PbtO2 at these different sites. METHODS A controlled cortical impact device was used to generate a focal lesion in the right frontal lobe in 12 anesthetized swine. PbtO2 was measured using Licox brain tissue oxygen probes placed at the site of contusion, in pericontusional tissue (proximal probe), in the right parietal region (distal probe), and in the contralateral hemisphere. PbtO2 was measured during normoxia, hyperoxia, hypoventilation, and hyperventilation. RESULTS Physiological interventions led to expected changes, including a large increase in partial pressure of oxygen in arterial blood with hyperoxia, increased intracranial pressure (ICP) with hypoventilation, and decreased ICP with hyperventilation. Importantly, PbtO2 decreased substantially with proximity to the focal injury (contusion and proximal probes), and this difference was maintained at different levels of fraction of inspired oxygen and partial pressure of carbon dioxide in arterial blood. In the distal and contralateral probes, hypoventilation and hyperventilation were associated with expected increased and decreased PbtO2 values, respectively. However, in the contusion and proximal probes, these effects were diminished, consistent with loss of cerebrovascular CO2 reactivity at and near the injury site. Similarly, hyperoxia led to the expected rise in PbtO2 only in the distal and contralateral probes, with little or no effect in the proximal and contusion probes, respectively. CONCLUSIONS PbtO2 measurements are strongly influenced by the distance from the

  10. Brain injury - discharge

    Science.gov (United States)

    ... and caregivers. Biausa.org. www.biausa.org/brain-injury-family-caregivers.htm#Manage the Home . Accessed December 8, 2016. ... Caregiver Alliance; National Center on Caregiving. Traumatic brain injury. ... www.caregiver.org/traumatic-brain-injury . Accessed ...

  11. Traumatic Brain Injury

    Science.gov (United States)

    Traumatic brain injury (TBI) happens when a bump, blow, jolt, or other head injury causes damage to the brain. Every year, millions of people in the U.S. suffer brain injuries. More than half are bad enough that ...

  12. Brain tissue partial pressure of oxygen predicts the outcome of severe traumatic brain injury under mild hypothermia treatment

    Directory of Open Access Journals (Sweden)

    Sun H

    2016-08-01

    Full Text Available Hongtao Sun,1,* Maohua Zheng,2,* Yanmin Wang,1 Yunfeng Diao,1 Wanyong Zhao,1 Zhengjun Wei1 1Sixth Department of Neurosurgery, Affiliated Hospital of Logistics University of People’s Armed Police Force, Tianjin, 2Department of Neurosurgery, The First Hospital of Lanzhou University, Lanzhou, People’s Republic of China *These authors contributed equally to this work Objective: The aim of this study was to investigate the clinical significance and changes of brain tissue partial pressure of oxygen (PbtO2 in the course of mild hypothermia treatment (MHT for treating severe traumatic brain injury (sTBI. Methods: There were 68 cases with sTBI undergoing MHT. PbtO2, intracranial pressure (ICP, jugular venous oxygen saturation (SjvO2, and cerebral perfusion pressure (CPP were continuously monitored, and clinical outcomes were evaluated using the Glasgow Outcome Scale score. Results: Of 68 patients with sTBI, PbtO2, SjvO2, and CPP were obviously increased, but decreased ICP level was observed throughout the MHT. PbtO2 and ICP were negatively linearly correlated, while there was a positive linear correlation between PbtO2 and SjvO2. Monitoring CPP and SjvO2 was performed under normal circumstances, and a large proportion of patients were detected with low PbtO2. Decreased PbtO2 was also found after MHT. Conclusion: Continuous PbtO2 monitoring could be introduced to evaluate the condition of regional cerebral oxygen metabolism, thereby guiding the clinical treatment and predicting the outcome. Keywords: severe traumatic brain injury, hypothermia, brain tissue partial pressure of oxygen, therapy

  13. Concentrations of Nitric Oxide in Rat Brain Tissues after Diffuse Brain Injury and Neuroprotection by the Selective Inducible Nitric Oxide Synthase Inhibitor Aminoguanidine

    Institute of Scientific and Technical Information of China (English)

    Yi-bao Wang; Shao-wu Ou; Guang-yu Li; Yun-hui Liu

    2005-01-01

    @@ To investigate the effects of nitric oxide (NO) and the selective inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (AG) on trauma, we explored the concentrations of nitric oxide in rat brain tissues at different time stamps after diffuse brain injury (DBI) with or without AG treatment.

  14. The quantitative analysis of S100 in the brain tissue and serum following diffuse brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    Wang Qi; Huang Ping; Xing Bo; Tuo Ya; Zhang Yongpan; Tian Weiping; Wang Zhenyuan

    2007-01-01

    Objective To investigate the dynamics of the level of S100 in cerebrum, brainstem, and serum following the diffuse brain injury in rats and provide the experimental evidences for estimating injury time. Methods ELISA was used to determine whether S100 protein is changed after diffuse brain injury in rats. Forty rats were sacrificed at 0.5 hour, 2 hours, 4 hours, 12 hours, 24 hours, 3 d and 7 d after diffuse brain injury and normal rats as control. Results The level of S100 in cerebrum, brainstem, and serum increased, followed by a decrease, and then further increased. The level of S100 could be detected to increase at 30 minutes and reached the peak at 4 hours after DBI. The level decreased gradually to the normal at 1d and till 3 d formed the second peak. The level returned to the normal at 7d following injury again. In the postmortem injury groups, there were no significant changes compared to the control group. Conclusion The present study showed that the time-dependent expression of S100 is obvious following diffuse brain injury in rats and suggested that S100 will be a suitable marker for diffuse brain injury age determination.

  15. A CD11d Monoclonal Antibody Treatment Reduces Tissue Injury and Improves Neurological Outcome after Fluid Percussion Brain Injury in Rats

    OpenAIRE

    2012-01-01

    Traumatic brain injury (TBI) is an international health concern often resulting in chronic neurological abnormalities, including cognitive deficits, emotional disturbances, and motor impairments. An anti-CD11d monoclonal antibody that blocks the CD11d/CD18 integrin and vascular cell adhesion molecule (VCAM)-1 interaction following experimental spinal cord injury improves functional recovery, while reducing the intraspinal number of neutrophils and macrophages, oxidative activity, and tissue d...

  16. Brain tissue oxygen-based therapy and outcome after severe traumatic brain injury: a systematic literature review.

    Science.gov (United States)

    Nangunoori, Raj; Maloney-Wilensky, Eileen; Stiefel, Michael; Park, Soojin; Andrew Kofke, W; Levine, Joshua M; Yang, Wei; Le Roux, Peter D

    2012-08-01

    Observational clinical studies demonstrate that brain hypoxia is associated with poor outcome after severe traumatic brain injury (TBI). In this study, available medical literature was reviewed to examine whether brain tissue oxygen (PbtO2)-based therapy is associated with improved patient outcome after severe TBI. Clinical studies published between 1993 and 2010 that compared PbtO2-based therapy combined with intracranial and cerebral perfusion pressure (ICP/CPP)-based therapy to ICP/CPP-based therapy alone were identified from electronic databases, Index Medicus, bibliographies of pertinent articles, and expert consultation. For analysis, each selected paper had to have adequate data to determine odds ratios (ORs) and confidence intervals (CIs) of outcome described by the Glasgow outcome score (GOS). Seven studies that compared ICP/CPP and PbtO2- to ICP/CPP-based therapy were identified. There were no randomized studies and no comparison studies in children. Four studies, published in 2003, 2009, and 2010 that included 491 evaluable patients were used in the final analysis. Among patients who received PbtO2-based therapy, 121(38.8%) had unfavorable and 191 (61.2%) had a favorable outcome. Among the patients who received ICP/CPP-based therapy 104 (58.1%) had unfavorable and 75 (41.9%) had a favorable outcome. Overall PbtO2-based therapy was associated with favorable outcome (OR 2.1; 95% CI 1.4-3.1). Summary results suggest that combined ICP/CPP- and PbtO2-based therapy is associated with better outcome after severe TBI than ICP/CPP-based therapy alone. Cross-organizational practice variances cannot be controlled for in this type of review and so we cannot answer whether PbtO2-based therapy improves outcome. However, the potentially large incremental value of PbtO2-based therapy provides justification for a randomized clinical trial.

  17. Mild Traumatic Brain Injury

    Science.gov (United States)

    ... Videos mild Traumatic Brain Injury 94447 reads Please Log in You must be logged in to access ... Brain Injury (DCoE) to promote the processes of building resilience, facilitating recovery and supporting reintegration of returning ...

  18. A Prospective Randomized Study of Brain Tissue Oxygen Pressure-Guided Management in Moderate and Severe Traumatic Brain Injury Patients

    Directory of Open Access Journals (Sweden)

    Chien-Min Lin

    2015-01-01

    Full Text Available The purpose of this study was to compare the effect of PbtO2-guided therapy with traditional intracranial pressure- (ICP- guided treatment on the management of cerebral variables, therapeutic interventions, survival rates, and neurological outcomes of moderate and severe traumatic brain injury (TBI patients. From 2009 to 2010, TBI patients with a Glasgow coma scale 20 mmHg, and 27 patients were treated with ICP-guided therapy (ICP 60 mmHg in the neurosurgical intensive care unit (NICU; demographic characteristics were similar across groups. The survival rate in the PbtO2-guided group was also significantly increased at 3 and 6 months after injury. Moreover, there was a significant correlation between the PbtO2 signal and Glasgow outcome scale-extended in patients from 1 to 6 months after injury. This finding demonstrates that therapy directed by PbtO2 monitoring is valuable for the treatment of patients with moderate and severe TBI and that increasing PaO2 to 150 mmHg may be efficacious for preventing cerebral hypoxic events after brain trauma.

  19. Contents of myelin-basic protein and S-100 in serum and brain tissue of neonatal rats with intrauterine infection-caused brain injury

    Institute of Scientific and Technical Information of China (English)

    Xiaojie Li; Hongying Li; Zhihai Lu

    2006-01-01

    BACKGROUND: The change of the content of myelin basic protein (MBP) in serum and brain tissue is the bio chemical diadynamic index of amyelination. S-100 is a specific and sensitive marker of central nervous system (CNS) injury. Whether or not the content of S-100 and MBP in blood and brain tissue can be used as the quan titative index for early diagnosing the intrauterine infection-caused brain injury still needs investigation. OBJECTIVE: To observe whether or not MBP and S-100 detection can be used as the biochemical indexes for early diagnosing the intrauterine infection-caused brain injury. DESIGN: Randomized controlled animal experiment. SETTING: Laboratory of Pediatric Neuro-rehabilitation, Medical College of Rehabilitation, Jiamusi University. MATERIALS: Sixty female and thirty male common Wistar rats, weighing from 180 to 240 g, were provided by the Experimental Animal Center of Jiamusi University. Reagent: Lipopolysaccharide(LPS, serological type 055: B5, SIGMA Company of USA); MBP enzyme linked immunosobent assay (ELISA) immunoreagent kit (Preclinicai Recombination DNA Laboratory, Chengdu Huaxi Medical Center, Sichuan Province); S-100 ELISA immunoreagent kit ( Department of Physiology, the Fourth Military Medical University of Chinese PLA) and bovine serum albumin(Haitaike Biotechnology Co.,Ltd.).METHODS: This experiment was carried out in the Laboratory of Pediatric Neuro-Rehabilitation, Experimental Animal Center, Department of Pathology and Central Laboratory of Jiamusi University from July 2005 to March 2006. ① Preparation of models and grouping: The female and male rats were placed in one cage at 2: 1 at 17:00 o'clock. Vaginal smear was checked at 8:00 on the next morning. Sperm was found and 0 day of pregnancy was recorded. Pregnant rats were bred in another cage. The pregnant 47 rats were randomly divided into 2 groups: control group (n =10) and experimental group (n =37). The experimental pregnant rats were intraperitoneally injected with LPS

  20. Two-dimensional zymography differentiates gelatinase isoforms in stimulated microglial cells and in brain tissues of acute brain injuries.

    Science.gov (United States)

    Chen, Shanyan; Meng, Fanjun; Chen, Zhenzhou; Tomlinson, Brittany N; Wesley, Jennifer M; Sun, Grace Y; Whaley-Connell, Adam T; Sowers, James R; Cui, Jiankun; Gu, Zezong

    2015-01-01

    Excessive activation of gelatinases (MMP-2/-9) is a key cause of detrimental outcomes in neurodegenerative diseases. A single-dimension zymography has been widely used to determine gelatinase expression and activity, but this method is inadequate in resolving complex enzyme isoforms, because gelatinase expression and activity could be modified at transcriptional and posttranslational levels. In this study, we investigated gelatinase isoforms under in vitro and in vivo conditions using two-dimensional (2D) gelatin zymography electrophoresis, a protocol allowing separation of proteins based on isoelectric points (pI) and molecular weights. We observed organomercuric chemical 4-aminophenylmercuric acetate-induced activation of MMP-2 isoforms with variant pI values in the conditioned medium of human fibrosarcoma HT1080 cells. Studies with murine BV-2 microglial cells indicated a series of proform MMP-9 spots separated by variant pI values due to stimulation with lipopolysaccharide (LPS). The MMP-9 pI values were shifted after treatment with alkaline phosphatase, suggesting presence of phosphorylated isoforms due to the proinflammatory stimulation. Similar MMP-9 isoforms with variant pI values in the same molecular weight were also found in mouse brains after ischemic and traumatic brain injuries. In contrast, there was no detectable pI differentiation of MMP-9 in the brains of chronic Zucker obese rats. These results demonstrated effective use of 2D zymography to separate modified MMP isoforms with variant pI values and to detect posttranslational modifications under different pathological conditions.

  1. Matrix metalloproteinases and their tissue inhibitors in serum and cerebrospinal fluid of patients with moderate and severe traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Kebin Zheng

    2013-01-01

    Full Text Available Objective: In this study, we investigated matrix metalloproteinases (MMPs and tissue inhibitor of metalloproteinase (TIMPs in cerebrospinal fluid (CSF and plasma of traumatic brain injury (TBI patients. Patients and Methods: A total of 30 patients with moderate and severe TBI and 15 age-matched controls were enrolled in this study. Plasma and CSF samples were collected within 24 h (as the initial value, at 72 and 120 h post injury. CSF and plasma MMP-9, MMP-2, TIMP-1 and TIMP-2 were estimated using ELISA. Different levels of these indexes were compared in the two groups and further investigated the correlation between each other. Results: There was a significant elevation in the levels of the initial MMP-9 in the CSF (P < 0.05, which lasted for 72 h post injury. TIMP-1 kept increasing within 120 h post injury and it was different compared with TIMP-1 at 24 and 72 h post injury. Plasma levels of MMP-9, MMP-2, TIMP-1 and TIMP-2 in TBI patients were also significantly different from those in controls. Furthermore the CSF MMP-9 in patients with severe TBI was higher than that in patients with moderate TBI. In addition, there was a positive relationship between the initial MMP-9 and TIMP-1 at 120 h post injury (r = 0.614, P < 0.01. Conclusion: MMPs and TIMPs are increased in both CSF and plasma of TBI patients. TIMP-1 has a positive correlation with MMP-9 and the initial MMP-9 is associated with the neurological outcomes.

  2. Study on changes of partial pressure of brain tissue oxygen and brain temperature in acute phase of severe head injury during mild hypothermia therapy

    Institute of Scientific and Technical Information of China (English)

    朱岩湘; 姚杰; 卢尚坤; 章更生; 周关仁

    2003-01-01

    Objective: To study the changes of partial pressure of brain tissue oxygen (PbtO2) and brain temperature in acute phase of severe head injury during mild hypothermia therapy and the clinical significance.Methods: One hundred and sixteen patients with severe head injury were selected and divided into a mild hypothermia group (n=58), and a control group (n=58) according to odd and even numbers of hospitalization. While mild hypothermia therapy was performed PbtO2 and brain temperature were monitored for 1-7 days (mean=86 hours), simultaneously, the intracranial pressure, rectum temperature, cerebral perfusion pressure, PaO2 and PaCO2 were also monitored. The patients were followed up for 6 months and the prognosis was evaluated with GOS (Glasgow outcome scale).Results: The mean value of PbtO2 within 24 hour monitoring in the 116 patients was 13.7 mm Hg±4.94 mm Hg, lower than the normal value (16 mm Hg±40 mm Hg) The time of PbtO2 recovering to the normal value in the mild hypothermia group was shortened by 10±4.15 hours compared with the control group (P<0.05). The survival rate of the mild hypothermia group was 60.43%, higher than that of the control group (46.55%). After the recovery of the brain temperature, PbtO2 increased with the rise of the brain temperature. Conclusions: Mild hypothermia can improve the survival rate of severe head injury. The technique of monitoring PbtO2 and the brain temperature is safe and reliable, and has important clinical significance in judging disease condition and instructing clinical therapy.

  3. Expression of GLUT4 mRNA of peripheral tissues and insulin resistance in rats with severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    CHEN Da-qing; ZHU Lie-lie; LI Yong-ling

    2007-01-01

    Objective: To evaluate the expression of glucose transporter-4 (GLUT4) mRNA in skeletal muscle and subcutaneous adipose tissues and investigate the mechanism of posttraumatic insulin resistance.Methods: Sixteen adult male Wistar rats were randomly divided into 2 group (n=8 in each group), i.e., severe traumatic brain injury (TBI) group due to falls from a height and normal control group. Blood glucose and serum insulin were measured at 0.5 h before trauma and 3 h, 24 h, 72 h, 7 d after trauma, respectively. And insulin sensitivity was calculated by insulin activity index (IAI) formula. Skeletal muscle and subcutaneous adipose tissue samples were collected at the same time when blood was sampled. The changes of expression of GLUT4 mRNA were observed using reverse transcription-polymerase chain reaction (RT-PCR).Results: Accompanied by the decrease of insulin sensitivity, the expression of GLUT4 mRNA was significantly decreased in adipose tissues at 24 h and 72 h after trauma (P<0.01), however, such phenomena did not appear in skeletal muscle samples.Conclusions: To some extent, the development of posttraumatic insulin resistance is related to the abnormality of transcription activity of GLUT4 gene. Adipose tissues show some difference in the transcriptional level of GLUT4 gene after trauma as compared with skeletal muscle tissues.

  4. Effect of mild hypothermia on partial pressure of oxygen in brain tissue and brain temperature in patients with severe head injury

    Institute of Scientific and Technical Information of China (English)

    张赛; 只达石; 林欣; 尚彦国; 牛玉德

    2002-01-01

    Objective: To study the changes of partial pressure of oxygen in brain tissue (PbtO2) and brain temperature (BT) in patients in acute phase of severe head injury, and to study the effect of mild hypothermia on PbtO2 and BT.   Methods: The PbtO2 and the BT of 18 patients with severe head injury were monitored, and the patients were treated with mild hypothermia within 20 hours after injury. The rectal temperature (RT) of the patients was kept on 31.5-34.9℃ for 1-7 days (57.7 hours±28.4 hours averagely), simultaneously, the indexes of PbtO2 and BT were monitored for 1-5 days (with an average of 54.8 hours±27.0 hours). According to Glasgow Outcome Scale (GOS), the prognosis of the patients was evaluated at 6 months after injury.   Results: Within 24 hours after severe head injury, the PbtO2 was significantly lower (9.6 mm Hg±6.8 mm Hg, 1 mm Hg=0.133 kPa) than the normal value (16-40 mm Hg). After treatment of mild hypothermia, the mean PbtO2 increased to 28.7 mm Hg±8.8 mm Hg during the first 24 hours, and the PbtO2 was still maintained within the range of normal value at 3 days after injury. The BT was higher than the RT in the patients in acute phase of severe head injury, and the difference between the BT and the RT significantly increased after treatment of mild hypothermia. Hyperventilation (the partial pressure of carbon dioxide in artery (PaCO2)≈25 mm Hg) decreased the high intracranial pressure (ICP) and significantly decreased the PbtO2.   Conclusions: This study demonstrates that PptO2 and BT monitoring is a safe, reliable and sensitive diagnostic method to follow cerebral oxygenation. It might become an important tool in our treatment regime for patients in the acute phase of severe head injury requiring hypothermia and hyperventilation.

  5. MRI of perinatal brain injury

    Energy Technology Data Exchange (ETDEWEB)

    Rutherford, Mary; Allsop, Joanna [Imperial College, Robert Steiner MR Unit, Perinatal Imaging, MRC Clinical Sciences Centre, Hammersmith Hospital, London (United Kingdom); Martinez Biarge, Miriam [La Paz University Hospital, Dept of Neonatology, Madrid (Spain); Counsell, Serena [Imperial College, Robert Steiner MR Unit, Neonatal Medicine, MRC Clinical Sciences Centre, Hammersmith Hospital, London (United Kingdom); Cowan, Frances [Imperial College, Dept of Paediatrics, Hammersmith Hospital, London (United Kingdom)

    2010-06-15

    MRI is invaluable in assessing the neonatal brain following suspected perinatal injury. Good quality imaging requires adaptations to both the hardware and the sequences used for adults or older children. The perinatal and postnatal details often predict the pattern of lesions sustained and should be available to aid interpretation of the imaging findings. Perinatal lesions, the pattern of which can predict neurodevelopmental outcome, are at their most obvious on conventional imaging between 1 and 2 weeks from birth. Very early imaging during the first week may be useful to make management decisions in ventilated neonates but brain abnormalities may still be subtle using conventional sequences. Diffusion-weighted imaging (DWI) is very useful for the early identification of ischaemic tissue in the neonatal brain but may underestimate the final extent of injury, particularly basal ganglia and thalamic lesions. MR imaging is an excellent predictor of outcome following perinatal brain injury and can therefore be used as a biomarker in interventional trials designed to reduce injury and improve neurodevelopmental outcome. (orig.)

  6. Concussion and Traumatic Brain Injury

    Science.gov (United States)

    ... turn JavaScript on. Feature: Concussion Concussion and Traumatic Brain Injury Past Issues / Summer 2015 Table of Contents Children ... body, may have a concussion or more serious brain injury. Concussion Signs Observed Can't recall events prior ...

  7. Brain Injury Association of America

    Science.gov (United States)

    ... 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 ...

  8. Brain Temperature: Physiology and Pathophysiology after Brain Injury

    Directory of Open Access Journals (Sweden)

    Ségolène Mrozek

    2012-01-01

    Full Text Available The regulation of brain temperature is largely dependent on the metabolic activity of brain tissue and remains complex. In intensive care clinical practice, the continuous monitoring of core temperature in patients with brain injury is currently highly recommended. After major brain injury, brain temperature is often higher than and can vary independently of systemic temperature. It has been shown that in cases of brain injury, the brain is extremely sensitive and vulnerable to small variations in temperature. The prevention of fever has been proposed as a therapeutic tool to limit neuronal injury. However, temperature control after traumatic brain injury, subarachnoid hemorrhage, or stroke can be challenging. Furthermore, fever may also have beneficial effects, especially in cases involving infections. While therapeutic hypothermia has shown beneficial effects in animal models, its use is still debated in clinical practice. This paper aims to describe the physiology and pathophysiology of changes in brain temperature after brain injury and to study the effects of controlling brain temperature after such injury.

  9. Effects of realgar on stress proteins, inflammatory mediators, and complement in brain tissue and serum of rats with inflammatory brain injury

    Institute of Scientific and Technical Information of China (English)

    Yishan Tang; Ningsheng Wang; Yinqing Zhang; Shaomei Ye; Weiping Ou

    2008-01-01

    BACKGROUND: The Chinese herbal compound realgar exerts detoxification effects as an adjuvant. It is suggested that realgar exerts detoxification via the following pathways: in the pathological state, realgar corrects the oxidative stress state by increasing stress levels, activating some endogenous protective factors and antagonizing the excessive release of inflammatory factors, as well as inhibiting complement activation.OBJECTIVE: To observe the changes in stress proteins, inflammatory mediators, and complement in the brain tissue and serum of rats with inflammatory brain injury, which have been treated with thc Chinese herbal compound Angong Niuhuang, and to compare the efficacy of Angong Niuhuang with that of realgar,to verify the mechanism of action of realgar.DESIGN, TIME AND SETTING: Randomized, controlled, cytological experiment, performed in the Institute of Clinical Pharmacology, Guangzhou University of Traditional Chinese Medicine in March 2006.MATERIALS: Thirty-six healthy, male, Sprague Dawley rats received 250 U/kg Bordetella pertussis via the common carotid artery within 15 seconds to induce inflammatory brain injury. Reagents and kits were as follows: Realgar and Angong Niuhuang powder (Foshan Second Pharmaceutical Factory, China), Bordetella pertussis diagnostic antigen (National Institute for the Control of Pharmaceutical and Biological Products,China), heat shock protein 70 (HSP70) enzyme-labeled immunosorbent assay (ELISA) kit (Stressgen, USA),tumor necrosis factor-α (TNF-α) ELISA kit (Biosource, USA), nitric oxide synthase (NOS) kit,Coomassie brilliant blue protein kit (Nanjing Jiancheng Bioengineering Co.,Ltd., China), and complements C3 and C4 (Shanghai Kehua Dongling Diagnositic Products Co.,Ltd., China),METHODS: Thirty-six rats were randomly and evenly divided into the following six groups: normal control,model, high-, middle-, and low-dose realgar-treated, and Angong Niuhuang-treated groups. At one hour prior to establishing the model

  10. A correlation study of the expression of resistin and glycometabolism in muscle tissue after traumatic brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    Jin Peng; Zhu Lielie; Zhang Jiasheng; Xie Songling; Pan Da; Wen Hao; Meng Weiyang

    2014-01-01

    Objective:To investigate the expression pattern of resistin (RSTN) in skeletal muscle tissue and its influence on glycometabolism in rats with traumatic brain injury (TBI).Methods:Seventy-eight SD rats were randomly divided into traumatic group (n=36),RSTN group (n=36) and sham operation group (n=6).Fluid percussion TBI model was developed in traumatic and RSTN groups and the latter received additional 1 mg RSTN antibody treatment for each rat.At respectively 12 h,24 h,72 h,1 w,2 w,and 4 w after operation,venous blood was collected and the right hind leg skeletal muscle tissue was sampled.We used real-time PCR to determine mRNA expression of RSTN in skeletal muscles,western blot to determine RSTN protein expression and ELISA to assess serum insulin as well as fasting blood glucose (FBG) levels.Calculation of the quantitative insulin sensitivity check index (Q value) was also conducted.The above mentioned indicators and their correction were statistically analyzed.Results:Compared with sham operation group,the RSTN expression in the skeletal muscle as well as serum insulin and FBG levels revealed significant elevation (P<0.05),and reduced Q value (P<0.05) in traumatic group.Single factor linear correlation analysis showed a significant negative correlation between RSTN expression and Q values (P<0.001) in traumatic group.Conclusion:The expression of RSTN has been greatly increased in the muscular tissue of TBI rats and it was closely related to the index of glycometabolism.RSTN may play an important role in the process of insulin resistance after TBI.

  11. CHANGES OF NITRIC OXIDE LEVEL IN BRAIN TISSUES AFTER EXPERIMENTAL FOCAL INJURY%实验性颅脑损伤后脑组织NO的变化

    Institute of Scientific and Technical Information of China (English)

    李志强; 袁先厚; 袁忠惠

    2001-01-01

    Objective To explore the changes of nitric oxide (NO) level and its relationship with brain edema in acutebrain injury.Methods After acute brain injury model was produced by free dropping of rats,brain tissues were obtained andits water concentration,Ca2 + and NO were measured.Results After brain injury,the water content,NO level and Ca2 + wereall increased.The peak levels of Ca2+ and NO emerged 4 hours and 8 hours after the injury respectively,and the increasing ofCa2 + tended to last for a longer time.Tests showed that No concentration was positively correlated with the water content inbrain tissues.Conclusion NO is involved in the occurrence of brain edema after acute brain injury.%目的探讨脑损伤后急性期局部一氧化氮(NO)含量变化及其与脑水肿的关系。方法采用自由落体法制造大鼠脑损伤后,于相应时间点取出脑组织测定其含水量、NO及Ca2+浓度。结果在损伤后急性期脑组织含水量、NO及Ca2+含量均升高,其中Ca2+浓度和NO含量分别于损伤后4h、8h达高峰,且Ca2+升高趋势持续时间长。经检验,NO含量与脑组织含水量呈正相关。结论 NO在脑损伤急性期参与了脑水肿的发生过程。

  12. Radiation Injury to the Brain

    Science.gov (United States)

    ... Tumors Brain Tumors Brain Disorders AVMs Radiosurgery Gamma Knife Linac Radiotherapy Overview Childhood Brain Tumors IMRT Radiation Therapy Radiation Injury Treatment Day Making a Decision Centers of Excellence Publications Definitions Q & ...

  13. Soft tissue twisting injuries of the knee

    Energy Technology Data Exchange (ETDEWEB)

    Magee, T.; Shapiro, M. [Neuroimaging Inst., Melbourne, FL (United States)

    2001-08-01

    Twisting injuries occur as a result of differential motion of different tissue types in injuries with some rotational force. These injuries are well described in brain injuries but, to our knowledge, have not been described in the musculoskeletal literature. We correlated the clinical examination and MR findings of 20 patients with twisting injuries of the soft tissues around the knee. Design and patients: We prospectively followed the clinical courses of 20 patients with knee injuries who had clinical histories and MR findings to suggest twisting injuries of the subcutaneous tissues. Patients with associated internal derangement of the knee (i.e., meniscal tears, ligamentous or bone injuries) were excluded from this study. MR findings to suggest twisting injuries included linear areas of abnormal dark signal on T1-weighted sequences and abnormal bright signal on T2-weighted or short tau inversion recovery (STIR) sequences and/or signal to suggest hemorrhage within the subcutaneous tissues. These MR criteria were adapted from those established for indirect musculotendinous junction injuries. Results: All 20 patients presented with considerable pain that suggested internal derangement on physical examination by the referring orthopedic surgeons. All presented with injuries associated with rotational force. The patients were placed on a course of protected weight-bearing of the affected extremity for 4 weeks. All patients had pain relief by clinical examination after this period of protected weight-bearing. Twisting injuries of the soft tissues can result in considerable pain that can be confused with internal derangement of the knee on physical examination. Soft tissue twisting injuries need to be recognized on MR examinations as they may be the cause of the patient's pain despite no MR evidence of internal derangement of the knee. The demonstration of soft tissue twisting injuries in a patient with severe knee pain but no documented internal derangement on MR

  14. Association between serum tissue inhibitor of matrix metalloproteinase-1 levels and mortality in patients with severe brain trauma injury.

    Directory of Open Access Journals (Sweden)

    Leonardo Lorente

    Full Text Available OBJECTIVE: Matrix metalloproteinases (MMPs and tissue inhibitors of matrix metalloproteinases (TIMPs play a role in neuroinflammation after brain trauma injury (TBI. Previous studies with small sample size have reported higher circulating MMP-2 and MMP-9 levels in patients with TBI, but no association between those levels and mortality. Thus, the aim of this study was to determine whether serum TIMP-1 and MMP-9 levels are associated with mortality in patients with severe TBI. METHODS: This was a multicenter, observational and prospective study carried out in six Spanish Intensive Care Units. Patients with severe TBI defined as Glasgow Coma Scale (GCS lower than 9 were included, while those with Injury Severity Score (ISS in non-cranial aspects higher than 9 were excluded. Serum levels of TIMP-1, MMP-9 and tumor necrosis factor (TNF-alpha, and plasma levels of tissue factor (TF and plasminogen activator inhibitor (PAI-1 plasma were measured in 100 patients with severe TBI at admission. Endpoint was 30-day mortality. RESULTS: Non-surviving TBI patients (n = 27 showed higher serum TIMP-1 levels than survivor ones (n = 73. We did not find differences in MMP-9 serum levels. Logistic regression analysis showed that serum TIMP-1 levels were associated 30-day mortality (OR = 1.01; 95% CI = 1.001-1.013; P = 0.03. Survival analysis showed that patients with serum TIMP-1 higher than 220 ng/mL presented increased 30-day mortality than patients with lower levels (Chi-square = 5.50; P = 0.02. The area under the curve (AUC for TIMP-1 as predictor of 30-day mortality was 0.73 (95% CI = 0.624-0.844; P<0.001. An association between TIMP-1 levels and APACHE-II score, TNF- alpha and TF was found. CONCLUSIONS: The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality

  15. Erythropoietin reduces apoptosis of brain tissue cells in rats after cerebral ischemia/reperfusion injury: a characteristic analysis using magnetic resonance imaging

    Directory of Open Access Journals (Sweden)

    Chun-juan Jiang

    2016-01-01

    Full Text Available Some in vitro experiments have shown that erythropoietin (EPO increases resistance to apoptosis and facilitates neuronal survival following cerebral ischemia. However, results from in vivo studies are rarely reported. Perfusion-weighted imaging (PWI and diffusion-weighted imaging (DWI have been applied successfully to distinguish acute cerebral ischemic necrosis and penumbra in living animals; therefore, we hypothesized that PWI and DWI could be used to provide imaging evidence in vivo for the conclusion that EPO could reduce apoptosis in brain areas injured by cerebral ischemia/reperfusion. To validate this hypothesis, we established a rat model of focal cerebral ischemia/reperfusion injury, and treated with intra-cerebroventricular injection of EPO (5,000 U/kg 20 minutes before injury. Brain tissue in the ischemic injury zone was sampled using MRI-guided localization. The relative area of abnormal tissue, changes in PWI and DWI in the ischemic injury zone, and the number of apoptotic cells based on TdT-mediated dUTP-biotin nick end-labeling (TUNEL were assessed. Our findings demonstrate that EPO reduces the relative area of abnormally high signal in PWI and DWI, increases cerebral blood volume, and decreases the number of apoptotic cells positive for TUNEL in the area injured by cerebral ischemia/reperfusion. The experiment provides imaging evidence in vivo for EPO treating cerebral ischemia/reperfusion injury.

  16. Erythropoietin reduces apoptosis of brain tissue cells in rats after cerebral ischemia/reperfusion injury:a characteristic analysis using magnetic resonance imaging

    Institute of Scientific and Technical Information of China (English)

    Chun-juan Jiang; Zhong-juan Wang; Yan-jun Zhao; Zhui-yang Zhang; Jing-jing Tao; Jian-yong Ma

    2016-01-01

    Somein vitro experiments have shown that erythropoietin (EPO) increases resistance to apoptosis and facilitates neuronal survival follow-ing cerebral ischemia. However, results fromin vivo studies are rarely reported. Perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) have been applied successfully to distinguish acute cerebral ischemic necrosis and penumbra in living animals; therefore, we hypothesized that PWI and DWI could be used to provide imaging evidencein vivo for the conclusion that EPO could reduce apoptosis in brain areas injured by cerebral ischemia/reperfusion. To validate this hypothesis, we established a rat model of focal cerebral ischemia/reperfusion injury, and treated with intra-cerebroventricular injection of EPO (5,000 U/kg) 20 minutes before injury. Brain tissue in the ischemic injury zone was sampled using MRI-guided localization. The relative area of abnormal tissue, changes in PWI and DWI in the ischemic injury zone, and the number of apoptotic cells based on TdT-mediated dUTP-biotin nick end-labeling (TUNEL) were assessed. Our ifndings demonstrate that EPO reduces the relative area of abnormally high signal in PWI and DWI, increases cerebral blood volume, and decreases the number of apoptotic cells positive for TUNEL in the area injured by cerebral ischemia/reperfusion. The experiment pro-vides imaging evidencein vivo for EPO treating cerebral ischemia/reperfusion injury.

  17. Erythropoietin reduces apoptosis of brain tissue cells in rats after cerebral ischemia/reperfusion injury: a characteristic analysis using magnetic resonance imaging.

    Science.gov (United States)

    Jiang, Chun-Juan; Wang, Zhong-Juan; Zhao, Yan-Jun; Zhang, Zhui-Yang; Tao, Jing-Jing; Ma, Jian-Yong

    2016-09-01

    Some in vitro experiments have shown that erythropoietin (EPO) increases resistance to apoptosis and facilitates neuronal survival following cerebral ischemia. However, results from in vivo studies are rarely reported. Perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) have been applied successfully to distinguish acute cerebral ischemic necrosis and penumbra in living animals; therefore, we hypothesized that PWI and DWI could be used to provide imaging evidence in vivo for the conclusion that EPO could reduce apoptosis in brain areas injured by cerebral ischemia/reperfusion. To validate this hypothesis, we established a rat model of focal cerebral ischemia/reperfusion injury, and treated with intra-cerebroventricular injection of EPO (5,000 U/kg) 20 minutes before injury. Brain tissue in the ischemic injury zone was sampled using MRI-guided localization. The relative area of abnormal tissue, changes in PWI and DWI in the ischemic injury zone, and the number of apoptotic cells based on TdT-mediated dUTP-biotin nick end-labeling (TUNEL) were assessed. Our findings demonstrate that EPO reduces the relative area of abnormally high signal in PWI and DWI, increases cerebral blood volume, and decreases the number of apoptotic cells positive for TUNEL in the area injured by cerebral ischemia/reperfusion. The experiment provides imaging evidence in vivo for EPO treating cerebral ischemia/reperfusion injury.

  18. PERSONALITY CHANGES IN BRAIN INJURY

    OpenAIRE

    Garcia, Patricia Gracia; Mielke, Michelle M.; Rosenberg, Paul; Bergey, Alyssa; Rao, Vani

    2011-01-01

    Traumatic brain injury (TBI) is frequently complicated by alterations in mood and behaviour and changes in personality. We report mild personality changes post-TBI as a possible indicator of traumatic brain injury, but not of injury severity or psychiatric complications.

  19. The quantitative analysis of S100 in the brain tissue and serum following diffusebrain injury in rats

    Institute of Scientific and Technical Information of China (English)

    王琪; 黄平; 邢博; 托娅; 张勇攀; 田卫平; 王振原

    2007-01-01

    Wound examination is one of the most i mpor-tant aspects inthe forensic practice,and forensic pa-thologists are often required to esti mate woundsage.The diffuse brain injury(DBI)exists in theforensic practices widely.At present,various kindsof biological substances such as c-fos,β-App,FN,and appolipoprotein Eare knownto be closely relat-ed to braininjury,but no effective methods can beused to differentiate the antemortem diffuse braininjuries from the post mortem injuries and exactlyesti mate the ti me of ...

  20. Novel roles for metallothionein-I + II (MT-I + II) in defense responses, neurogenesis, and tissue restoration after traumatic brain injury: insights from global gene expression profiling in wild-type and MT-I + II knockout mice

    DEFF Research Database (Denmark)

    Penkowa, Milena; Cáceres, Mario; Borup, Rehannah

    2006-01-01

    Traumatic injury to the brain is one of the leading causes of injury-related death or disability, especially among young people. Inflammatory processes and oxidative stress likely underlie much of the damage elicited by injury, but the full repertoire of responses involved is not well known...... times consistent with the processes involved in the initial tissue injury and later regeneration of the parenchyma, as well as a prominent effect of MT-I + II deficiency. The results thoroughly confirmed the importance of the antioxidant proteins MT-I + II in the response of the brain to injury...

  1. [Biochemical and immunohistochemical markers of brain injury].

    Science.gov (United States)

    Vajtr, D; Průsa, R; Houst'ava, L; Sámal, F; Kukacka, J; Pachl, J

    2006-07-01

    Proteins released to circulation from affected tissues during primary or secondary trauma brain injury might be used as serum markers of glial or ganglial cells damage (neuron specific enolasis and S100 B protein). Other markers of trauma can be proved as relatively specific of diffuse axonal injury by immunohistochemical detectoin (amyloid prekurzor protein, neuron specific enolasis, glial fibrilar acidic protein and superficial antigen receptor CD 68). Some markers are associated with blood brain barrier damage (matrix metaloproteinases (MMP-2, MMP-9) and synthase of nitric oxide (iNOS)). We aimed in our short communication on biomechanics of developed of trauma, primary or secondary kinds of trauma brain injury and use of trauma brain injury markers for clinical diagnostics and management of patients.

  2. Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice

    OpenAIRE

    2011-01-01

    Traumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and mortality. Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes 1,2. Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4. ...

  3. Neuroprotective effects of vagus nerve stimulation on traumatic brain injury.

    Science.gov (United States)

    Zhou, Long; Lin, Jinhuang; Lin, Junming; Kui, Guoju; Zhang, Jianhua; Yu, Yigang

    2014-09-01

    Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and brain tissues, and water content in brain tissues was measured. Results showed that vagus nerve stimulation could reduce the degree of brain edema, decrease tumor necrosis factor-α and interleukin-1β concentrations, and increase interleukin-10 concentration after brain explosive injury in rabbits. These data suggest that vagus nerve stimulation may exert neuroprotective effects against explosive injury via regulating the expression of tumor necrosis factor-α, interleukin-1β and interleukin-10 in the serum and brain tissue.

  4. Neuroprotective effects of vagus nerve stimulation on traumatic brain injury

    Science.gov (United States)

    Zhou, Long; Lin, Jinhuang; Lin, Junming; Kui, Guoju; Zhang, Jianhua; Yu, Yigang

    2014-01-01

    Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and brain tissues, and water content in brain tissues was measured. Results showed that vagus nerve stimulation could reduce the degree of brain edema, decrease tumor necrosis factor-α and interleukin-1β concentrations, and increase interleukin-10 concentration after brain explosive injury in rabbits. These data suggest that vagus nerve stimulation may exert neuroprotective effects against explosive injury via regulating the expression of tumor necrosis factor-α, interleukin-1β and interleukin-10 in the serum and brain tissue. PMID:25368644

  5. Spectromicroscopy of Brain Tissue

    Science.gov (United States)

    Frazer, Bradley; Cannara, Rachel; Gilbert, Benjamin; Destasio, Gelsomina; Ogg, Mandy; Gough, Kathy

    2001-03-01

    X-ray PhotoElectron Emission Microscopy (X-PEEM) was originally developed for studying the surface microchemistry of materials science specimens. It has then evolved into a valuable tool to investigate the magnetic properties of materials and the microchemistry of cells and tissues. We used the MEPHISTO X-PEEM instrument, installed at the UW-Synchrotron Radiation Center to detect trace concentrations of non-physiological elements in senile brain tissue specimens. These tissues contain a large number of plaques, in which all the compounds and elements that the brain does not need are disposed and stored. We hypothesized that plaques should contain elements, such as Si, B, and Al which are very abundant on the Earth crust but absent from healthy tissues. We verified this hypothesis with MEPHISTO and found evidence of Si and B, and suspect Al. We also found a higher than normal concentration of Fe.

  6. Mechanical Tissue Resuscitation Treatment Reduces Brain Tissue Volume and Intracerebral Hemorrhage and Increases Blood Perfusion in a Traumatic Brain Injury Model in Swine

    Science.gov (United States)

    2010-01-01

    extremities.(Covey, 2006; Geiger, 2008; Leininger , 2006) It is also used to successfully treat injuries associated with high energy trauma...case report and the role of vacuum-assisted wound closure dressing. J Orthop Trauma 19:748- 50. Leininger BE, Rasmussen TE, Smith DL, Jenkins DH

  7. Evaluation after Traumatic Brain Injury

    Science.gov (United States)

    Trudel, Tina M.; Halper, James; Pines, Hayley; Cancro, Lorraine

    2010-01-01

    It is important to determine if a traumatic brain injury (TBI) has occurred when an individual is assessed in a hospital emergency room after a car accident, fall, or other injury that affects the head. This determination influences decisions about treatment. It is essential to screen for the injury, because the sooner they begin appropriate…

  8. Brain Injury: A Manual For Educators.

    Science.gov (United States)

    Connor, Karen; Dettmer, Judy; Dise-lewis, Jeanne E.; Murphy, Mary; Santistevan, Barbette; Seckinger, Barbara

    This manual provides Colorado educators with guidelines for serving students with brain injuries. Following an introductory chapter, chapter 2 provides basic information on the brain including definitions of brain injury and its severity, incidence of brain injury, and characteristics of students with brain injury. Chapter 3 considers…

  9. Cytokines and perinatal brain injury.

    Science.gov (United States)

    Silverstein, F S; Barks, J D; Hagan, P; Liu, X H; Ivacko, J; Szaflarski, J

    1997-01-01

    A rapidly expanding body of data provides support for the hypothesis that pro-inflammatory cytokines including interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) are expressed acutely in injured brain and contribute to progressive neuronal damage. Little is known about the pathogenetic role of these cytokines in perinatal brain injury. Recent experimental studies have incorporated two closely related in vivo perinatal rodent brain injury models to evaluate the role(s) of pro-inflammatory cytokines in the progression of neuronal injury: a perinatal stroke model, elicited by unilateral carotid artery ligation and subsequent timed exposure to 8% oxygen in 7-day-old rats, and a model of excitotoxic injury, elicited by stereotactic intra-cerebral injection of the selective excitatory amino acid agonist NMDA. Each of these lesioning methods results in reproducible, quantifiable focal forebrain injury at this developmental stage. Acute brain injury, evoked by cerebral hypoxia-ischemia or excitotoxin lesioning, results in transient marked increases in expression of IL-1 beta, and TNF-alpha mRNA in brain regions susceptible to irreversible injury, and there is evidence that pharmacological antagonism of IL-1 receptors can attenuate injury in both models. Recent studies also suggest that complementary strategies, based on pharmacological antagonism of platelet activating factor and on neutrophil depletion can also limit the extent of irreversible injury. In summary, current data suggest that pro-inflammatory cytokines contribute to the progression of perinatal brain injury, and that these mediators are important targets for neuroprotective interventions in the acute post-injury period.

  10. Traumatic Brain Injury Registry (TBI)

    Data.gov (United States)

    Department of Veterans Affairs — As the number of Operation Enduring Freedom/Operation Iraqi Freedom (OEF/OIF) Traumatic Brain Injury (TBI) patients has grown, so has the need to track and monitor...

  11. Traumatic Brain Injury Inpatient Rehabilitation

    Science.gov (United States)

    Im, Brian; Schrer, Marcia J.; Gaeta, Raphael; Elias, Eileen

    2010-01-01

    Traumatic brain injuries (TBI) can cause multiple medical and functional problems. As the brain is involved in regulating nearly every bodily function, a TBI can affect any part of the body and aspect of cognitive, behavioral, and physical functioning. However, TBI affects each individual differently. Optimal management requires understanding the…

  12. AT2 Receptor and Tissue Injury

    DEFF Research Database (Denmark)

    Namsolleck, Pawel; Recarti, Chiara; Foulquier, Sébastien;

    2014-01-01

    The renin-angiotensin system (RAS) plays an important role in the initiation and progression of tissue injuries in the cardiovascular and nervous systems. The detrimental actions of the AT1 receptor (AT1R) in hypertension and vascular injury, myocardial infarction and brain ischemia are well...... established. In the past twenty years, protective actions of the RAS, not only in the cardiovascular, but also in the nervous system, have been demonstrated. The so-called protective arm of the RAS includes AT2-receptors and Mas receptors (AT2R and MasR) and is characterized by effects different from...

  13. Biophysical mechanisms of traumatic brain injuries.

    Science.gov (United States)

    Young, Lee Ann; Rule, Gregory T; Bocchieri, Robert T; Burns, Jennie M

    2015-02-01

    Despite years of effort to prevent traumatic brain injuries (TBIs), the occurrence of TBI in the United States alone has reached epidemic proportions. When an external force is applied to the head, it is converted into stresses that must be absorbed into the brain or redirected by a helmet or other protective equipment. Complex interactions of the head, neck, and jaw kinematics result in strains in the brain. Even relatively mild mechanical trauma to these tissues can initiate a neurochemical cascade that leads to TBI. Civilians and warfighters can experience head injuries in both combat and noncombat situations from a variety of threats, including ballistic and blunt impact, acceleration, and blast. It is critical to understand the physics created by these threats to develop meaningful improvements to clinical care, injury prevention, and mitigation. Here the authors review the current state of understanding of the complex loading conditions that lead to TBI and characterize how these loads are transmitted through soft tissue, the skull and into the brain, resulting in TBI. In addition, gaps in knowledge and injury thresholds are reviewed, as these must be addressed to better design strategies that reduce TBI incidence and severity.

  14. Therapeutic hypothermia for acute brain injuries.

    Science.gov (United States)

    Andresen, Max; Gazmuri, Jose Tomás; Marín, Arnaldo; Regueira, Tomas; Rovegno, Maximiliano

    2015-06-05

    Therapeutic hypothermia, recently termed target temperature management (TTM), is the cornerstone of neuroprotective strategy. Dating to the pioneer works of Fay, nearly 75 years of basic and clinical evidence support its therapeutic value. Although hypothermia decreases the metabolic rate to restore the supply and demand of O₂, it has other tissue-specific effects, such as decreasing excitotoxicity, limiting inflammation, preventing ATP depletion, reducing free radical production and also intracellular calcium overload to avoid apoptosis. Currently, mild hypothermia (33°C) has become a standard in post-resuscitative care and perinatal asphyxia. However, evidence indicates that hypothermia could be useful in neurologic injuries, such as stroke, subarachnoid hemorrhage and traumatic brain injury. In this review, we discuss the basic and clinical evidence supporting the use of TTM in critical care for acute brain injury that extends beyond care after cardiac arrest, such as for ischemic and hemorrhagic strokes, subarachnoid hemorrhage, and traumatic brain injury. We review the historical perspectives of TTM, provide an overview of the techniques and protocols and the pathophysiologic consequences of hypothermia. In addition, we include our experience of managing patients with acute brain injuries treated using endovascular hypothermia.

  15. Fluorescence diagnosis in tissue injury

    Science.gov (United States)

    Maciel, Vitória H.; Ferreira, Juliana; Bagnato, Vanderlei S.

    2009-06-01

    Background and Objectives: The paper aim was to evaluate the efficacy of the fluorescence spectroscopy in the detection of UV-induced skin change of Wistar rats. Study Design/ Materials and Methods: In a group male Wistar rats, the skin damage was produced by an UV-C lamp, periodically monitored using the laser-induced fluorescence, until complete healing process. After determining a characteristic emission band present in the fluorescence spectra of the induced injuries, the amplitude band monitoring allowed the follow up on the injury and the recovery. Results: We observed the appearance of two new emission bands more evident at the injury spectra when compared to the spectrums from normal non-exposed tissue. Following such spectral bands was possible to observe the establishment and recovery. Conclusions: The fluorescence spectroscopy is a promising technique in distinguishing between normal and UV induced skin change helping the evaluation of changes which are irreversible cancer tissue characteristics.

  16. Interleukin-1α expression precedes IL-1β after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues

    OpenAIRE

    Luheshi Nadia M; Kovács Krisztina J; Lopez-Castejon Gloria; Brough David; Denes Adam

    2011-01-01

    Abstract Background Cerebral ischemia is a devastating condition in which the outcome is heavily influenced by inflammatory processes, which can augment primary injury caused by reduced blood supply. The cytokines interleukin-1α (IL-1α) and IL-1β are key contributors to ischemic brain injury. However, there is very little evidence that IL-1 expression occurs at the protein level early enough (within hours) to influence brain damage after stroke. In order to determine this we investigated the ...

  17. Reducing Secondary Insults in Traumatic Brain Injury

    Science.gov (United States)

    2015-03-01

    distinguished by aligning data from the data logger accelerometer against the simultaneous data streams of ICP, mean anerial pressure, and cerebral ... edema of central nervous system tissue within the closed confines of the cranial vault. The ability to estab- lish and maintain an appropriate...source of cerebral ischemia following severe brain injury in the Trau- matic Coma Data Bank . Acta Neurochir Suppl (Wien) 1993; 59: 121-5. II. Jeremitsky

  18. Traumatic Brain Injury: FDA Research and Actions

    Science.gov (United States)

    ... Control—Traumatic Brain Injury Public Workshop: Advancing the Development of Biomarkers in Traumatic Brain Injury, March 3, 2016 ... Health Cosmetics Dietary Supplements Drugs Food Medical Devices Nutrition Radiation-Emitting Products Tobacco Products Vaccines, Blood & Biologics ...

  19. Traumatic Brain Injury (TBI) Data and Statistics

    Science.gov (United States)

    ... The CDC Cancel Submit Search The CDC Traumatic Brain Injury & Concussion Note: Javascript is disabled or is not ... please visit this page: About CDC.gov . Traumatic Brain Injury & Concussion Basic Information Get the Facts Signs and ...

  20. Brain Injury Safety Tips and Prevention

    Science.gov (United States)

    ... Address What's this? Submit What's this? Submit Button Brain Injury Safety Tips and Prevention Recommend on Facebook ... not grass or dirt. More HEADS UP Video: Brain Injury Safety and Prevention frame support disabled and/ ...

  1. Use of diffusion tensor imaging to assess the impact of normobaric hyperoxia within at-risk pericontusional tissue after traumatic brain injury.

    Science.gov (United States)

    Veenith, Tonny V; Carter, Eleanor L; Grossac, Julia; Newcombe, Virginia F; Outtrim, Joanne G; Nallapareddy, Sridhar; Lupson, Victoria; Correia, Marta M; Mada, Marius M; Williams, Guy B; Menon, David K; Coles, Jonathan P

    2014-10-01

    Ischemia and metabolic dysfunction remain important causes of neuronal loss after head injury, and we have shown that normobaric hyperoxia may rescue such metabolic compromise. This study examines the impact of hyperoxia within injured brain using diffusion tensor imaging (DTI). Fourteen patients underwent DTI at baseline and after 1 hour of 80% oxygen. Using the apparent diffusion coefficient (ADC) we assessed the impact of hyperoxia within contusions and a 1 cm border zone of normal appearing pericontusion, and within a rim of perilesional reduced ADC consistent with cytotoxic edema and metabolic compromise. Seven healthy volunteers underwent imaging at 21%, 60%, and 100% oxygen. In volunteers there was no ADC change with hyperoxia, and contusion and pericontusion ADC values were higher than volunteers (P<0.01). There was no ADC change after hyperoxia within contusion, but an increase within pericontusion (P<0.05). We identified a rim of perilesional cytotoxic edema in 13 patients, and hyperoxia resulted in an ADC increase towards normal (P=0.02). We demonstrate that hyperoxia may result in benefit within the perilesional rim of cytotoxic edema. Future studies should address whether a longer period of hyperoxia has a favorable impact on the evolution of tissue injury.

  2. Imaging of Traumatic Brain Injury

    NARCIS (Netherlands)

    Zagorchev, L.; McAllister, T.

    2011-01-01

    Traumatic brain injury (TBI) represents an enormous public health challenge and is often associated with life long neurobehavioral sequelae in survivors. Several factors including higher percentages of individuals surviving TBI, as well as increasing concern about potential long term sequelae of ev

  3. Traumatic brain injury : from impact to rehabilitation

    NARCIS (Netherlands)

    Halliday, J.; Absalom, A. R.

    2008-01-01

    Traumatic brain injury is a significant cause of mortality and morbidity in our society, particularly among the young. This review discusses the pathophysiology of traumatic brain injury, and current management from the acute phase through to rehabilitation of the traumatic brain injury patient.

  4. Assessment of Students with Traumatic Brain Injury

    Science.gov (United States)

    Chesire, David J.; Buckley, Valerie A.; Canto, Angela I.

    2011-01-01

    The incidence of brain injuries, as well as their impact on individuals who sustain them, has received growing attention from American media in recent years. This attention is likely the result of high profile individuals suffering brain injuries. Greater public awareness of traumatic brain injuries (TBIs) has also been promoted by sources such as…

  5. Knowledge of Traumatic Brain Injury among Educators

    Science.gov (United States)

    Ernst, William J.; Gallo, Adrienne B.; Sellers, Amanda L.; Mulrine, Jessica; MacNamara, Luciana; Abrahamson, Allison; Kneavel, Meredith

    2016-01-01

    The purpose of this study is to determine knowledge of traumatic brain injury among educators. Few studies have examined knowledge of traumatic brain injury in this population and fewer still have included a substantial proportion of general education teachers. Examining knowledge of traumatic brain injury in educators is important as the vast…

  6. Traumatic brain injury and reserve.

    Science.gov (United States)

    Bigler, Erin D; Stern, Yaakov

    2015-01-01

    The potential role of brain and cognitive reserve in traumatic brain injury (TBI) is reviewed. Brain reserve capacity (BRC) refers to preinjury quantitative measures such as brain size that relate to outcome. Higher BRC implies threshold differences when clinical deficits will become apparent after injury, where those individuals with higher BRC require more pathology to reach that threshold. Cognitive reserve (CR) refers to how flexibly and efficiently the individual makes use of available brain resources. The CR model suggests the brain actively attempts to cope with brain damage by using pre-existing cognitive processing approaches or by enlisting compensatory approaches. Standard proxies for CR include education and IQ although this has expanded to include literacy, occupational attainment, engagement in leisure activities, and the integrity of social networks. Most research on BRC and CR has taken place in aging and degenerative disease but these concepts likely apply to the effects of TBI, especially with regards to recovery. Since high rates of TBI occur in those under age 35, both CR and BRC factors likely relate to how the individual copes with TBI over the lifespan. These factors may be particularly relevant to the relationship of developing dementia in the individual who has sustained a TBI earlier in life.

  7. Temperature Effects on Brain Tissue in Compression

    CERN Document Server

    Rashid, Badar; Gilchrist, Michael; 10.1016/j.jmbbm.2012.04.005

    2013-01-01

    Extensive research has been carried out for at least 50 years to understand the mechanical properties of brain tissue in order to understand the mechanisms of traumatic brain injury (TBI). The observed large variability in experimental results may be due to the inhomogeneous nature of brain tissue and to the broad range of test conditions. However, test temperature is also considered as one of the factors influencing the properties of brain tissue. In this research, the mechanical properties of porcine brain have been investigated at 22C (room temperature) and at 37C (body temperature) while maintaining a constant preservation temperature of approximately 4-5C. Unconfined compression tests were performed at dynamic strain rates of 30 and 50/s using a custom made test apparatus. There was no significant difference (p = 0.8559 - 0.9290) between the average engineering stresses of the brain tissue at the two different temperature conditions. The results of this study should help to understand the behavior of bra...

  8. BPSD following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Renato Anghinah

    Full Text Available ABSTRACT Annually, 700,000 people are hospitalized with brain injury acquired after traumatic brain injury (TBI in Brazil. Objective: We aim to review the basic concepts related to TBI, and the most common Behavioral and Psychological Symptoms of Dementia (BPSD findings in moderate and severe TBI survivors. We also discussed our strategies used to manage such patients in the post-acute period. Methods: Fifteen TBI outpatients followed at the Center for Cognitive Rehabilitation Post-TBI of the Clinicas Hospital of the University of São Paulo were submitted to a neurological, neuropsychological, speech and occupational therapy evaluation, including the Mini-Mental State Examination. Rehabilitation strategies will then be developed, together with the interdisciplinary team, for each patient individually. Where necessary, the pharmacological approach will be adopted. Results: Our study will discuss options of pharmacologic treatment choices for cognitive, behavioral, or affective disorders following TBI, providing relevant information related to a structured cognitive rehabilitation service and certainly will offer an alternative for patients and families afflicted by TBI. Conclusion: Traumatic brain injury can cause a variety of potentially disabling psychiatric symptoms and syndromes. Combined behavioral and pharmacological strategies, in the treatment of a set of highly challenging behavioral problems, appears to be essential for good patient recovery.

  9. Severe cerebral vasospasm after traumatic brain injury.

    Science.gov (United States)

    Fehnel, Corey R; Wendell, Linda C; Potter, N Stevenson; Klinge, Petra; Thompson, Bradford B

    2014-07-01

    Severe traumatic brain injury is associated with both acute and delayed neuro- logical injury. Cerebral vasospasm is commonly associated with delayed neurological decline in aneurysmal subarachnoid hemorrhage patients. However, the role played by vasospasm in traumatic brain injury is less clear. Vasospasm occurs earlier, for a shorter duration, and often without significant neurological consequence among traumatic brain injury patients. Detection and management strategies for vasospasm in aneurysmal subarachnoid hemorrhage are not easily transferrable to traumatic brain injury patients. We present a patient with a severe traumatic brain injury who had dramatic improvement following emergent decompressive hemicraniectomy. Two weeks after initial presentation he suffered a precipitous decline despite intensive surveillance. This case illustrates the distinct challenges of diagnosing cerebral vasospasm in the setting of severe traumatic brain injury.

  10. Cerebrospinal fluid enzymes in acute brain injury

    NARCIS (Netherlands)

    A.I.R. Maas (Andrew)

    1977-01-01

    textabstractSevere brain injury is a major cause of death, especially in young men. In 1972, over 20% of all deaths occurring in England and Wales in men aged 15-25 years were due to head injury (Field, 1976). The mortality rate after severe brain injuries is higb. Jennett et al. (1977) reporting on

  11. Traumatic brain injury-induced sleep disorders

    Directory of Open Access Journals (Sweden)

    Viola-Saltzman M

    2016-02-01

    Full Text Available Mari Viola-Saltzman, Camelia Musleh Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA Abstract: Sleep disturbances are frequently identified following traumatic brain injury, affecting 30%–70% of persons, and often occur after mild head injury. Insomnia, fatigue, and sleepiness are the most frequent sleep complaints after traumatic brain injury. Sleep apnea, narcolepsy, periodic limb movement disorder, and parasomnias may also occur after a head injury. In addition, depression, anxiety, and pain are common brain injury comorbidities with significant influence on sleep quality. Two types of traumatic brain injury that may negatively impact sleep are acceleration/deceleration injuries causing generalized brain damage and contact injuries causing focal brain damage. Polysomnography, multiple sleep latency testing, and/or actigraphy may be utilized to diagnose sleep disorders after a head injury. Depending on the disorder, treatment may include the use of medications, positive airway pressure, and/or behavioral modifications. Unfortunately, the treatment of sleep disorders associated with traumatic brain injury may not improve neuropsychological function or sleepiness. Keywords: traumatic brain injury, insomnia, hypersomnia, sleep apnea, periodic limb movement disorder, fatigue

  12. Relationship between Morphofunctional Changes in Open Traumatic Brain Injury and the Severity of Brain Damage in Rats.

    Science.gov (United States)

    Shakova, F M; Barskov, I V; Gulyaev, M V; Prokhorenko, S V; Romanova, G A; Grechko, A V

    2016-07-01

    A correlation between the severity of morphofunctional disturbances and the volume of brain tissue injury determined by MRT was demonstrated on the model of open traumatic brain injury in rats. A relationship between the studied parameters (limb placing and beam walking tests and histological changes) and impact force (the height of load fell onto exposed brain surface) was revealed.

  13. Traumatic brain injury among Indiana state prisoners.

    Science.gov (United States)

    Ray, Bradley; Sapp, Dona; Kincaid, Ashley

    2014-09-01

    Research on traumatic brain injury among inmates has focused on comparing the rate of traumatic brain injury among offenders to the general population, but also how best to screen for traumatic brain injury among this population. This study administered the short version of the Ohio State University Traumatic Brain Injury Identification Method to all male inmates admitted into Indiana state prisons were screened for a month (N = 831). Results indicate that 35.7% of the inmates reported experiencing a traumatic brain injury during their lifetime and that these inmates were more likely to have a psychiatric disorder and a prior period of incarceration than those without. Logistic regression analysis finds that a traumatic brain injury predicts the likelihood of prior incarceration net of age, race, education, and psychiatric disorder. This study suggests that brief instruments can be successfully implemented into prison screenings to help divert inmates into needed treatment.

  14. Mesenchymal Stem Cells in the Treatment of Traumatic Brain Injury

    Science.gov (United States)

    Hasan, Anwarul; Deeb, George; Rahal, Rahaf; Atwi, Khairallah; Mondello, Stefania; Marei, Hany Elsayed; Gali, Amr; Sleiman, Eliana

    2017-01-01

    Traumatic brain injury (TBI) is characterized by a disruption in the normal function of the brain due to an injury following a trauma, which can potentially cause severe physical, cognitive, and emotional impairment. The primary insult to the brain initiates secondary injury cascades consisting of multiple complex biochemical responses of the brain that significantly influence the overall severity of the brain damage and clinical sequelae. The use of mesenchymal stem cells (MSCs) offers huge potential for application in the treatment of TBI. MSCs have immunosuppressive properties that reduce inflammation in injured tissue. As such, they could be used to modulate the secondary mechanisms of injury and halt the progression of the secondary insult in the brain after injury. Particularly, MSCs are capable of secreting growth factors that facilitate the regrowth of neurons in the brain. The relative abundance of harvest sources of MSCs also makes them particularly appealing. Recently, numerous studies have investigated the effects of infusion of MSCs into animal models of TBI. The results have shown significant improvement in the motor function of the damaged brain tissues. In this review, we summarize the recent advances in the application of MSCs in the treatment of TBI. The review starts with a brief introduction of the pathophysiology of TBI, followed by the biology of MSCs, and the application of MSCs in TBI treatment. The challenges associated with the application of MSCs in the treatment of TBI and strategies to address those challenges in the future have also been discussed.

  15. Cell Delivery System for Traumatic Brain Injury

    Science.gov (United States)

    2008-03-21

    REPORT Cell Delivery System for Traumatic Brain Injury 14. ABSTRACT 16. SECURITY CLASSIFICATION OF: We have met all of the milestones outlined in this...COVERED (From - To) 18-Sep-2006 Standard Form 298 (Rev 8/98) Prescribed by ANSI Std. Z39.18 - 17-Mar-2008 Cell Delivery System for Traumatic Brain Injury Report...Manassero*, Justin Kim*, Maureen St Georges*, Nicole Esclamado* and Elizabeth Orwin. “Development of a Cell Delivery System for Traumatic Brain Injury Using

  16. Traumatic Brain Injury: Same or Different

    Science.gov (United States)

    2011-07-22

    TRAUMATIC BRAIN INJURY : SAME OR DIFFERENT Kimberly Meyer, ACNP-BC, CNRN Report Documentation Page Form ApprovedOMB No. 0704-0188 Public reporting...TITLE AND SUBTITLE Traumatic Brain Injury : Same or Different 5a. CONTRACT NUMBER 5b. GRANT NUMBER 5c. PROGRAM ELEMENT NUMBER 6. AUTHOR(S) 5d. PROJECT...official policy of the Department of the Army, Department of Defense, or U.S. Government. DISCLOSURES Nothing to disclose TRAUMATIC BRAIN INJURY Mild

  17. [Mild brain injuries in emergency medicine].

    Science.gov (United States)

    Liimatainen, Suvi; Niskakangas, Tero; Ohman, Juha

    2011-01-01

    Diagnostics and correct classification of mild brain injuries is challenging. Problems caused by insufficient documentation at the acute phase become more obvious in situations in which legal insurance issues are to be considered. A small proportion of patients with mild brain injury suffer from prolonged symptoms. Medical recording and classification of the brain injury at the initial phase should therefore be carried out in a structured manner. The review deals with the diagnostic problems of mild brain injuries and presents a treatment protocol for adult patients at the acute phase, aiming at avoiding prolonged problems.

  18. Hypopituitarism after traumatic brain injury.

    Science.gov (United States)

    Fernandez-Rodriguez, Eva; Bernabeu, Ignacio; Castro, Ana I; Casanueva, Felipe F

    2015-03-01

    The prevalence of hypopituitarism after traumatic brain (TBI) injury is widely variable in the literature; a meta-analysis determined a pooled prevalence of anterior hypopituitarism of 27.5%. Growth hormone deficiency is the most prevalent hormone insufficiency after TBI; however, the prevalence of each type of pituitary deficiency is influenced by the assays used for diagnosis, severity of head trauma, and time of evaluation. Recent studies have demonstrated improvement in cognitive function and cognitive quality of life with substitution therapy in GH-deficient patients after TBI.

  19. Traumatic Brain Injury (TBI) in Kids

    Science.gov (United States)

    ... Research Information Clinical Trials Resources and Publications Traumatic Brain Injury (TBI): Condition Information Skip sharing on social ... external force that affects the functioning of the brain. It can be caused by a bump or ...

  20. Quality of Life Following Brain Injury: Perspectives from Brain Injury Association of America State Affiliates

    Science.gov (United States)

    Degeneffe, Charles Edmund; Tucker, Mark

    2012-01-01

    Objective: to examine the perspectives of brain injury professionals concerning family members' feelings about the quality of life experienced by individuals with brain injuries. Participants: participating in the study were 28 individuals in leadership positions with the state affiliates of the Brain Injury Association of America (BIAA). Methods:…

  1. Chronic issues related to traumatic brain injury : traumatic brain injury is not an incident

    NARCIS (Netherlands)

    Grauwmeijer, Erik; van der Naalt, Joukje; ribbers, gerard

    2016-01-01

    Despite an increased awareness of the long-term consequences of traumatic brain injury, health care professionals often consider traumatic brain injury as an incident. However, patients with traumatic brain injury may experience long-term neurological, cognitive and behavioural problems. Due to the

  2. Increased leakage of brain antigens after traumatic brain injury and effect of immune tolerance induced by cells on traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    YAN Hua; ZHANG Hong-wei; WU Qiao-li; ZHANG Guo-bin; LIU Kui; ZHI Da-shi; HU Zhen-bo; ZENG Xian-wei

    2012-01-01

    Background Although traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances (including water) into brain tissue,few studies of brain antigens leaking into the blood and the pathways have been reported.Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies,but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue.The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury,and provide some new methods to inhibit the immune injury.Methods In part one,methylene blue was injected into the rabbits' cisterna magna after traumatic brain injury,and concentrations of methylene blue and tumor necrosis factor (TNF)-α in blood were detected to determine the permeability of arachnoid granulations.In part two,umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins,and concentrations of interleukin 1 (IL-1),IL-10,interferon (IFN)-y,transforming growth factor (TGF)-β,anti-brain antibodies (ABAb),and IL-12 were measured by ELISA on days 1,3,7,14 and 21 after injury,and the numbers of leukocytes in the blood were counted.Twenty-one days after injury,expression of glutamate in brain tissue was determined by immunohistochemical staining,and neuronal degeneration was detected by H&E staining.Results In part one,blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group (P <0.05).Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid (CSF)injected group were higher than in the control cerebrospinal fluid injected group (P <0.05).In part two,concentrations of IL-1,IFN-y,ABAb,IL-12,expression of glutamate (Glu),neuronal degeneration and number of peripheral blood leukocytes were lower in the group with cell treatment compared to the

  3. 创伤性颅脑损伤后脑组织中TLR4表达的实验研究%Expression of Toll like receptor 4 in injured brain tissue after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    李光照; 赵飞; 杨非; 杭春华

    2011-01-01

    目的 研究创伤性脑损伤(TBI)后损伤灶周围脑组织Toll样受体4(TLR4)的表达,探讨TLR4/NF-κB信号通路在TBI中的作用机制.方法 SD大鼠36只按随机数字表法分为对照组(n=12)、TBI后1d组(n=6)、TBI后3d组(n=12)和TBI后7d组(n=6),后3组采用Feeney自由落体撞击法制作TBI模型,对照组仅行右侧顶部开窗而无TBI.应用RT-PCR、凝胶电泳迁移率实验(EMSA)、ELISA分别检测4组大鼠挫伤脑组织TLR4 mRNA、NF-κB活性、TNF-α和IL-6浓度的变化;免疫组化染色检测对照组和TBI后3d组大鼠挫伤脑组织TLR4的表达.结果 与对照组比较,TBI后1d、3d、7d组TLR4 mRNA表达、NF-κB活性、TNF-α和IL-6浓度均增加,差异有统计学意义(P<0.05);对照组脑组织TLR4表达较少,TBI后3d组创伤灶周围可见大量TLR4阳性细胞,主要表达在皮层胶质细胞、神经元中;NF-κB活性与TLR4 mRNA的表达呈正相关关系(r=0.786,P=-0.000).TNF-α、IL-6与TLR4的表达也呈正相关关系(r=0.517,P=0.010;r=0.503,P=0.012).结论 TBI可引起损伤区脑组织TLR4的表达和下游NF-κB、促炎症因子水平的增加,TLR4/NF-κB信号通路可能在脑组织的继发性损害中起重要作用.%Objective To investigate the expression of Toll like receptor 4(TLR4)in the injured brain tissue atter traumatic brain injury(TBI) and explore the potential role of TLR4/NF-κB in the secondary brain injury.Methods Thirty-six SD rats were randomly divided into control group(n=1 2),TBI inducement for 1 d group(n=6),TBI inducement for 3 d group(n=12)and TBI inducement for 7 d group(n=6).TBI models of the later 3 groups were induced by Feendy's free-falling,and rats of the control group are only performed exposure ofdura of the right parietal lobe.TLR4 mRNA expression in the injured brain tissue was studied by RT-PCR,NF-κB binding activity was detected by electrophoretic mobility shift assay (EMSA),and the TNF-α and IL-6 levels were detected by enzyme linked

  4. Interleukin-1α expression precedes IL-1β after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues

    Directory of Open Access Journals (Sweden)

    Luheshi Nadia M

    2011-12-01

    Full Text Available Abstract Background Cerebral ischemia is a devastating condition in which the outcome is heavily influenced by inflammatory processes, which can augment primary injury caused by reduced blood supply. The cytokines interleukin-1α (IL-1α and IL-1β are key contributors to ischemic brain injury. However, there is very little evidence that IL-1 expression occurs at the protein level early enough (within hours to influence brain damage after stroke. In order to determine this we investigated the temporal and spatial profiles of IL-1α and IL-1β expression after cerebral ischemia. Findings We report here that in mice, as early as 4 h after reperfusion following ischemia induced by occlusion of the middle cerebral artery, IL-1α, but not IL-1β, is expressed by microglia-like cells in the ischemic hemisphere, which parallels an upregulation of IL-1α mRNA. 24 h after ischemia IL-1α expression is closely associated with areas of focal blood brain barrier breakdown and neuronal death, mostly near the penumbra surrounding the infarct. The sub-cellular distribution of IL-1α in injured areas is not uniform suggesting that it is regulated. Conclusions The early expression of IL-1α in areas of focal neuronal injury suggests that it is the major form of IL-1 contributing to inflammation early after cerebral ischemia. This adds to the growing body of evidence that IL-1α is a key mediator of the sterile inflammatory response.

  5. Epidemiology of traumatic brain injury in Europe

    NARCIS (Netherlands)

    W. Peeters (Wouter); R. van den Brande (Ruben); S. Polinder (Suzanne); A. Brazinova (Alexandra); E.W. Steyerberg (Ewout); H.F. Lingsma (Hester); A.I.R. Maas (Andrew)

    2015-01-01

    textabstractBackground: Traumatic brain injury (TBI) is a critical public health and socio-economic problem throughout the world, making epidemiological monitoring of incidence, prevalence and outcome of TBI necessary. We aimed to describe the epidemiology of traumatic brain injury in Europe and to

  6. Treatment of very severe brain injuries

    Institute of Scientific and Technical Information of China (English)

    杨振九; 杨佳勇; 冯承宣; 宋伟健; 孙强

    2004-01-01

    Objective: To sum up the experience in treating very severe traumatic brain injuries.Methods: Retrospective analysis of 68 patients with very severe traumatic brain injuries treated in our hospital from 1997 to 2002 was done.Results: Forty-one (60%) patients died. In the 50 patients treated surgically 27 (40%) survived, 8 recovered well, 9 had moderate disability and 10 had sever deficits. The 18 patients treated non-operatively all died.Conclusions: Much attention should be given to the observation of the changes of severe brain injuries with cranial base injury. Timely operative decompression, basic life support, keeping effective brain blood perfusion and effective oxygen supply, improving cerebral microcirculation and preventing or controlling complications are the main methods to raise the successful rate of treating very severe brain injuries and the life quality of the patients.

  7. Novel roles for metallothionein-I + II (MT-I + II) in defense responses, neurogenesis, and tissue restoration after traumatic brain injury: insights from global gene expression profiling in wild-type and MT-I + II knockout mice.

    Science.gov (United States)

    Penkowa, Milena; Cáceres, Mario; Borup, Rehannah; Nielsen, Finn Cilius; Poulsen, Christian Bjørn; Quintana, Albert; Molinero, Amalia; Carrasco, Javier; Florit, Sergi; Giralt, Mercedes; Hidalgo, Juan

    2006-11-15

    Traumatic injury to the brain is one of the leading causes of injury-related death or disability, especially among young people. Inflammatory processes and oxidative stress likely underlie much of the damage elicited by injury, but the full repertoire of responses involved is not well known. A genomic approach, such as the use of microarrays, provides much insight in this regard, especially if combined with the use of gene-targeted animals. We report here the results of one of these studies comparing wild-type and metallothionein-I + II knockout mice subjected to a cryolesion of the somatosensorial cortex and killed at 0, 1, 4, 8, and 16 days postlesion (dpl) using Affymetrix genechips/oligonucleotide arrays interrogating approximately 10,000 different murine genes (MG_U74Av2). Hierarchical clustering analysis of these genes readily shows an orderly pattern of gene responses at specific times consistent with the processes involved in the initial tissue injury and later regeneration of the parenchyma, as well as a prominent effect of MT-I + II deficiency. The results thoroughly confirmed the importance of the antioxidant proteins MT-I + II in the response of the brain to injury and opened new avenues that were confirmed by immunohistochemistry. Data in KO, MT-I-overexpressing, and MT-II-injected mice strongly suggest a role of these proteins in postlesional activation of neural stem cells.

  8. Anesthesia for Patients with Traumatic Brain Injuries.

    Science.gov (United States)

    Bhattacharya, Bishwajit; Maung, Adrian A

    2016-12-01

    Traumatic brain injury (TBI) represents a wide spectrum of disease and disease severity. Because the primary brain injury occurs before the patient enters the health care system, medical interventions seek principally to prevent secondary injury. Anesthesia teams that provide care for patients with TBI both in and out of the operating room should be aware of the specific therapies and needs of this unique and complex patient population.

  9. Effect of AVP on brain edema following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    XU Miao; SU Wei; HUANG Wei-dong; LU Yuan-qiang; XU Qiu-ping; CHEN Zhao-jun

    2007-01-01

    Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤ 8) and moderate traumatic brain injury group (MTBI, GCS>8).Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group)and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan.Results: plasma AVP levels (ng/L) were (mean±SD): control, 3.06±1.49; MTBI, 38.12±7.25; and STBI, 66.61±17.10.The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0.01). And the AVP level was correlated with the severity (STBI r=0.919, P<0.01; MTBI r=0.724, P<0.01) and the duration of brain edema (STBI r=0.790, P<0.01; MTBI r=0.712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.

  10. Family needs after brain injury

    DEFF Research Database (Denmark)

    Norup, Anne; Perrin, Paul B; Cuberos-Urbano, Gustavo

    2015-01-01

    OBJECTIVE: The objective of this study was to explore differences by country in the importance of family needs after traumatic brain injury (TBI), as well as differences in met/unmet needs. METHOD: Two hundred and seventy-one family members of an individual with TBI in Mexico, Colombia, Spain......, Denmark, and Norway completed the Family Needs Questionnaire. RESULTS: Eight of the ten needs rated as most important globally were from the Health Information subscale. Importance ratings on the Health Information, Professional Support, and Involvement With Care subscales were similar across countries......, but Mexican family members rated Instrumental Support needs as less important than Colombian, Spanish, and Danish family members, and also rated their Community Support needs as less important than Danish and Spanish family members. Mexican family member's rated emotional support needs as less important than...

  11. Traumatic Brain Injury in Kenya

    Directory of Open Access Journals (Sweden)

    Benson Kinyanjui

    2016-03-01

    Full Text Available Kenya has a disproportionately high rate of road traffic accidents each year, many of them resulting in traumatic brain injuries (TBIs. A review of articles written on issues pertaining to the medical treatment of people with TBI in the past 15 years in Kenya indicates a significantly high incidence of TBIs and a high mortality rate. This article reviews the available literature as a first step in exploring the status of rehabilitation of Kenyans with cognitive impairments and other disabilities resulting from TBIs. From this preliminary review, it is apparent that despite TBI being a pervasive public health problem in Kenya, it has not received due attention in the public and private sectors as evidenced by a serious lack of post-acute rehabilitation services for people with TBIs. Implications for this lack of services are discussed and recommendations are made for potential approaches to this problem.

  12. Hypopituitarism in Traumatic Brain Injury

    DEFF Research Database (Denmark)

    Klose, Marianne; Feldt-Rasmussen, Ulla

    2015-01-01

    While hypopituitarism after traumatic brain injury (TBI) was previously considered rare, it is now thought to be a major cause of treatable morbidity among TBI survivors. Consequently, recommendations for assessment of pituitary function and replacement in TBI were recently introduced. Given...... the high incidence of TBI with more than 100 pr. 100,000 inhabitants, TBI would be by far the most common cause of hypopituitarism if the recently reported prevalence rates hold true. The disproportion between this proposed incidence and the occasional cases of post-TBI hypopituitarism in clinical practice...... justifies reflection as to whether hypopituitarism has been unrecognized in TBI patients or whether diagnostic testing designed for high risk populations such as patients with obvious pituitary pathology has overestimated the true risk and thereby the disease burden of hypopituitarism in TBI. The findings...

  13. Increased CD133+ cell infiltration in the rat brain following fluid percussion injury

    Institute of Scientific and Technical Information of China (English)

    Ming Wei; Ziwei Zhou; Shenghui Li; Chengwei Jing; Dashi Zhi; Jianning Zhang

    2012-01-01

    The prominin-1/CD133 epitope is expressed in undifferentiated cells. Studies have reported that craniocerebral trauma in animal models of fluid percussion injury induces production of a specific stem cell subgroup. It has been hypothesized that fluid percussion injury induces CD133+ cell infiltration in the brain tissue. The present study established a traumatic brain injury model through fluid percussion injury. Immunohistochemical staining showed significantly increased CD133 antigen expression in the rat brain following injury. CD133+ cells were mainly distributed in hippocampal CA1-3 regions, as well as the dentate gyrus and hilus, of the lesioned hemisphere. Occasional cells were also detected in the cortex. In addition, reverse transcription-PCR revealed that no change in CD133 mRNA expression in injured brain tissue. These results suggested that fluid percussion injury induced CD133 antigen expression in the brain tissues as a result of conformational epitope changes, but not transcriptional expression.

  14. 尼莫同对大鼠创伤性脑损伤后脑组织NF-κB表达和活化的影响%Effect of nimotop on expression and activation of NF-κB in the rat brain tissues after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    陈兵; 吴华伟; 尹延庆; 彭浩; 龙霄翱; 梁远生; 徐军发; 陈东

    2009-01-01

    Objective To explore the effect of nimotop on expression and activation of NF-κB after traumatic brain injury. Methods Local traumatic brain injury was made in rats by strike with freefalling hammer. Then, the rats were injected with dexamethasone and nimotop respectively to detect expressions of NF-κB P65 and IκBα in rat brain tissues by means of immunohistochemistry. Results The expression of NF-κB P65 in brain tissue was obviously increased after traumatic brain injury and reached peak at 24 hours, which lasted for 96 hours. The expression of IκB was obviously decreased after traumatic brain injury and lowered to the least at 24 hours. Both dexamethasone and nimotop could decrease the expression of NF-κB P65 and increase the expression of IκBα in rat brain tissues after traumatic brain injury (P<0.01), when nimotop was better than dexamethasone (P<0.05). Conclusions Nimotop can inhibit the expression and activation of NF-κB and hence regulate inflammatory reaction after traumatic brain injury.%目的 观察尼莫同对大鼠创伤性脑损伤(traumatic brain injury,TBI)后NF-κB表达和活化的影响. 方法制作SD大鼠落体撞击脑损伤模型,分别给予地塞米松和尼莫同干预,检测脑组织NF-κB P65和IκBα的表达. 结果 TBI后脑组织NF-κB P65的表达明显增加,伤后24 h最低,持续到96 h仍有明显表达;IκBα表达明显减弱,伤后24 h达到低峰.尼莫同与地塞米松可以显著降低TBI后NF-κB P65的表达和增加IκBα的表达(P<0.01),尼莫同作用优于地塞米松(P<0.05). 结论尼莫同可以抑制TBI后NF-κB表达和活化,从而调节脑损伤后的炎症反应.

  15. Clinimetric measurement in traumatic brain injuries.

    Science.gov (United States)

    Opara, J A; Małecka, E; Szczygiel, J

    2014-06-15

    Traumatic brain injury is a leading cause of death and disability worldwide. Every year, about 1.5 million affected people die and several millions receive emergency treatment. Most of the burden (90%) is in low and middle-income countries. The costs of care depend on the level of disability. The burden of care after traumatic brain injury is caused by disability as well as by psychosocial and emotional sequelae of injury. The final consequence of brain injury is the reduction of quality of life. It is very difficult to predict the outcome after traumatic brain injury. The basic clinical model included four predictors: age, score in Glasgow coma scale, pupil reactivity, and the presence of major extracranial injury. These are the neuroradiological markers of recovery after TBI (CT, MRI and PET) and biomarkers: genetic markers of ApoE Gene, ectoenzyme CD 38 (cluster of differentiation 38), serum S100B, myelin basic protein (MBP), neuron specific endolase (NSE), and glial fibrillary acidic protein (GPAP). These are many clinimetric scales which are helpful in prognosing after head injury. In this review paper, the most commonly used scales evaluating the level of consciousness after traumatic brain injury have been presented.

  16. Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1.

    Science.gov (United States)

    Henninger, Nils; Bouley, James; Sikoglu, Elif M; An, Jiyan; Moore, Constance M; King, Jean A; Bowser, Robert; Freeman, Marc R; Brown, Robert H

    2016-04-01

    Axonal degeneration is a critical, early event in many acute and chronic neurological disorders. It has been consistently observed after traumatic brain injury, but whether axon degeneration is a driver of traumatic brain injury remains unclear. Molecular pathways underlying the pathology of traumatic brain injury have not been defined, and there is no efficacious treatment for traumatic brain injury. Here we show that mice lacking the mouse Toll receptor adaptor Sarm1 (sterile α/Armadillo/Toll-Interleukin receptor homology domain protein) gene, a key mediator of Wallerian degeneration, demonstrate multiple improved traumatic brain injury-associated phenotypes after injury in a closed-head mild traumatic brain injury model. Sarm1(-/-) mice developed fewer β-amyloid precursor protein aggregates in axons of the corpus callosum after traumatic brain injury as compared to Sarm1(+/+) mice. Furthermore, mice lacking Sarm1 had reduced plasma concentrations of the phophorylated axonal neurofilament subunit H, indicating that axonal integrity is maintained after traumatic brain injury. Strikingly, whereas wild-type mice exibited a number of behavioural deficits after traumatic brain injury, we observed a strong, early preservation of neurological function in Sarm1(-/-) animals. Finally, using in vivo proton magnetic resonance spectroscopy we found tissue signatures consistent with substantially preserved neuronal energy metabolism in Sarm1(-/-) mice compared to controls immediately following traumatic brain injury. Our results indicate that the SARM1-mediated prodegenerative pathway promotes pathogenesis in traumatic brain injury and suggest that anti-SARM1 therapeutics are a viable approach for preserving neurological function after traumatic brain injury.

  17. [Cellular and molecular mechanisms of radiation-induced brain injury: can peripheral markers be detected?].

    Science.gov (United States)

    Piskunov, A K; Nikitin, K V; Potapov, A A

    2015-01-01

    Investigation of the mechanisms of radiation-induced brain injury is a relevant fundamental objective of radiobiology and neuroradiology. Damage to the healthy brain tissue is the key factor limiting the application of radiation therapy in patients with nervous systems neoplasms. Furthermore, postradiation brain injury can be clinically indiscernible from continued tumor growth and requires differential diagnosis. Thus, there exists high demand for biomarkers of radiation effects on the brain in neurosurgery and radiobiology. These markers could be used for better understanding and quantifying the effects of ionizing radiation on brain tissues, as well as for elaborating personalized therapy. Despite the high demand, biomarkers of radiation-induced brain injury have not been identified thus far. The cellular and molecular mechanisms of the effect of ionizing radiation on the brain were analyzed in this review in order to identify potential biomarkers of radiation-induced injury to nervous tissue.

  18. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Science.gov (United States)

    2010-10-01

    ... 45 Public Welfare 4 2010-10-01 2010-10-01 false Eligibility criteria: Traumatic brain injury. 1308... DISABILITIES Health Services Performance Standards § 1308.16 Eligibility criteria: Traumatic brain injury. A child is classified as having traumatic brain injury whose brain injuries are caused by an...

  19. Cognitive impairments in patients with brain injury

    Directory of Open Access Journals (Sweden)

    Vladimir Vladimirovich Zakharov

    2013-01-01

    Full Text Available The paper gives the data of Russian and foreign authors and the results of this paper authors’ investigation of higher cerebral functions in patients who have sustained brain injury (BI. It shows their high prevalence, the predominance of cognitive impairments (CI over neurological disorders in patients with mild and moderate injury, presents their quantitative and qualitative features (a preponderance of focal symptoms in severe injury and neurodynamic disorders in mild injury, describes the predictors of their course and prognosis (the degree of injury is one of the most important predictors, and discusses current trends in the medical correction of detected abnormalities.

  20. Nonsurgical interventions after mild traumatic brain injury

    DEFF Research Database (Denmark)

    Nygren-de Boussard, Catharina; Holm, Lena W; Cancelliere, Carol;

    2014-01-01

    OBJECTIVE: To synthesize the best available evidence regarding the impact of nonsurgical interventions on persistent symptoms after mild traumatic brain injury (MTBI). DATA SOURCES: MEDLINE and other databases were searched (2001-2012) with terms including "rehabilitation." Inclusion criteria wer...

  1. Reducing Secondary Insults in Traumatic Brain Injury

    Science.gov (United States)

    2013-04-01

    persons, and leaves 99,000 persons permanently disabled [1]. The total cost for treatment and rehabilitation of patients with brain injuries is...registry based or retrospective or include only secondary insults that occur in the intensive care unit ( ICU ) setting. Most prior investigations have...in the surgical and neurosurgical ICU diagnosed with a traumatic brain injury requiring a diagnostic procedure were eligible for the study. The study

  2. Mesenchymal stromal cells for traumatic brain injury

    OpenAIRE

    Pischiutta,

    2014-01-01

    The multiple pathological cascades activated after traumatic brain injury (TBI) and their extended nature offer the possibility for therapeutic interventions possibly affecting multiple injury mechanisms simultaneously. Mesenchymal stromal cell (MSC) therapy matches this need, being a bioreactor of a variety of molecules able to interact and modify the injured brain microenvironment. Compared to autologous MSCs, bank stored GMP-graded allogenic MSCs appear to be a realistic choice for TBI ...

  3. Traumatic brain injuries: Forensic and expertise aspects

    OpenAIRE

    Vuleković Petar; Simić Milan; Mišić-Pavkov Gordana; Cigić Tomislav; Kojadinović Željko; Đilvesi Đula

    2008-01-01

    Introduction. Traumatic brain injuries have major socio-economic importance due to their frequency, high mortality and serious consequences. According to their nature the consequences of these injuries may be classified as neurological, psychiatric and esthetic. Various lesions of brain structures cause neurological consequences such as disturbance of motor functions, sensibility, coordination or involuntary movements, speech disturbances and other deviations, as well as epilepsy. Psychiatric...

  4. Spectroscopic Monitoring of Kidney Tissue Ischemic Injury

    Energy Technology Data Exchange (ETDEWEB)

    Demos, S G; Fitzgerald, J T; Michalopoulou, A P; Troppmann, C

    2004-03-11

    Noninvasive evaluation of tissue viability of donor kidneys used for transplantation is an issue that current technology is not able to address. In this work, we explore optical spectroscopy for its potential to assess the degree of ischemic damage in kidney tissue. We hypothesized that ischemic damage to kidney tissue will give rise to changes in its optical properties which in turn may be used to asses the degree of tissue injury. The experimental results demonstrate that the autofluorescence intensity of the injured kidney is decreasing as a function of time exposed to ischemic injury. Changes were also observed in the NIR light scattering intensities most probably arising from changes due to injury and death of the tissue.

  5. Understanding Traumatic Brain Injury: An Introduction

    Science.gov (United States)

    Trudel, Tina M.; Scherer, Marcia J.; Elias, Eileen

    2009-01-01

    This article is the first of a multi-part series on traumatic brain injury (TBI). Historically, TBI has received very limited national public policy attention and support. However since it has become the signature injury of the military conflicts in Iraq and Afghanistan, TBI has gained the attention of elected officials, military leaders,…

  6. Perioperative management of traumatic brain injury

    OpenAIRE

    Curry, Parichat; Viernes, Darwin; Sharma, Deepak

    2011-01-01

    Traumatic brain injury (TBI) is a major public health problem and the leading cause of death and disability worldwide. Despite the modern diagnosis and treatment, the prognosis for patients with TBI remains poor. While severity of primary injury is the major factor determining the outcomes, the secondary injury caused by physiological insults such as hypotension, hypoxemia, hypercarbia, hypocarbia, hyperglycemia and hypoglycemia, etc. that develop over time after the onset of the initial inju...

  7. Occupational Therapy and Community Reintegration of Persons with Brain Injury

    Science.gov (United States)

    Fact Sheet Occupational Therapy and Community Reintegration of Persons With Brain Injury Brain injuries can affect motor, sensory, cognitive, and behavioral functioning. A person who has sustained a brain ...

  8. Traumatic brain injuries: Forensic and expertise aspects

    Directory of Open Access Journals (Sweden)

    Vuleković Petar

    2008-01-01

    Full Text Available Introduction. Traumatic brain injuries have major socio-economic importance due to their frequency, high mortality and serious consequences. According to their nature the consequences of these injuries may be classified as neurological, psychiatric and esthetic. Various lesions of brain structures cause neurological consequences such as disturbance of motor functions, sensibility, coordination or involuntary movements, speech disturbances and other deviations, as well as epilepsy. Psychiatric consequences include cognitive deficit, emotional disturbances and behavior disturbances. Criminal-legal aspect of traumatic brain injuries and litigation. Criminal-legal aspect of traumatic brain injuries expertise understands the qualification of these injuries as mild, serious and qualified serious body injuries as well as the expertise about the mechanisms of their occurrence. Litigation expertise includes the estimation of pain, fear, diminished, i.e. lost vital activity and disability, esthetic marring, and psychological suffer based on the diminished general vital activity and esthetic marring. Competence and timing of expertise. Evaluation of consequences of traumatic brain injuries should be performed only when it can be positively confirmed that they are permanent, i.e. at least one year after the injury. Expertise of these injuries is interdisciplinary. Among clinical doctors the most competent medical expert is the one who is in charge for diagnostics and injury treatment, with the recommendation to avoid, if possible, the doctor who conducted treatment. For the estimation of general vital activity, the neurological consequences, pain and esthetic marring expertise, the most competent doctors are neurosurgeon and neurologist. Psychological psychiatric consequences and fear expertise have to be performed by the psychiatrist. Specialists of forensic medicine contribute with knowledge of criminal low and legal expertise.

  9. Modeling Blast-Related Brain Injury

    Science.gov (United States)

    2008-12-01

    02139 D. Moore Defense and Veterans Brain Injury Center (WRAMC) 6900 Georgia Ave. NW, Washington, DC 20307 L. Noels University of Liege Chemin des...chevreuils 1, B4000 Liege , Belgium ABSTRACT Recent military conflicts in Iraq and Afghanistan have highlighted the wartime effect of traumatic brain in

  10. The role of free radicals in traumatic brain injury.

    Science.gov (United States)

    O'Connell, Karen M; Littleton-Kearney, Marguerite T

    2013-07-01

    Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.

  11. [Differentiated treatment of acute diffuse brain injuries].

    Science.gov (United States)

    Pedachenko, E G; Dziak, L A; Sirko, A G

    2012-01-01

    Diagnosis and treatment results of 57 patients with acute diffuse brain injury have been analyzed. Patients were divided into two groups: first study period 2000-2005; second study period 2006-2010. The main differences between the first and the second study periods were in health condition and brain functions monitoring parameters, therapy approaches and goals. Increasing of axial and lateral dislocation symptoms during progression from the first type of diffuse injury to the fourth one is related to intracranial hypertension (ICH) occurrence rate and significance it's significance. During the second study period, ICH was found in 25% patients with the second type of injury, 57% patients with the third type of injury, and 80%, with the fourth type of injury. Mean ICP in the group of patients with the second type of diffuse injury comprised 14.4 +/- 6.6 mmHg; with the third type of injury, 30 +/- 20.6 mmHg; with the fourth type of injuty, 37.6 +/- 14.1 mmHg. Introduction of differentiated approach to conservative or surgical treatment method application to acute diffuse brain injuries patients based on ICP monitoring data led to 13.8% reduction in mortality in the second study period compared with the first study period.

  12. TRAUMATIC BRAIN INJURY CHILDREN: A LITERATURE REVIEW

    Directory of Open Access Journals (Sweden)

    Denismar Borges de Miranda

    2013-09-01

    Full Text Available Objective: to know the scientific literature on head injury in children. Method: this study is an integrative review of published articles in the database SciELO the period 2000-2010. Results: 10 articles were analyzed, from which emerged four categories: causes of traumatic brain child infant prognosis of traumatic brain child, treating children victims of child head injury and complications of therapy used for child victims of traumatic brain injury in children. Conclusions: there is consensus among the authors investigated the factors associated with better prognosis of traumatic brain child, remain vague and uncertain. They add that the success of this customer service related to the control of complications arising from cerebral trauma and mostly are treatable and / or preventable.

  13. Recovery after Brain Injury: Mechanisms and Principles

    Directory of Open Access Journals (Sweden)

    Randolph J. Nudo

    2013-12-01

    Full Text Available The past 20 years have represented an important period in the development of principles underlying neuroplasticity, especially as they apply to recovery from neurological injury. It is now generally accepted that acquired brain injuries, such as occur in stroke or trauma, initiate a cascade of regenerative events that last for at least several weeks, if not months. Many investigators have pointed out striking parallels between post-injury plasticity and the molecular and cellular events that take place during normal brain development. As evidence for the principles and mechanisms underlying post-injury neuroplasticity has been gleaned from both animal models and human populations, novel approaches to therapeutic intervention have been proposed. One important theme has persisted as the sophistication of clinicians and scientists in their knowledge of neuroplasticity mechanisms has grown: Behavioral experience is the most potent modulator of brain plasticity. While there is substantial evidence for this principle in normal, healthy brains, the injured brain is particularly malleable. Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways. This paper reviews selected studies that have demonstrated the neurophysiological and neuroanatomical changes that are triggered by motor experience, by injury, and the interaction of these processes. In addition, recent studies using new and elegant techniques are providing novel perspectives on the events that take place in the injured brain, providing a real-time window into post-injury plasticity. These new approaches are likely to accelerate the pace of basic research, and provide a wealth of opportunities to translate basic principles into therapeutic methodologies.

  14. Traumatic brain injury, neuroimaging, and neurodegeneration.

    Science.gov (United States)

    Bigler, Erin D

    2013-01-01

    Depending on severity, traumatic brain injury (TBI) induces immediate neuropathological effects that in the mildest form may be transient but as severity increases results in neural damage and degeneration. The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase. This review examines how neuroimaging may be used in TBI to understand (1) the dynamic changes that occur in brain development relevant to understanding the effects of TBI and how these relate to developmental stage when the brain is injured, (2) how TBI interferes with age-typical brain development and the effects of aging thereafter, and (3) how TBI results in greater frontotemporolimbic damage, results in cerebral atrophy, and is more disruptive to white matter neural connectivity. Neuroimaging quantification in TBI demonstrates degenerative effects from brain injury over time. An adverse synergistic influence of TBI with aging may predispose the brain injured individual for the development of neuropsychiatric and neurodegenerative disorders long after surviving the brain injury.

  15. Traumatic brain injury, neuroimaging, and neurodegeneration

    Directory of Open Access Journals (Sweden)

    Erin D. Bigler

    2013-08-01

    Full Text Available Depending on severity, traumatic brain injury (TBI induces immediate neuropathological effects that in the mildest form may be transient but as severity increases results in neural damage and degeneration. The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase. This review examines how neuroimaging may be used in TBI to understand (1 the dynamic changes that occur in brain development relevant to understanding the effects of TBI and how these relate to developmental stage when the brain is injured, (2 how TBI interferes with age-typical brain development and the effects of aging thereafter, and (3 how TBI results in greater frontotemporolimbic damage, results in cerebral atrophy, and is more disruptive to white matter neural connectivity. Neuroimaging quantification in TBI demonstrates degenerative effects from brain injury over time. An adverse synergistic influence of TBI with aging may predispose the brain injured individual for the development of neuropsychiatric and neurodegenerative disorders long after surviving the brain injury.

  16. Traumatic brain injury and obesity induce persistent central insulin resistance.

    Science.gov (United States)

    Karelina, Kate; Sarac, Benjamin; Freeman, Lindsey M; Gaier, Kristopher R; Weil, Zachary M

    2016-04-01

    Traumatic brain injury (TBI)-induced impairments in cerebral energy metabolism impede tissue repair and contribute to delayed functional recovery. Moreover, the transient alteration in brain glucose utilization corresponds to a period of increased vulnerability to the negative effects of a subsequent TBI. In order to better understand the factors contributing to TBI-induced central metabolic dysfunction, we examined the effect of single and repeated TBIs on brain insulin signalling. Here we show that TBI induced acute brain insulin resistance, which resolved within 7 days following a single injury but persisted until 28 days following repeated injuries. Obesity, which causes brain insulin resistance and neuroinflammation, exacerbated the consequences of TBI. Obese mice that underwent a TBI exhibited a prolonged reduction of Akt (also known as protein kinase B) signalling, exacerbated neuroinflammation (microglial activation), learning and memory deficits, and anxiety-like behaviours. Taken together, the transient changes in brain insulin sensitivity following TBI suggest a reduced capacity of the injured brain to respond to the neuroprotective and anti-inflammatory actions of insulin and Akt signalling, and thus may be a contributing factor for the damaging neuroinflammation and long-lasting deficits that occur following TBI.

  17. Influence of indomethacin on free radical reactions in brain tissues ofrabbits with brain injury%消炎痛对兔脑外伤后脑组织氧自由基反应的影响

    Institute of Scientific and Technical Information of China (English)

    谭占国; 柴宗举; 冯祖荫

    2001-01-01

    目的:探讨消炎痛对急性实验性脑外伤后兔脑组织氧自由基反应的影响。方法:30只家兔随机分为A组(正常对照组)、B组(生理盐水治疗组)及C组(消炎痛治疗组),每组10只动物。其中A组不致脑外伤,作为正常对照。B、C2组采用自由落体打击法建立兔闭合性脑外伤模型。C组于外伤后.10min开始,经耳缘静脉缓慢注入消炎痛针剂。B组于外伤后相同时间同样方法注入等量的生理盐水,作为生理盐水治疗对照。B、C2组于外伤后4h将动物处死,完整取出大脑半球以干湿重比较法测定大脑含水量;取挫伤灶周边脑组织制成匀浆,生化测定脑组织中过氧化物歧化酶(SOD)活性和脂质过氧化物(LPO)含量。结果:B组动物致脑外伤后4h,脑组织含水量及LPO含量分别为(79.918±1.449)%和(143.5±24.9)nmol/g,较对照组显著为高(P0.05);SOD活性为(2.25±0.21)Nu/mg,较B组明显升高(P 0.05). The mean value of SOD activity was (2.25 + 0.21 ) Nu/mg, higher than that in group B ( P < 0.05). Conclusion:IM treatment at the early stage of brain injury could attenuate oxygen free radical reaction in injured brain tissues, protect bloodbrain barrier, prevent traumatic cerebral edema being formed and developing fmther.

  18. Catecholamines and cognition after traumatic brain injury.

    Science.gov (United States)

    Jenkins, Peter O; Mehta, Mitul A; Sharp, David J

    2016-09-01

    Cognitive problems are one of the main causes of ongoing disability after traumatic brain injury. The heterogeneity of the injuries sustained and the variability of the resulting cognitive deficits makes treating these problems difficult. Identifying the underlying pathology allows a targeted treatment approach aimed at cognitive enhancement. For example, damage to neuromodulatory neurotransmitter systems is common after traumatic brain injury and is an important cause of cognitive impairment. Here, we discuss the evidence implicating disruption of the catecholamines (dopamine and noradrenaline) and review the efficacy of catecholaminergic drugs in treating post-traumatic brain injury cognitive impairments. The response to these therapies is often variable, a likely consequence of the heterogeneous patterns of injury as well as a non-linear relationship between catecholamine levels and cognitive functions. This individual variability means that measuring the structure and function of a person's catecholaminergic systems is likely to allow more refined therapy. Advanced structural and molecular imaging techniques offer the potential to identify disruption to the catecholaminergic systems and to provide a direct measure of catecholamine levels. In addition, measures of structural and functional connectivity can be used to identify common patterns of injury and to measure the functioning of brain 'networks' that are important for normal cognitive functioning. As the catecholamine systems modulate these cognitive networks, these measures could potentially be used to stratify treatment selection and monitor response to treatment in a more sophisticated manner.

  19. Oxygen radicals, inflammation, and tissue injury.

    Science.gov (United States)

    Ward, P A; Warren, J S; Johnson, K J

    1988-01-01

    Inflammatory reactions often result in the activation and recruitment of phagocytic cells (e.g., neutrophils and/or tissue macrophages) whose products result in injury to the tissue. In killing of endothelial cells by activated neutrophils as well as in lung injury produced by either activated neutrophils or activated macrophages there is evidence that H2O2 and iron play a role. HO. may be a key oxygen product related to the process of injury. Endothelial cells in some vascular compartments may be susceptible to neutrophil mediated injury in a manner that is independent of oxygen radicals. On the basis of in vitro observations, a synergy exits between platelets and neutrophils, resulting in enhanced oxygen radical formation by the latter. Finally, the cytokines, interleukin 1 and tumor necrosis factor, released from macrophages have both direct stimulatory effects on oxygen radical formation in neutrophils and can "prime" macrophages for enhanced oxygen radical responses to other agonists. Cytokines may also alter endothelial cells rendering them more susceptible to oxygen radical mediated injury by neutrophils. This suggests a complex network of interactions between phagocytic cells and peptide mediators, the result of which is acute, oxygen radical mediated tissue injury.

  20. A High Rate Tension Device for Characterizing Brain Tissue

    CERN Document Server

    Rashid, Badar; Gilchrist, Michael; 10.1177/1754337112436900

    2013-01-01

    The mechanical characterization of brain tissue at high loading velocities is vital for understanding and modeling Traumatic Brain Injury (TBI). The most severe form of TBI is diffuse axonal injury (DAI) which involves damage to individual nerve cells (neurons). DAI in animals and humans occurs at strains > 10% and strain rates > 10/s. The mechanical properties of brain tissues at these strains and strain rates are of particular significance, as they can be used in finite element human head models to accurately predict brain injuries under different impact conditions. Existing conventional tensile testing machines can only achieve maximum loading velocities of 500 mm/min, whereas the Kolsky bar apparatus is more suitable for strain rates > 100/s. In this study, a custom-designed high rate tension device is developed and calibrated to estimate the mechanical properties of brain tissue in tension at strain rates < 90/s, while maintaining a uniform velocity. The range of strain can also be extended to 100% de...

  1. Hyperthermia and fever control in brain injury.

    Science.gov (United States)

    Badjatia, Neeraj

    2009-07-01

    Fever in the neurocritical care setting is common and has a negative impact on outcome of all disease types. Meta-analyses have demonstrated that fever at onset and in the acute setting after ischemic brain injury, intracerebral hemorrhage, and cardiac arrest has a negative impact on morbidity and mortality. Data support that the impact of fever is sustained for longer durations after subarachnoid hemorrhage and traumatic brain injury. Recent advances have made eliminating fever and maintaining normothermia feasible. However, there are no prospective randomized trials demonstrating the benefit of fever control in these patient populations, and important questions regarding indications and timing remain. The purpose of this review is to analyze the data surrounding the impact of fever across a range of neurologic injuries to better understand the optimal timing and duration of fever control. Prospective randomized trials are needed to determine whether the beneficial impact of secondary injury prevention is outweighed by the potential risks of prolonged fever control.

  2. Molecular Mechanisms of Neonatal Brain Injury

    Directory of Open Access Journals (Sweden)

    Claire Thornton

    2012-01-01

    Full Text Available Fetal/neonatal brain injury is an important cause of neurological disability. Hypoxia-ischemia and excitotoxicity are considered important insults, and, in spite of their acute nature, brain injury develops over a protracted time period during the primary, secondary, and tertiary phases. The concept that most of the injury develops with a delay after the insult makes it possible to provide effective neuroprotective treatment after the insult. Indeed, hypothermia applied within 6 hours after birth in neonatal encephalopathy reduces neurological disability in clinical trials. In order to develop the next generation of treatment, we need to know more about the pathophysiological mechanism during the secondary and tertiary phases of injury. We review some of the critical molecular events related to mitochondrial dysfunction and apoptosis during the secondary phase and report some recent evidence that intervention may be feasible also days-weeks after the insult.

  3. Fatigue in adults with traumatic brain injury

    DEFF Research Database (Denmark)

    Mollayeva, Tatyana; Kendzerska, Tetyana; Mollayeva, Shirin;

    2013-01-01

    . CONCLUSIONS: The review will summarize the current knowledge in the field with the aim of increasing understanding and guiding future research on the associations between fatigue and clinically important factors, as well as the consequences of fatigue in traumatic brain injury. PROSPERO registry number: CRD......BACKGROUND: Despite strong indications that fatigue is the most common and debilitating symptom after traumatic brain injury, little is known about its frequency, natural history, or relation to other factors. The current protocol outlines a strategy for a systematic review that will identify......, assess, and critically appraise studies that assessed predictors for fatigue and the consequences of fatigue on at least two separate time points following traumatic brain injury. METHODS/DESIGN: MEDLINE, EMBASE, the Cochrane Database of Systematic Reviews, CINAHL, and PsycINFO will be systematically...

  4. Diffusion-weighted imaging predicts cognition in pediatric brain injury.

    Science.gov (United States)

    Babikian, Talin; Tong, Karen A; Galloway, Nicholas R; Freier-Randall, Mary-Catherin; Obenaus, André; Ashwal, Stephen

    2009-12-01

    Apparent diffusion coefficient maps from diffusion-weighted imaging predict gross neurologic outcome in adults with traumatic brain injury. Few studies in children have been reported, and none have used apparent diffusion coefficient maps to predict long-term (>1 year) neurocognitive outcomes. In this study, pooled regional and total brain diffusion coefficients were used to predict long-term outcomes in 17 pediatric brain injury patients. Apparent diffusion coefficient values were grouped into peripheral and deep gray and white matter, posterior fossa, and total brain. Regions of interest excluded areas that appeared abnormal on T(2)-weighted images. Apparent diffusion coefficient values from peripheral regions were inversely correlated with cognitive functioning. No significant correlations were apparent between the cognitive scores and apparent diffusion coefficient values for deep tissue or the posterior fossa. Regression analyses suggested that combined peripheral gray and white matter apparent diffusion coefficients explained 42% of the variance in the combined neurocognitive index. Peripheral gray diffusion coefficients alone explained an additional 20% of variance after accounting for clinical variables. These results suggest that obtaining apparent diffusion coefficient values, specifically from peripheral brain regions, may predict long-term outcome after pediatric brain injury. Discrepancies in the literature on this topic, as well as possible explanations, including sampling and clinical considerations, are discussed.

  5. Managing traumatic brain injury secondary to explosions

    Directory of Open Access Journals (Sweden)

    Burgess Paula

    2010-01-01

    Full Text Available Explosions and bombings are the most common deliberate cause of disasters with large numbers of casualties. Despite this fact, disaster medical response training has traditionally focused on the management of injuries following natural disasters and terrorist attacks with biological, chemical, and nuclear agents. The following article is a clinical primer for physicians regarding traumatic brain injury (TBI caused by explosions and bombings. The history, physics, and treatment of TBI are outlined.

  6. Functional Recovery After Severe Traumatic Brain Injury

    DEFF Research Database (Denmark)

    Hart, Tessa; Kozlowski, Allan; Whyte, John

    2014-01-01

    OBJECTIVE: To examine person, injury, and treatment characteristics associated with recovery trajectories of people with severe traumatic brain injury (TBI) during inpatient rehabilitation. DESIGN: Observational prospective longitudinal study. SETTING: Two specialized inpatient TBI rehabilitation...... functional levels received more treatment and more treatment was associated with slower recovery, presumably because treatment was allocated according to need. Thus, effects of treatment on outcome could not be disentangled from effects of case mix factors. CONCLUSIONS: FIM gain during inpatient recovery...

  7. Mild Traumatic Brain Injury – Case Report

    Directory of Open Access Journals (Sweden)

    2015-06-01

    Full Text Available A mild traumatic brain injury or a concussion represents the majority of all traumatic brain injuries. The consequences show on physical, cognitive, and emotional functioning and even though the injury classifies as mild, it can have a significant effect on a patient, patient’s family and their quality of life. Defects are often overlooked as objective clinical methods are lacking. Neuropsychological evaluation can aid in appraisal of the defect magnitude and determine factors that influence the outcome of the injured. The following case report addresses the importance of neuropsychological evaluation in treating cognitive defects along with the Cognitive Behavioral therapy approach toward emotional and behavioral disorders treatment in mild traumatic brain injury. It has been shown how important it is to find possible causes for slow recovery. The annuity tendencies have been noted as an important factor for prolongation of the post-concussion syndrome. We can detect the symptom simulation with appropriate psychological instruments. Described is a case of 38-year-old man who suffered a mild traumatic brain injury.

  8. Neuropsychiatric aspects of severe brain injuries

    Directory of Open Access Journals (Sweden)

    O. S. Zaitsev

    2012-01-01

    Full Text Available The state-of-the-art of Russian neuropsychiatry and priority developments in different psychopathological syndromes in severe brain injuries are assessed. Many cognitive and emotional impairments are explained in terms of the idea on the organization of psychic activity over time. It is emphasized that to achieve the premorbid levels of an interhemispheric interaction and functional asymmetry of the cerebral hemispheres affords psychic activity recovery. The experience in investigating, classifying, and treating various mental disorders occurring after severe brain injuries is generalized. The basic principles of psychopharmacotherapy and rehabilitation of victims are stated.

  9. Surgical management of traumatic brain injury

    DEFF Research Database (Denmark)

    Hartings, Jed A; Vidgeon, Steven; Strong, Anthony J;

    2014-01-01

    OBJECT: Mass lesions from traumatic brain injury (TBI) often require surgical evacuation as a life-saving measure and to improve outcomes, but optimal timing and surgical technique, including decompressive craniectomy, have not been fully defined. The authors compared neurosurgical approaches...... enrolled in the Co-Operative Studies on Brain Injury Depolarizations (COSBID) at King's College Hospital (KCH, n = 27) and Virginia Commonwealth University (VCU, n = 24) from July 2004 to March 2010. Subdural electrode strips were placed at the time of surgery for subsequent electrocorticographic...

  10. Mild Traumatic Brain Injury in Translation

    OpenAIRE

    Levin, Harvey S.; Robertson, Claudia S.

    2013-01-01

    This Introduction to a Special Issue on Mild Traumatic Brain Injury (mTBI) highlights the methodological challenges in outcome studies and clinical trials involving patients who sustain mTBI. Recent advances in brain imaging and portable, computerized cognitive tasks have contributed to protocols that are sensitive to the effects of mTBI and efficient in time for completion. Investigation of civilian mTBI has been extended to single and repeated injuries in athletes and blast-related mTBI in ...

  11. Time dysperception perspective for acquired brain injury

    Directory of Open Access Journals (Sweden)

    Federica ePiras

    2014-01-01

    Full Text Available Distortions of time perception are presented by a number of neuropsychiatric disorders. Here we survey timing abilities in clinical populations with acquired brain injuries in key cerebral areas recently implicated in human studies of timing. We purposely analyzed the complex relationship between cognitive and contextual factors involved in time estimation, as to characterize the correlation between timed and other cognitive behaviors in each group. We assume that interval timing is a solid construct to study cognitive dysfunctions following brain injury, as timing performance is a sensitive metric of information processing, while temporal cognition has the potential of influencing a wide range of cognitive processes. Moreover, temporal performance is a sensitive assay of damage to the underlying neural substrate after a brain insult. Further research in neurological and psychiatric patients will definitively answer the question of whether time distortions are manifestations of cognitive and behavioral symptoms of brain damage and definitively clarify their mechanisms.

  12. Prehospital Care of Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    TVSP Murthy

    2008-01-01

    Full Text Available Traumatic brain injury (TBI occurs when a sudden trauma causes brain damage. Depending on the severity, outcome can be anything from complete recovery to permanent disability or death. Emergency medical services play a dominant role in provision of primary care at the site of injury. Since little can be done to reverse the initial brain damage due to trauma, attempts to prevent further brain damage and stabilize the patient before he can be brought to a specialized trauma care centre play a pivotal role in the final outcome. Recognition and early treatment of hypoten-sion, hypoxemia, and hypoglycemia, objective neurological assessment based on GCS and pupils, and safe transport to an optimal care centre are the key elements of prehospital care of a TBI patient.

  13. Endogenous lipoid pneumonia in a cachectic patient after brain injury.

    Science.gov (United States)

    Zhang, Ji; Mu, Jiao; Lin, Wei; Dong, Hongmei

    2015-01-01

    Endogenous lipoid pneumonia (EnLP) is an uncommon non-life-threatening inflammatory lung disease that usually occurs in patients with conditions such as lung cancers, primary sclerosing cholangitis, and undifferentiated connective tissue disease. Here we report a case of EnLP in a paralytic and cachectic patient with bronchopneumonia after brain injury. A 40-year-old man experienced a severe brain injury in an automobile accident. He was treated for 1 month and his status plateaued. However, he became paralyzed and developed cachexia and ultimately died 145 days after the accident. Macroscopically, multifocal yellowish firm nodules were visible on scattered gross lesions throughout the lungs. Histologically, many foam cells had accumulated within the alveoli and alveolar walls accompanied by a surrounding interstitial infiltration of lymphocytes. The findings were in accordance with a diagnosis of EnLP. Bronchopneumonia was also noted. To our knowledge, there have been few reports of EnLP associated with bronchopneumonia and cachexia after brain injury. This uncommon pathogenesis should be well recognized by clinicians and forensic pathologists. The case reported here should prompt medical staff to increase the nutritional status and fight pulmonary infections in patients with brain injury to prevent the development of EnLP.

  14. Interleukin-1 and acute brain injury.

    Science.gov (United States)

    Murray, Katie N; Parry-Jones, Adrian R; Allan, Stuart M

    2015-01-01

    Inflammation is the key host-defense response to infection and injury, yet also a major contributor to a diverse range of diseases, both peripheral and central in origin. Brain injury as a result of stroke or trauma is a leading cause of death and disability worldwide, yet there are no effective treatments, resulting in enormous social and economic costs. Increasing evidence, both preclinical and clinical, highlights inflammation as an important factor in stroke, both in determining outcome and as a contributor to risk. A number of inflammatory mediators have been proposed as key targets for intervention to reduce the burden of stroke, several reaching clinical trial, but as yet yielding no success. Many factors could explain these failures, including the lack of robust preclinical evidence and poorly designed clinical trials, in addition to the complex nature of the clinical condition. Lack of consideration in preclinical studies of associated co-morbidities prevalent in the clinical stroke population is now seen as an important omission in previous work. These co-morbidities (atherosclerosis, hypertension, diabetes, infection) have a strong inflammatory component, supporting the need for greater understanding of how inflammation contributes to acute brain injury. Interleukin (IL)-1 is the prototypical pro-inflammatory cytokine, first identified many years ago as the endogenous pyrogen. Research over the last 20 years or so reveals that IL-1 is an important mediator of neuronal injury and blocking the actions of IL-1 is beneficial in a number of experimental models of brain damage. Mechanisms underlying the actions of IL-1 in brain injury remain unclear, though increasing evidence indicates the cerebrovasculature as a key target. Recent literature supporting this and other aspects of how IL-1 and systemic inflammation in general contribute to acute brain injury are discussed in this review.

  15. Interleukin-1 and acute brain injury

    Directory of Open Access Journals (Sweden)

    Katie N Murray

    2015-02-01

    Full Text Available Inflammation is the key host-defense response to infection and injury, yet also a major contributor to a diverse range of diseases, both peripheral and central in origin. Brain injury as a result of stroke or trauma is a leading cause of death and disability worldwide, yet there are no effective treatments, resulting in enormous social and economic costs. Increasing evidence, both preclinical and clinical, highlights inflammation as an important factor in stroke, both in determining outcome and as a contributor to risk. A number of inflammatory mediators have been proposed as key targets for intervention to reduce the burden of stroke, several reaching clinical trial, but as yet yielding no success. Many factors could explain these failures, including the lack of robust preclinical evidence and poorly designed clinical trials, in addition to the complex nature of the clinical condition. Lack of consideration in preclinical studies of associated co-morbidities prevalent in the clinical stroke population is now seen as an important omission in previous work. These co-morbidities (atherosclerosis, hypertension, diabetes, infection have a strong inflammatory component, supporting the need for greater understanding of how inflammation contributes to acute brain injury. Interleukin (IL-1 is the prototypical pro-inflammatory cytokine, first identified many years ago as the endogenous pyrogen. Research over the last 20 years or so reveals that IL-1 is an important mediator of neuronal injury and blocking the actions of IL-1 is beneficial in a number of experimental models of brain damage. Mechanisms underlying the actions of IL-1 in brain injury remain unclear, though increasing evidence indicates the cerebrovasculature as a key target. Recent literature supporting this and other aspects of how IL-1 and systemic inflammation in general contribute to acute brain injury are discussed in this review.

  16. An experimental protocol for mimicking pathomechanisms of traumatic brain injury in mice

    Directory of Open Access Journals (Sweden)

    Albert-Weißenberger Christiane

    2012-02-01

    Full Text Available Abstract Traumatic brain injury (TBI is a result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events. In order to examine injury processes associated with TBI, a number of rodent models to induce brain trauma have been described. However, none of these models covers the entire spectrum of events that might occur in TBI. Here we provide a thorough methodological description of a straightforward closed head weight drop mouse model to assess brain injuries close to the clinical conditions of human TBI.

  17. Recovery of resting brain connectivity ensuing mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Rose Dawn Bharath

    2015-09-01

    Full Text Available Brains reveal amplified plasticity as they recover from an injury. We aimed to define time dependent plasticity changes in patients recovering from mild traumatic brain injury (mTBI. 25 subjects with mild head injury were longitudinally evaluated within 36 hours, 3 and 6 months using resting state functional connectivity (RSFC. Region of interest (ROI based connectivity differences over time within the patient group and in comparison with a healthy control group were analyzed at p<0.005. We found 33 distinct ROI pairs that revealed significant changes in their connectivity strength with time. Within three months, the majority of the ROI pairs had decreased connectivity in mTBI population, which increased and became comparable to healthy controls at 6 months. Initial imaging within 36 hours of injury revealed hyper connectivity predominantly involving the salience network and default mode network, which reduced at 3 months when lingual, inferior frontal and fronto-parietal networks revealed hyper connectivity. At six months all the evaluated networks revealed hyper connectivity and became comparable to the healthy controls. Our findings in a fairly homogenous group of patients with mTBI evaluated during the 6 month window of recovery defines time varying brain connectivity changes as the brain recovers from an injury. A majority of these changes were seen in the frontal and parietal lobes between 3-6 months after injury. Hyper connectivity of several networks supported normal recovery in the first six months and it remains to be seen in future studies whether this can predict an early and efficient recovery of brain function.

  18. Future directions in brain injury research.

    Science.gov (United States)

    Gennarelli, Thomas A

    2014-01-01

    This paper reviews the potential future directions that are important for brain injury research, especially with regard to concussion. The avenues of proposed research are categorized according to current concepts of concussion, types of concussion, and a global schema for globally reducing the burden of concussion.

  19. Monitoring Agitated Behavior After acquired Brain Injury

    DEFF Research Database (Denmark)

    Aadal, Lena; Mortensen, Jesper; Nielsen, Jørgen Feldbaek

    2016-01-01

    Purpose: To describe the onset, duration, intensity, and nursing shift variation of agitated behavior in patients with acquired brain injury (ABI) at a rehabilitation hospital. Design: Prospective descriptive study. Methods: A total of 11 patients with agitated behavior were included. Agitated...

  20. School Reentry Following Traumatic Brain Injury

    Science.gov (United States)

    Deidrick, Kathleen K. M.; Farmer, Janet E.

    2005-01-01

    Successful school reentry following traumatic brain injury (TBI) is critical to recovery. Physical, cognitive, behavioral, academic, and social problems can affect a child's school performance after a TBI. However, early intervention has the potential to improve child academic outcomes and promote effective coping with any persistent changes in…

  1. Working with Students with Traumatic Brain Injury

    Science.gov (United States)

    Lucas, Matthew D.

    2010-01-01

    The participation of a student with Traumatic Brain Injury (TBI) in general physical education can often be challenging and rewarding for the student and physical education teacher. This article addresses common characteristics of students with TBI and presents basic solutions to improve the education of students with TBI in the general physical…

  2. Executive Functioning after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2008-07-01

    Full Text Available The Behavior Rating Inventory of Executive Function (BRIEF, a caregiver-report questionnaire, was used to measure changes in executive function in the first year after traumatic brain injury (TBI in a study of children, aged 5 to 15 years, at University of Minnesota, Minneapolis, and Johns Hopkins University School of Medicine, Baltimore, MD.

  3. Brain Injury with Sickle Cell Disease

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2003-11-01

    Full Text Available The relationship between brain injury and vasculopathy in 146 sickle cell (SCD patients with hemoglobin SS, the most serious form of SCD, was evaluated by MRI and MRA at St Jude Children’s Research Hospital, Memphis, TN.

  4. Traumatic Brain Injury: Nuclear Medicine Neuroimaging

    NARCIS (Netherlands)

    Sánchez-Catasús, Carlos A; Vállez Garcia, David; Le Riverend Morales, Eloísa; Galvizu Sánchez, Reinaldo; Dierckx, Rudi; Dierckx, Rudi AJO; Otte, Andreas; de Vries, Erik FJ; van Waarde, Aren; Leenders, Klaus L

    2014-01-01

    This chapter provides an up-to-date review of nuclear medicine neuroimaging in traumatic brain injury (TBI). 18F-FDG PET will remain a valuable tool in researching complex mechanisms associated with early metabolic dysfunction in TBI. Although evidence-based imaging studies are needed, 18F-FDG PET i

  5. Narrative Language in Traumatic Brain Injury

    Science.gov (United States)

    Marini, Andrea; Galetto, Valentina; Zampieri, Elisa; Vorano, Lorenza; Zettin, Marina; Carlomagno, Sergio

    2011-01-01

    Persons with traumatic brain injury (TBI) often show impaired linguistic and/or narrative abilities. The present study aimed to document the features of narrative discourse impairment in a group of adults with TBI. 14 severe TBI non-aphasic speakers (GCS less than 8) in the phase of neurological stability and 14 neurologically intact participants…

  6. Perioperative Management of Adult Traumatic Brain Injury

    OpenAIRE

    Sharma, Deepak; Vavilala, Monica S.

    2012-01-01

    This article presents an overview of the management of traumatic brain injury (TBI) as relevant to the practicing anesthesiologist. Key concepts surrounding the pathophysiology, anesthetic principles are used to describe potential ways to reduce secondary insults and improve outcomes after TBI.

  7. Traumatic brain injury and olfactory deficits

    DEFF Research Database (Denmark)

    Fortin, Audrey; Lefebvre, Mathilde Beaulieu; Ptito, Maurice

    2010-01-01

    PRIMARY OBJECTIVE: Olfactory functions are not systematically evaluated following traumatic brain injury (TBI). This study aimed at comparing two smell tests that are used in a clinical setting. RESEARCH DESIGN: The University of Pennsylvania Smell Identification Test (UPSIT) and the Alberta Smell...

  8. MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY

    Directory of Open Access Journals (Sweden)

    Diana G Hernadez-Ontiveros

    2013-03-01

    Full Text Available Traumatic brain injury (TBI has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuroprotective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglia response despite these inflammatory cells’ detrimental effects on the brain. Another relevant point to consider is the veracity of results of animal experiments due to deficiencies in experimental design, such as incomplete or inadequate method description, data misinterpretation and reporting may introduce bias and give false-positive results. Thus, scientific publications should follow strict guidelines that include randomization, blinding, sample-size estimation and accurate handling of all data (Landis et al., 2012. A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer’s disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Here, we discuss inflammatory mechanisms that accompany TBI in an effort to increase our understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI.

  9. Relatives of patients with severe brain injury

    DEFF Research Database (Denmark)

    Norup, Anne; Petersen, Janne; Lykke Mortensen, Erik

    2015-01-01

    PRIMARY OBJECTIVE: To investigate trajectories and predictors of trajectories of anxiety and depression in relatives of patients with a severe brain injury during the first year after injury. RESEARCH DESIGN: A prospective longitudinal study with four repeated measurements. SUBJECTS: Ninety...... relatives of patients with severe brain injury. METHODS: The relatives were assessed on the anxiety and depression scales from the Symptom Checklist-90-Revised and latent variable growth curve models were used to model the trajectories. The effects of patient's age, patient's Glasgow Coma Score, level...... improvement. Higher initial level of symptoms of depression was seen in female relatives. Higher initial level of anxiety was associated with younger patient age, lower level of function and consciousness in the patient and the relative being female or the spouse. CONCLUSION: Future research and interventions...

  10. Centralized rehabilitation after servere traumatic brain injury

    DEFF Research Database (Denmark)

    Engberg, Aase Worså; Liebach, Annette; Nordenbo, Annette Mosbæk

    2006-01-01

    OBJECTIVES: To present results from the first 3 years of centralized subacute rehabilitation after very severe traumatic brain injury (TBI), and to compare results of centralized versus decentralized rehabilitation. MATERIAL AND METHODS: Prospectively, the most severely injured group of adults from...... an uptake area of 2.4 million in Denmark were included at admission to a regional brain injury unit (BIU), on average 19 days after injury. Patients in the retrospective study used for comparison were randomly chosen from the national hospital register. RESULTS AND CONCLUSIONS: Out of 117 patients...... post-trauma was 0.29, and at 1 year 0.055 per 100,000 population. By comparison of 39 patients from the centralized unit injured in 2000-2003 with 21 patients injured in 1982, 1987 or 1992 and with similar PTA- and age distributions and male/female ratio, Glasgow Outcome Scale score at discharge...

  11. Discriminating military and civilian traumatic brain injuries.

    Science.gov (United States)

    Reid, Matthew W; Velez, Carmen S

    2015-05-01

    Traumatic brain injury (TBI) occurs at higher rates among service members than civilians. Explosions from improvised explosive devices and mines are the leading cause of TBI in the military. As such, TBI is frequently accompanied by other injuries, which makes its diagnosis and treatment difficult. In addition to postconcussion symptoms, those who sustain a TBI commonly report chronic pain and posttraumatic stress symptoms. This combination of symptoms is so typical they have been referred to as the "polytrauma clinical triad" among injured service members. We explore whether these symptoms discriminate civilian occurrences of TBI from those of service members, as well as the possibility that repeated blast exposure contributes to the development of chronic traumatic encephalopathy (CTE). This article is part of a Special Issue entitled 'Traumatic Brain Injury'.

  12. Centralized rehabilitation after servere traumatic brain injury

    DEFF Research Database (Denmark)

    Engberg, Aase Worså; Liebach, Annette; Nordenbo, Annette Mosbæk

    2006-01-01

    post-trauma was 0.29, and at 1 year 0.055 per 100,000 population. By comparison of 39 patients from the centralized unit injured in 2000-2003 with 21 patients injured in 1982, 1987 or 1992 and with similar PTA- and age distributions and male/female ratio, Glasgow Outcome Scale score at discharge......OBJECTIVES: To present results from the first 3 years of centralized subacute rehabilitation after very severe traumatic brain injury (TBI), and to compare results of centralized versus decentralized rehabilitation. MATERIAL AND METHODS: Prospectively, the most severely injured group of adults from...... an uptake area of 2.4 million in Denmark were included at admission to a regional brain injury unit (BIU), on average 19 days after injury. Patients in the retrospective study used for comparison were randomly chosen from the national hospital register. RESULTS AND CONCLUSIONS: Out of 117 patients...

  13. Language Abilities Following Prematurity, Periventricular Brain Injury, and Cerebral Palsy.

    Science.gov (United States)

    Feldman, Heidi M.; And Others

    1994-01-01

    This study compared language abilities in three groups of preschool children (total n=18) who were born prematurely: children with bilateral spastic cerebral palsy associated with perinatal brain injury, with similar brain injury but no motor impairment, and with no brain injuries. No significant differences were observed among the groups on any…

  14. Traumatic Brain Injury (TBI) Studies at Grady Memorial Hospital

    Science.gov (United States)

    2010-09-01

    management of adult, blunt-mechanism traumatic brain injury ( TBI ) patients and assess the overall mortality of this cohort at Grady...this study is to determine the current compliance with widely accepted guidelines for the management of severe traumatic brain injury ( TBI ) patients...AD_________________ Award Number: W81XWH-09-2-0145 Study Title: Traumatic Brain Injury ( TBI

  15. Brain response to traumatic brain injury in wild-type and interleukin-6 knockout mice: a microarray analysis

    DEFF Research Database (Denmark)

    Poulsen, Christian Bjørn; Penkowa, Milena; Borup, Rehannah

    2005-01-01

    Traumatic injury to the brain is one of the leading causes of injury-related death or disability. Brain response to injury is orchestrated by cytokines, such as interleukin (IL)-6, but the full repertoire of responses involved is not well known. We here report the results obtained with microarrays...... in the initial tissue injury and later regeneration of the parenchyma. IL-6 deficiency showed a dramatic effect in the expression of many genes, especially in the 1 day post-lesion timing, which presumably underlies the poor capacity of IL-6 knockout mice to cope with brain damage. The results highlight...... the importance of IL-6 controlling the response of the brain to injury as well as the suitability of microarrays for identifying specific targets worthy of further study....

  16. Dual diagnosis: traumatic brain injury with spinal cord injury.

    Science.gov (United States)

    Kushner, David S; Alvarez, Gemayaret

    2014-08-01

    Spinal cord injury (SCI) patients should be assessed for a co-occurring traumatic brain injury (TBI) on admission to a rehabilitation program. Incidence of a dual diagnosis may approach 60% with certain risk factors. Diagnosis of mild-moderate severity TBIs may be missed during acute care hospitalizations of SCI. Neuropsychological symptoms of a missed TBI diagnosis may be perceived during rehabilitation as noncompliance, inability to learn, maladaptive reactions to SCI, and poor motivation. There are life-threatening and quality-of-life-threatening complications of TBI that also may be missed if a dual diagnosis is not made.

  17. Research progress of immune tolerance in the treatment of brain injury

    Directory of Open Access Journals (Sweden)

    Hua YAN

    2014-08-01

    Full Text Available Due to its special anatomical structures and immune pathophysiological mechanisms, brain damage repair is greatly different from damage repair of other systems. Secondary brain injury and inflammation are closely related. As a "double-edged sword", inflammation scavenges hazardous substances on the early stage of injury, but has side effects on normal brain tissue. The use of immunosuppressive therapy or hypothermia can inhibit immune injury, but the presence of reduced immunity may result in infection and tumorigenesis in the long term. Only reducing the autoimmune attack against brain tissue without affecting other immune capacity of the body will be optimized solution, and this paper will make a review on the research of immune tolerance in the treatment of brain injury with optimized program. doi: 10.3969/j.issn.1672-6731.2014.08.017

  18. Combat Helmets and Blast Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Duncan Wallace

    2012-01-01

    Full Text Available Background: The conflicts in Iraq and Afghanistan and the prominence of traumatic brain injury (TBI, mostly from improvised explosive devices, have focused attention on the effectiveness of combat helmets. Purpose: This paper examines the importance of TBI, the role and history of the development of combat helmets, current helmet designs and effectiveness, helmet design methodology, helmet sensors, future research and recommendations. Method: A literature review was conducted using search terms – combat helmets, traumatic brain injury, concussion, Iraq, Afghanistan and helmet sensors, searching PubMed, MEDLINE, ProQuest and Google Scholar. Conclusions: At present, no existing helmet is able to fully protect against all threats faced on the battlefield. The prominence of traumatic brain injury from improvised explosive devices in the current conflicts in Iraq and Afghanistan has highlighted the limitations in knowledge about blast and how to provide protection from it. As a result, considerable research is currently occurring in how to protect the head from blast over-pressure. Helmet sensors may provide valuable data. Some new combat helmets may be able to protect against rifle rounds, but may result in injuries occurring behind body armour. Optimal combat helmet design requires a balance between the need for protection from trauma and the comfort and practicality of the helmet for the user to ensure the best outcomes.

  19. The neuropathology and neurobiology of traumatic brain injury.

    Science.gov (United States)

    Blennow, Kaj; Hardy, John; Zetterberg, Henrik

    2012-12-06

    The acute and long-term consequences of traumatic brain injury (TBI) have received increased attention in recent years. In this Review, we discuss the neuropathology and neural mechanisms associated with TBI, drawing on findings from sports-induced TBI in athletes, in whom acute TBI damages axons and elicits both regenerative and degenerative tissue responses in the brain and in whom repeated concussions may initiate a long-term neurodegenerative process called dementia pugilistica or chronic traumatic encephalopathy (CTE). We also consider how the neuropathology and neurobiology of CTE in many ways resembles other neurodegenerative illnesses such as Alzheimer's disease, particularly with respect to mismetabolism and aggregation of tau, β-amyloid, and TDP-43. Finally, we explore how translational research in animal models of acceleration/deceleration types of injury relevant for concussion together with clinical studies employing imaging and biochemical markers may further elucidate the neurobiology of TBI and CTE.

  20. Kevlar Vest Protection Against Blast Overpressure Brain Injury: Systemic Contributions to Injury Etiology

    Science.gov (United States)

    2014-11-01

    Award Number: W81XWH-08-2-0017 TITLE: " Kevlar Vest Protection Against Blast Overpressure Brain Injury: Systemic Contributions to Injury Etiology...TITLE AND SUBTITLE 5a. CONTRACT NUMBER “ Kevlar Vest Protection Against Blast Overpressure Brain Injury: Systemic Contributions to Injury Etiology...traumatic brain injury (bTBI) is largely undefined. Along with reducing mortality, in preliminary experiments Kevlar vests significantly protected

  1. Surviving severe traumatic brain injury in Denmark

    DEFF Research Database (Denmark)

    Odgaard, Lene; Poulsen, Ingrid; Kammersgaard, Lars Peter;

    2015-01-01

    PURPOSE: To identify all hospitalized patients surviving severe traumatic brain injury (TBI) in Denmark and to compare these patients to TBI patients admitted to highly specialized rehabilitation (HS-rehabilitation). PATIENTS AND METHODS: Patients surviving severe TBI were identified from...... severe TBI were admitted to HS-rehabilitation. Female sex, older age, and non-working status pre-injury were independent predictors of no HS-rehabilitation among patients surviving severe TBI. CONCLUSION: The incidence rate of hospitalized patients surviving severe TBI was stable in Denmark...

  2. Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Hai-jun Bao

    2016-01-01

    Full Text Available The adipocytokine, apelin-13, is an abundantly expressed peptide in the nervous system. Apelin-13 protects the brain against ischemia/reperfusion injury and attenuates traumatic brain injury by suppressing autophagy. However, secondary apelin-13 effects on traumatic brain injury-induced neural cell death and blood-brain barrier integrity are still not clear. Here, we found that apelin-13 significantly decreases cerebral water content, mitigates blood-brain barrier destruction, reduces aquaporin-4 expression, diminishes caspase-3 and Bax expression in the cerebral cortex and hippocampus, and reduces apoptosis. These results show that apelin-13 attenuates secondary injury after traumatic brain injury and exerts a neuroprotective effect

  3. Resveratrol attenuates peripheral and brain inflammation and reduces ischemic brain injury in aged female mice.

    Science.gov (United States)

    Jeong, Sae Im; Shin, Jin A; Cho, Sunghee; Kim, Hye Won; Lee, Ji Yoon; Kang, Jihee Lee; Park, Eun-Mi

    2016-08-01

    Resveratrol is known to improve metabolic dysfunction associated with obesity. Visceral obesity is a sign of aging and is considered a risk factor for ischemic stroke. In this study, we investigated the effects of resveratrol on inflammation in visceral adipose tissue and the brain and its effects on ischemic brain injury in aged female mice. Mice treated with resveratrol (0.1 mg/kg, p.o.) for 10 days showed reduced levels of interleukin-1β and tumor necrosis factor-α, as well as a reduction in the size of adipocytes in visceral adipose tissue. Resveratrol also reduced interleukin-1β and tumor necrosis factor-α protein levels and immunoglobulin G extravasation in the brain. Mice treated with resveratrol demonstrated smaller infarct size, improved neurological function, and blunted peripheral inflammation at 3 days postischemic stroke. These results showed that resveratrol counteracted inflammation in visceral adipose tissue and in the brain and reduced stroke-induced brain injury and peripheral inflammation in aged female mice. Therefore, resveratrol administration can be a valuable strategy for the prevention of age-associated and disease-provoked inflammation in postmenopausal women.

  4. Glyburide - Novel Prophylaxis and Effective Treatment for Traumatic Brain Injury

    Science.gov (United States)

    2012-08-01

    ABSTRACT The overall subject of this project is blast- traumatic brain injury (blast- TBI ) and the role of the SUR1-regulated NCCa-ATP channel in blast- TBI ...project is blast- traumatic brain injury (blast- TBI ) and the role of the SUR1-regulated NCCa-ATP channel in secondary injury following blast- TBI . The...effective treatment for traumatic brain injury PRINCIPAL INVESTIGATOR: J. Marc Simard, M.D., Ph.D

  5. A Blast Model of Traumatic Brain Injury in Swine

    Science.gov (United States)

    2009-05-01

    public release; distribution unlimited Although blast-induced traumatic brain injury (BI- TBI ) is a significant cause of morbidity and behavioral...survival model of BI- TBI in swine. Traumatic Brain Injury , Swine, Blast, Model Development U U U 7 USAMRMC W81XWH-08-2-0082... Injury , TBI Scientific Advisor, Defense Center of Excellence for Psychological Health and Traumatic Brain Injury ) and Dr. Tamara Crowder at the DoD

  6. An animal-to-human scaling law for blast-induced traumatic brain injury risk assessment.

    Science.gov (United States)

    Jean, Aurélie; Nyein, Michelle K; Zheng, James Q; Moore, David F; Joannopoulos, John D; Radovitzky, Raúl

    2014-10-28

    Despite recent efforts to understand blast effects on the human brain, there are still no widely accepted injury criteria for humans. Recent animal studies have resulted in important advances in the understanding of brain injury due to intense dynamic loads. However, the applicability of animal brain injury results to humans remains uncertain. Here, we use advanced computational models to derive a scaling law relating blast wave intensity to the mechanical response of brain tissue across species. Detailed simulations of blast effects on the brain are conducted for different mammals using image-based biofidelic models. The intensity of the stress waves computed for different external blast conditions is compared across species. It is found that mass scaling, which successfully estimates blast tolerance of the thorax, fails to capture the brain mechanical response to blast across mammals. Instead, we show that an appropriate scaling variable must account for the mass of protective tissues relative to the brain, as well as their acoustic impedance. Peak stresses transmitted to the brain tissue by the blast are then shown to be a power function of the scaling parameter for a range of blast conditions relevant to TBI. In particular, it is found that human brain vulnerability to blast is higher than for any other mammalian species, which is in distinct contrast to previously proposed scaling laws based on body or brain mass. An application of the scaling law to recent experiments on rabbits furnishes the first physics-based injury estimate for blast-induced TBI in humans.

  7. The neuroethics and neurolaw of brain injury.

    Science.gov (United States)

    Aggarwal, Neil Krishan; Ford, Elizabeth

    2013-01-01

    Neuroethics and neurolaw are fields of study that involve the interface of neuroscience with clinical and legal decision-making. The past two decades have seen increasing attention being paid to both fields, in large part because of the advances in neuroimaging techniques and improved ability to visualize and measure brain structure and function. Traumatic brain injury (TBI), along with its acute and chronic sequelae, has emerged as a focus of neuroethical issues, such as informed consent for treatment and research, diagnostic and prognostic uncertainties, and the subjectivity of interpretation of data. The law has also more frequently considered TBI in criminal settings for exculpation, mitigation and sentencing purposes and in tort and administrative law for personal injury, disability and worker's compensation cases. This article provides an overview of these topics with an emphasis on the current challenges that the neuroscience of TBI faces in the medicolegal arena.

  8. Barbiturates for acute traumatic brain injury.

    OpenAIRE

    Roberts, I.; Sydenham, E

    2012-01-01

    BACKGROUND: Raised intracranial pressure (ICP) is an important complication of severe brain injury, and is associated with high mortality. Barbiturates are believed to reduce ICP by suppressing cerebral metabolism, thus reducing cerebral metabolic demands and cerebral blood volume. However, barbiturates also reduce blood pressure and may, therefore, adversely effect cerebral perfusion pressure. OBJECTIVES: To assess the effects of barbiturates in reducing mortality, disability and raised ICP ...

  9. Caregiver stress in traumatic brain injury

    OpenAIRE

    Blake, Holly

    2013-01-01

    Aims\\ud Many patients experience physical, behavioural, cognitive and emotional problems following traumatic brain injury (TBI). They may require continuing care for many years, most of which is provided by informal caregivers, such as spouses, parents, or other family members. The caregiving role is associated with a range of adverse effects including anxiety, depression, poor physical health and lowered quality of life. This article explores issues around caregiver stress; highlighting inte...

  10. Traumatic Brain Injury, Microglia, and Beta Amyloid

    OpenAIRE

    Mannix, Rebekah C.; Whalen, Michael J

    2012-01-01

    Recently, there has been growing interest in the association between traumatic brain injury (TBI) and Alzheimer's Disease (AD). TBI and AD share many pathologic features including chronic inflammation and the accumulation of beta amyloid (A\\(\\beta\\)). Data from both AD and TBI studies suggest that microglia play a central role in A\\(\\beta\\) accumulation after TBI. This paper focuses on the current research on the role of microglia response to A\\(\\beta\\) after TBI.

  11. Cerebral Vasospasm in Traumatic Brain Injury

    OpenAIRE

    Kramer, Daniel R.; Winer, Jesse L.; B. A. Matthew Pease; Arun P. Amar; Mack, William J.

    2013-01-01

    Vasospasm following traumatic brain injury (TBI) may dramatically affect the neurological and functional recovery of a vulnerable patient population. While the reported incidence of traumatic vasospasm ranges from 19%–68%, the true incidence remains unknown due to variability in protocols for its detection. Only 3.9%–16.6% of patients exhibit clinical deficits. Compared to vasospasm resulting from aneurysmal SAH (aSAH), the onset occurs earlier and the duration is shorter. Overall, the clinic...

  12. Traumatic brain injury in modern war

    Science.gov (United States)

    Ling, Geoffrey S. F.; Hawley, Jason; Grimes, Jamie; Macedonia, Christian; Hancock, James; Jaffee, Michael; Dombroski, Todd; Ecklund, James M.

    2013-05-01

    Traumatic brain injury (TBI) is common and especially with military service. In Iraq and Afghanistan, explosive blast related TBI has become prominent and is mainly from improvised explosive devices (IED). Civilian standard of care clinical practice guidelines (CPG) were appropriate has been applied to the combat setting. When such CPGs do not exist or are not applicable, new practice standards for the military are created, as for TBI. Thus, CPGs for prehospital care of combat TBI CPG [1] and mild TBI/concussion [2] were introduced as was a DoD system-wide clinical care program, the first large scale system wide effort to address all severities of TBI in a comprehensive organized way. As TBI remains incompletely understood, substantial research is underway. For the DoD, leading this effort are The Defense and Veterans Brain Injury Center, National Intrepid Center of Excellence and the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury. This program is a beginning, a work in progress ready to leverage advances made scientifically and always with the intent of providing the best care to its military beneficiaries.

  13. Radiation-induced brain injury: A review

    Directory of Open Access Journals (Sweden)

    Michael eRobbins

    2012-07-01

    Full Text Available Approximately 100,000 primary and metastatic brain tumor patients/year in the US survive long enough (> 6 months to experience radiation-induced brain injury. Prior to 1970, the human brain was thought to be highly radioresistant; the acute CNS syndrome occurs after single doses > 30 Gy; white matter necrosis occurs at fractionated doses > 60 Gy. Although white matter necrosis is uncommon with modern techniques, functional deficits, including progressive impairments in memory, attention, and executive function have become important, because they have profound effects on quality of life. Preclinical studies have provided valuable insights into the pathogenesis of radiation-induced cognitive impairment. Given its central role in memory and neurogenesis, the majority of these studies have focused on the hippocampus. Irradiating pediatric and young adult rodent brains leads to several hippocampal changes including neuroinflammation and a marked reduction in neurogenesis. These data have been interpreted to suggest that shielding the hippocampus will prevent clinical radiation-induced cognitive impairment. However, this interpretation may be overly simplistic. Studies using older rodents, that more closely match the adult human brain tumor population, indicate that, unlike pediatric and young adult rats, older rats fail to show a radiation-induced decrease in neurogenesis or a loss of mature neurons. Nevertheless, older rats still exhibit cognitive impairment. This occurs in the absence of demyelination and/or white matter necrosis similar to what is observed clinically, suggesting that more subtle molecular, cellular and/or microanatomic modifications are involved in this radiation-induced brain injury. Given that radiation-induced cognitive impairment likely reflects damage to both hippocampal- and non-hippocampal-dependent domains, there is a critical need to investigate the microanatomic and functional effects of radiation in various brain

  14. Biomarkers of Traumatic Injury Are Transported from Brain to Blood via the Glymphatic System

    OpenAIRE

    2015-01-01

    The nonspecific and variable presentation of traumatic brain injury (TBI) has motivated an intense search for blood-based biomarkers that can objectively predict the severity of injury. However, it is not known how cytosolic proteins released from traumatized brain tissue reach the peripheral blood. Here we show in a murine TBI model that CSF movement through the recently characterized glymphatic pathway transports biomarkers to blood via the cervical lymphatics. Clinically relevant manipulat...

  15. Effects of Acanthopanax senticosus on learning and memory in a mouse model of Alzheimer's disease and protection against free radical injury to brain tissue

    Institute of Scientific and Technical Information of China (English)

    Yanji Xu; Chunji Han; Songji Xu; Xing Yu; Guozhe Jiang; Chunhua Nan

    2008-01-01

    BACKGROUND:Acanthopanax senticosus,a plant of the Araliaceae family,is used in traditional Chinese medicine.It can be used to replenish Qi,strengthen the spleen,tonify the kidney,and relieve mental strain.OBJECTIVE:To observe effects ofAcanthopanax senticosus on learning and memory in a mouse model of Alzheimer's disease and abnormal biochemical changes in the brain tissue.DESIGN:A completely randomized grouping,controlled animal experiment.SETTING:Department of Preventive Medicine,School of Basic Medical Sciences,Yanbian University.MATERIALS:A total of 50 Kunming mice,aged 1-1.5 months,equal numbers of males and females,were provided by the Laboratory Animal Center,Yanbian University Medical College.The study was performed in accordance with ethical guidelines for the use and care of animals.Acanthopanax was provided by Yanbian Chengda Pharmaceutical Co.,Ltd.Acanthopanax senticosus(0.5 kg)was soaked in water for 1 hour and transferred to 1.5 kg distilled water for extraction.It was boiled for 1 hour and extracted after 1 hour of boiling.The procedure was repeated 3 times.The extract was condensed to 500 mL and then adjusted to 500 and 1 000 g/L with water.Piracetam tablets were produced by Shandong Luoxin Pharmaceutical Corporation, China.Malonaldehyde(MDA),superoxide dismutase(SOD),and acetylcholinesterase(ACHE)kits were purchased from Nanjing Jiancheng Bioengineering Co.,Ltd.,China. METHODS:This study was performed at the Department of Preventive Medicine,School of Basic Medical Sciences,Yanbian University from January to June 2007.All mice were randomly divided into 5 groups with 10 mice in each:control group,model group,low-,and high-dose Acanthopanax senticosus-treated groups, and piracetam-treated group.All groups were administered 0.1 mL/10 g.In the control and model groups, mice were intragastrically administered saline each morning for 5 days prior to experimentation.Five days later,they were intraperitoneally perfused with saline and aluminum trichloride

  16. Secondary Damage after Traumatic Brain Injury: Epidemiology, Pathophysiology and Therapy

    NARCIS (Netherlands)

    D.C. Engel (Doortje Caroline)

    2008-01-01

    textabstractTraumatic brain injury (TBI) is defined as a microscopic or macroscopic injury to the brain caused by external physical forces. Road traffic accidents, falls, sports injuries (i.e. boxing), recreational accidents (i.e. parachute jumping), the use of firearms, assault, child abuse, and se

  17. Patterns of neonatal hypoxic-ischaemic brain injury

    Energy Technology Data Exchange (ETDEWEB)

    Vries, Linda S. de [University Medical Centre, Department of Neonatology, Wilhelmina Children' s Hospital, Utrecht (Netherlands); Wilhelmina Children' s Hospital, University Medical Centre, Department of Neonatology, KE 04.123.1, P.O. Box 85090, Utrecht (Netherlands); Groenendaal, Floris [University Medical Centre, Department of Neonatology, Wilhelmina Children' s Hospital, Utrecht (Netherlands)

    2010-06-15

    Enormous progress has been made in assessing the neonatal brain, using magnetic resonance imaging (MRI). In this review, we will describe the use of MRI and proton magnetic resonance spectroscopy in detecting different patterns of brain injury in (full-term) human neonates following hypoxic-ischaemic brain injury and indicate the relevance of these findings in predicting neurodevelopmental outcome. (orig.)

  18. Early monitoring of PtiO2, PtiCO2, pH and brain temperat ure in patients with brain injuries and the clinical significanc e

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To explore the regulation of early br ain tissue metabolic changing after brain injuries and the clinical significance .   Methods: There were 17 patients with brain injuries. Early dire ct monitoring of PtiO2, PtiCO2, pH and brain temperature, dynami c observation of the relation between various parameters and clinics after brai n injuries were performed.   Results: Early changes of PtiO2, PtiCO2 and pH we re closely correlated with outcome. The death rate obviously increased when P tiO2 was continuously lower than 9 mm?Hg within 24 hours after injuries. Secondary brain injury prolonged and aggravated brain tissue metabolic disturban ce. When intracerebral pressure was over 30 mm?Hg PtiO2 began to de crea se. The brain temperature in brain death patients was evidently lower than axill ary temperature.   Conclusions: The direct monitoring of PtiO2, PtiC O2, pH and brain temperature is safe and accurate and can find early anoxia da mage to brain tissue and provide reliable basis for clinical therapy. It ha s an instructive significance in selecting and studying a new treatment method i n brain injuries. And it can be taken as a criterion in clinical judging brain d eaths.

  19. The influence of cationic liposome-mediated APOE2 gene transfer on brain structural changes after experimental traumatic brain injury

    OpenAIRE

    Pedachenko E.G.; Biloshytsky V.V.; Semenova V.M.; Gridina N.Ya.; Tsyba L. O.

    2009-01-01

    The possibilities to prevent the evolution of structural changes caused by secondary damage after traumatic brain injury by means of gene therapy aimed at the induction of apoE2 synthesis in brain tissue were studied. Traumatic brain injury in rats was inflicted under an overall anesthesia by free falling load weighing 450 g, falling from a 1.5 m elevation. The mixture of DOTAP liposome and 25 μg of plasmid vector pCMV•SPORT6 with cDNA of APOE2 gene was infused intraventricularly. At day 10 a...

  20. Aquaporin 9 in rat brain after severe traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Hui Liu

    2012-03-01

    Full Text Available OBJECTIVE: To reveal the expression and possible roles of aquaporin 9 (AQP9 in rat brain, after severe traumatic brain injury (TBI. METHODS: Brain water content (BWC, tetrazolium chloride staining, Evans blue staining, immunohistochemistry (IHC, immunofluorescence (IF, western blot, and real-time polymerase chain reaction were used. RESULTS: The BWC reached the first and second (highest peaks at 6 and 72 hours, and the blood brain barrier (BBB was severely destroyed at six hours after the TBI. The worst brain ischemia occurred at 72 hours after TBI. Widespread AQP9-positive astrocytes and neurons in the hypothalamus were detected by means of IHC and IF after TBI. The abundance of AQP9 and its mRNA increased after TBI and reached two peaks at 6 and 72 hours, respectively, after TBI. CONCLUSIONS: Increased AQP9 might contribute to clearance of excess water and lactate in the early stage of TBI. Widespread AQP9-positive astrocytes might help lactate move into neurons and result in cellular brain edema in the later stage of TBI. AQP9-positive neurons suggest that AQP9 plays a role in energy balance after TBI.

  1. Optical microangiography enabling visualization of change in meninges after traumatic brain injury in mice in vivo

    Science.gov (United States)

    Choi, Woo June; Qin, Wan; Qi, Xiaoli; Wang, Ruikang K.

    2016-03-01

    Traumatic brain injury (TBI) is a form of brain injury caused by sudden impact on brain by an external mechanical force. Following the damage caused at the moment of injury, TBI influences pathophysiology in the brain that takes place within the minutes or hours involving alterations in the brain tissue morphology, cerebral blood flow (CBF), and pressure within skull, which become important contributors to morbidity after TBI. While many studies for the TBI pathophysiology have been investigated with brain cortex, the effect of trauma on intracranial tissues has been poorly studied. Here, we report use of high-resolution optical microangiography (OMAG) to monitor the changes in cranial meninges beneath the skull of mouse after TBI. TBI is induced on a brain of anesthetized mouse by thinning the skull using a soft drill where a series of drilling exert mechanical stress on the brain through the skull, resulting in mild brain injury. Intracranial OMAG imaging of the injured mouse brain during post-TBI phase shows interesting pathophysiological findings in the meningeal layers such as widening of subdural space as well as vasodilation of subarachnoid vessels. These processes are acute and reversible within hours. The results indicate potential of OMAG to explore mechanism involved following TBI on small animals in vivo.

  2. Assessment of brain tissue injury after moderate hypothermia in neonates with hypoxic–ischaemic encephalopathy: a nested substudy of a randomised controlled trial

    OpenAIRE

    Rutherford, Mary; Ramenghi, Luca A; Edwards, A. David; Brocklehurst, Peter; Halliday, Henry; Levene, Malcolm; Strohm, Brenda; Thoresen, Marianne; Whitelaw, Andrew; Azzopardi, Denis

    2010-01-01

    Summary Background Moderate hypothermia in neonates with hypoxic–ischaemic encephalopathy might improve survival and neurological outcomes at up to 18 months of age, although complete neurological assessment at this age is difficult. To ascertain more precisely the effect of therapeutic hypothermia on neonatal cerebral injury, we assessed cerebral lesions on MRI scans of infants who participated in the Total Body Hypothermia for Neonatal Encephalopathy (TOBY) trial. Methods In the TOBY trial ...

  3. Transplantation of autologous bone marrow-derived mesenchymal stem cells for traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Jindou Jiang; Xingyao Bu; Meng Liu; Peixun Cheng

    2012-01-01

    Results from the present study demonstrated that transplantation of autologous bone marrow-derived mesenchymal stem cells into the lesion site in rat brain significantly ameliorated brain tissue pathological changes and brain edema, attenuated glial cell proliferation, and increased brain-derived neurotrophic factor expression. In addition, the number of cells double-labeled for 5-bromodeoxyuridine/glial fibrillary acidic protein and cells expressing nestin increased. Finally, blood vessels were newly generated, and the rats exhibited improved motor and cognitive functions. These results suggested that transplantation of autologous bone marrow-derived mesenchymal stem cells promoted brain remodeling and improved neurological functions following traumatic brain injury.

  4. Cushing's ulcer in traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Biteghe-bi-Nzeng Alain; WANG Yun-jie

    2008-01-01

    Traumatic brain injury(TBI)remains a complicated and urgent disease in our modernized cities. It becomes now a public health disease. We have got more and more patients in Neurosurgery Intensive Care Unit following motor vehicle accidents and others causes. TBI brings multiple disorders,from the primary injury to secondary injury. The body received the disturbances in the brain,in the hypothalamo-pituitary-adrenocortical(HPA)axis,in the gastric mucosa,in the immune and neuroendocrine systems.The mortality of TBI is more than 50 000 deaths/year, the third of the mortality of all iniuries. Cushing ulcer is one of the severe complications of TBI and its mortality rate is more than 50%. Many studies have improved the management of TBI and the associated complications to give patients a better outcome. Furthers studies need to be done based on the similar methodology to clarify the different steps of the HPA axis and the neuroendocrine change associated. The aim of the present review is to assess the clinical and endocrinal features of hypopituitarism and stress ulcer following TBI.

  5. Distribution of cysteinyl leukotriene receptor 2 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    Hua HU; Er-qing WEI; Gao CHEN; Jian-min ZHANG; Wei-ping ZHANG; Lei ZHANG; Qiu-fu GE; Hong-tian YAO; Wei DING; Zhong CHEN

    2005-01-01

    Aim: To determine the distribution of cysteinyl leukotriene receptor 2 (CysLT2),one of the cysteinyl leukotriene receptors, in human brains with traumatic injury and tumors. Methods: Brain specimens were obtained from patients who underwent brain surgery. CysLT2 in brain tissues was examined using immunohistochemical analysis. Results: CysLT2 was expressed in the smooth muscle cells (not in the endothelial cells) of arteries and veins. CysLT2 was also expressed in the granulocytes in both vessels and in the brain parenchyma. In addition, CysLT2 was detected in neuron- and glial-appearing cells in either the late stages of traumatic injury or in the area surrounding the tumors. Microvessels regenerated 8 d after trauma and CysLT2 expression was recorded in their endothelial cells.Conclusion: CysLT2 is distributed in vascular smooth muscle cells and granulocytes, and brain trauma and tumor can induce its expression in vascular endothelial cells and in a number of other cells.

  6. Regional brain morphometry predicts memory rehabilitation outcome after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Gary E Strangman

    2010-10-01

    Full Text Available Cognitive deficits following traumatic brain injury (TBI commonly include difficulties with memory, attention, and executive dysfunction. These deficits are amenable to cognitive rehabilitation, but optimally selecting rehabilitation programs for individual patients remains a challenge. Recent methods for quantifying regional brain morphometry allow for automated quantification of tissue volumes in numerous distinct brain structures. We hypothesized that such quantitative structural information could help identify individuals more or less likely to benefit from memory rehabilitation. Fifty individuals with TBI of all severities who reported having memory difficulties first underwent structural MRI scanning. They then participated in a 12 session memory rehabilitation program emphasizing internal memory strategies (I-MEMS. Primary outcome measures (HVLT, RBMT were collected at the time of the MRI scan, immediately following therapy, and again at one month post-therapy. Regional brain volumes were used to predict outcome, adjusting for standard predictors (e.g., injury severity, age, education, pretest scores. We identified several brain regions that provided significant predictions of rehabilitation outcome, including the volume of the hippocampus, the lateral prefrontal cortex, the thalamus, and several subregions of the cingulate cortex. The prediction range of regional brain volumes were in some cases nearly equal in magnitude to prediction ranges provided by pretest scores on the outcome variable. We conclude that specific cerebral networks including these regions may contribute to learning during I-MEMS rehabilitation, and suggest that morphometric measures may provide substantial predictive value for rehabilitation outcome in other cognitive interventions as well.

  7. Differential role of tumor necrosis factor receptors in mouse brain inflammatory responses in cryolesion brain injury

    DEFF Research Database (Denmark)

    Quintana, Albert; Giralt, Mercedes; Rojas, Santiago

    2005-01-01

    Tumor necrosis factor-alpha (TNF-alpha) is one of the mediators dramatically increased after traumatic brain injury that leads to the activation, proliferation, and hypertrophy of mononuclear, phagocytic cells and gliosis. Eventually, TNF-alpha can induce both apoptosis and necrosis via intracell......Tumor necrosis factor-alpha (TNF-alpha) is one of the mediators dramatically increased after traumatic brain injury that leads to the activation, proliferation, and hypertrophy of mononuclear, phagocytic cells and gliosis. Eventually, TNF-alpha can induce both apoptosis and necrosis via...... signaling also affected the expression of apoptosis/cell death-related genes (Fas, Rip, p53), matrix metalloproteinases (MMP3, MMP9, MMP12), and their inhibitors (TIMP1), suggesting a role of TNFR1 in extracellular matrix remodeling after injury. However, GDNF, NGF, and BDNF expression were not affected...... by TNFR1 deficiency. Overall, these results suggest that TNFR1 is involved in the early establishment of the inflammatory response and that its deficiency causes a decreased inflammatory response and tissue damage following brain injury....

  8. Hypersexuality or altered sexual preference following brain injury.

    OpenAIRE

    Miller, B.L.; Cummings, J L; McIntyre, H.; Ebers, G; Grode, M

    1986-01-01

    Eight patients are described in whom either hypersexuality (four cases) or change in sexual preference (four cases) occurred following brain injury. In this series disinhibition of sexual activity and hypersexuality followed medial basal-frontal or diencephalic injury. This contrasted with the patients demonstrating altered sexual preference whose injuries involved limbic system structures. In some patients altered sexual behaviour may be the presenting or dominant feature of brain injury.

  9. A case of hypoglycemic brain injuries with cortical laminar necrosis.

    Science.gov (United States)

    Lee, Byung-Wan; Jin, Eun Sun; Hwang, Hyung-Sik; Yoo, Hyung-Joon; Jeong, Je Hoon

    2010-06-01

    We report a case of 68-yr-old male who died from brain injuries following an episode of prolonged hypoglycemia. While exploring controversies surrounding magnetic resonance imaging (MRI) findings indicating the bad prognosis in patients with hypoglycemia-induced brain injuries, we here discuss interesting diffusion-MRI of hypoglycemic brain injuries and their prognostic importance focusing on laminar necrosis of the cerebral cortex.

  10. Neuroprotective effects of vagus nerve stimulation on traumatic brain injury

    OpenAIRE

    Zhou, Long; Lin, Jinhuang; Lin, Junming; Kui, Guoju; Zhang, Jianhua; Yu, Yigang

    2014-01-01

    Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and b...

  11. Treatment of Traumatic Brain Injury by Localized Application of Sub-atmospheric Pressure to the Site of Cortical Impact

    Science.gov (United States)

    2013-07-01

    Resuscitation (MTR – the controlled application of vacuum) to the cerebral cortex following a controlled cortical impact (CCI) injury reduces brain... edema and the extent of injury, modulates metabolites in injured neuronal tissues, preserves neuronal tissue, and improves functional recovery. The...hyperintense region ipsilateral to the injured site. There was a large area of T2 hyperintensity ( edema ) sometimes associated with hypointensity

  12. Sports-related traumatic brain injury.

    Science.gov (United States)

    Phillips, Shawn; Woessner, Derek

    2015-06-01

    Concussions have garnered more attention in the medical literature, media, and social media. As such, in the nomenclature according to the Centers for Disease Control and Prevention, the term concussion has been supplanted by the term mild traumatic brain injury. Current numbers indicate that 1.7 million TBIs are documented annually, with estimates around 3 million annually (173,285 sports- and recreation-related TBIs among children and adolescents). The Sideline Concussion Assessment Tool 3 and the NFL Sideline Concussion Assessment Tool are commonly used sideline tools.

  13. [Updates on severe traumatic brain injury management].

    Science.gov (United States)

    Alted López, Emilio; Aznárez, Susana Bermejo; Fernández, Mario Chico

    2009-01-01

    Traumatic brain injury (TBI) is an important reason of morbidity-mortality all over the world, affecting young males more and generating Public Health problem. Unfortunately, the advances in the pathophysiology knowledge have not followed a similar development in therapeutic options, there currently not being any contrasted neuroprotectants. In this article, we have reviewed the epidemiology, pathophysiology and therapeutic measures used in the management of patient with severe TBI. The general measures as well as those aimed at controlling intracranial hypertension, the role of the surgery and some more innovative therapeutic options currently under evaluation in these patients are analyzed.

  14. Visceral adipose tissue inflammation is associated with age-related brain changes and ischemic brain damage in aged mice.

    Science.gov (United States)

    Shin, Jin A; Jeong, Sae Im; Kim, Minsuk; Yoon, Joo Chun; Kim, Hee-Sun; Park, Eun-Mi

    2015-11-01

    Visceral adipose tissue is accumulated with aging. An increase in visceral fat accompanied by low-grade inflammation is associated with several adult-onset diseases. However, the effects of visceral adipose tissue inflammation on the normal and ischemic brains of aged are not clearly defined. To examine the role of visceral adipose tissue inflammation, we evaluated inflammatory cytokines in the serum, visceral adipose tissue, and brain as well as blood-brain barrier (BBB) permeability in aged male mice (20 months) underwent sham or visceral fat removal surgery compared with the young mice (2.5 months). Additionally, ischemic brain injury was compared in young and aged mice with sham and visceral fat removal surgery. Interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels in examined organs were increased in aged mice compared with the young mice, and these levels were reduced in the mice with visceral fat removal. Increased BBB permeability with reduced expression of tight junction proteins in aged sham mice were also decreased in mice with visceral fat removal. After focal ischemic injury, aged mice with visceral fat removal showed a reduction in infarct volumes, BBB permeability, and levels of proinflammatory cytokines in the ischemic brain compared with sham mice, although the neurological outcomes were not significantly improved. In addition, further upregulated visceral adipose tissue inflammation in response to ischemic brain injury was attenuated in mice with visceral fat removal. These results suggest that visceral adipose tissue inflammation is associated with age-related changes in the brain and contributes to the ischemic brain damage in the aged mice. We suggest that visceral adiposity should be considered as a factor affecting brain health and ischemic brain damage in the aged population.

  15. Multimodal neuromonitoring for traumatic brain injury: A shift towards individualized therapy.

    Science.gov (United States)

    Makarenko, Serge; Griesdale, Donald E; Gooderham, Peter; Sekhon, Mypinder S

    2016-04-01

    Multimodal neuromonitoring in the management of traumatic brain injury (TBI) enables clinicians to make individualized management decisions to prevent secondary ischemic brain injury. Traditionally, neuromonitoring in TBI patients has consisted of a combination of clinical examination, neuroimaging and intracranial pressure monitoring. Unfortunately, each of these modalities has its limitations and although pragmatic, this simplistic approach has failed to demonstrate improved outcomes, likely owing to an inability to consider the underlying heterogeneity of various injury patterns. As neurocritical care has evolved, so has our understanding of underlying disease pathophysiology and patient specific considerations. Recent additions to the multimodal neuromonitoring platform include measures of cerebrovascular autoregulation, brain tissue oxygenation, microdialysis and continuous electroencephalography. The implementation of neurocritical care teams to manage patients with advanced brain injury has led to improved outcomes. Herein, we present a narrative review of the recent advances in multimodal neuromonitoring and highlight the utility of dedicated neurocritical care.

  16. Critical care management of severe traumatic brain injury in adults

    OpenAIRE

    Haddad Samir H; Arabi Yaseen M

    2012-01-01

    Abstract Traumatic brain injury (TBI) is a major medical and socio-economic problem, and is the leading cause of death in children and young adults. The critical care management of severe TBI is largely derived from the "Guidelines for the Management of Severe Traumatic Brain Injury" that have been published by the Brain Trauma Foundation. The main objectives are prevention and treatment of intracranial hypertension and secondary brain insults, preservation of cerebral perfusion pressure (CPP...

  17. Neuroglobin expression in rats after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Xin Lin; Min Li; Aijia Shang; Yazhuo Hu; Xiao Yang; Ling Ye; Suyan Bian; Zhongfeng Wang; Dingbiao Zhou

    2012-01-01

    In this study, we used a rat model of severe closed traumatic brain injury to explore the relationship between neuroglobin, brain injury and neuronal apoptosis. Real-time PCR showed that neuroglobin mRNA expression rapidly increased in the rat cerebral cortex, and peaked at 30 minutes and 48 hours following traumatic brain injury. Immunohistochemical staining demonstrated that neuroglobin expression increased and remained high 2 hours to 5 days following injury. The rate of increase in the apoptosis-related Bax/Bcl-2 ratio greatly decreased between 30 minutes and 1 hour as well as between 48 and 72 hours post injury. Expression of neuroglobin and the anti-apoptotic factor Bcl-2 greatly increased, while that of the proapoptotic factor decreased, in the cerebral cortex post severe closed traumatic brain injury. It suggests that neuroglobin might protect neurons from apoptosis after traumatic injury by regulating Bax/Bcl-2 pathway.

  18. Robust whole-brain segmentation: application to traumatic brain injury.

    Science.gov (United States)

    Ledig, Christian; Heckemann, Rolf A; Hammers, Alexander; Lopez, Juan Carlos; Newcombe, Virginia F J; Makropoulos, Antonios; Lötjönen, Jyrki; Menon, David K; Rueckert, Daniel

    2015-04-01

    We propose a framework for the robust and fully-automatic segmentation of magnetic resonance (MR) brain images called "Multi-Atlas Label Propagation with Expectation-Maximisation based refinement" (MALP-EM). The presented approach is based on a robust registration approach (MAPER), highly performant label fusion (joint label fusion) and intensity-based label refinement using EM. We further adapt this framework to be applicable for the segmentation of brain images with gross changes in anatomy. We propose to account for consistent registration errors by relaxing anatomical priors obtained by multi-atlas propagation and a weighting scheme to locally combine anatomical atlas priors and intensity-refined posterior probabilities. The method is evaluated on a benchmark dataset used in a recent MICCAI segmentation challenge. In this context we show that MALP-EM is competitive for the segmentation of MR brain scans of healthy adults when compared to state-of-the-art automatic labelling techniques. To demonstrate the versatility of the proposed approach, we employed MALP-EM to segment 125 MR brain images into 134 regions from subjects who had sustained traumatic brain injury (TBI). We employ a protocol to assess segmentation quality if no manual reference labels are available. Based on this protocol, three independent, blinded raters confirmed on 13 MR brain scans with pathology that MALP-EM is superior to established label fusion techniques. We visually confirm the robustness of our segmentation approach on the full cohort and investigate the potential of derived symmetry-based imaging biomarkers that correlate with and predict clinically relevant variables in TBI such as the Marshall Classification (MC) or Glasgow Outcome Score (GOS). Specifically, we show that we are able to stratify TBI patients with favourable outcomes from non-favourable outcomes with 64.7% accuracy using acute-phase MR images and 66.8% accuracy using follow-up MR images. Furthermore, we are able to

  19. Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    HU Hua; YAO Hong-tian; ZHANG Wei-ping; ZHANG LEI; DING Wei; ZHANG Shi-hong; CHEN Zhong; WEI Er-qing

    2005-01-01

    Objective: To characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors. Methods: Nineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression. Results: AQP4 expression was increased from 15h to at least 8 d after injury. AQP4immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung.Conclusion: AQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.

  20. Neuropsychological rehabilitation for traumatic brain injury patients

    Directory of Open Access Journals (Sweden)

    Marzena Chantsoulis

    2015-05-01

    Full Text Available The aim of this review is to discuss the basic forms of neuropsychological rehabilitation for patients with traumatic brain injury (TBI. More broadly, we discussed cognitive rehabilitation therapy (CRT which constitutes a fundamental component in therapeutic interaction at many centres worldwide. Equally presented is a comprehensive model of rehabilitation, the fundamental component of which is CRT. It should be noted that the principles of this approach first arose in Poland in the 1970s, in other words, several decades before their appearance in other programmemes. Taken into consideration are four factors conditioning the effectiveness of such a process: comprehensiveness, earlier interaction, universality and its individualized character. A comprehensive programmeme of rehabilitation covers: cognitive rehabilitation, individual and group rehabilitation with the application of a therapeutic environment, specialist vocational rehabilitation, as well as family psychotherapy. These training programmemes are conducted within the scope of the ‘Academy of Life,’ which provides support for the patients in their efforts and shows them the means by which they can overcome existing difficulties. Equally emphasized is the close cooperation of the whole team of specialists, as well as the active participation of the family as an essential condition for the effectiveness of rehabilitation and, in effect, a return of the patient to a relatively normal life. Also presented are newly developing neurothechnologies and the neuromarkers of brain injuries. This enables a correct diagnosis to be made and, as a result, the selection of appropriate methods for neuropsychological rehabilitation, including neurotherapy.

  1. Psychiatric disorders and traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Marcelo Schwarzbold

    2008-09-01

    Full Text Available Marcelo Schwarzbold1, Alexandre Diaz1, Evandro Tostes Martins2, Armanda Rufino1, Lúcia Nazareth Amante1,3, Maria Emília Thais1, João Quevedo4, Alexandre Hohl1, Marcelo Neves Linhares1,5,6, Roger Walz1,61Núcleo de Pesquisas em Neurologia Clínica e Experimental (NUPNEC, Departamento de Clínica Médica, Hospital Universitário, UFSC, Florianópolis, SC, Brazil; 2Unidade de Terapia Intensiva, Hospital Governador Celso Ramos, Florianópolis, SC, Brazil; 3Departamento de Enfermagem, UFSC, Florianópolis, SC, Brazil; 4Laboratório de Neurociências, UNESC, Criciúma, SC, Brazil; 5Departamento de Cirurgia, Hospital Universitário, UFSC, Florianópolis, SC, Brazil; 6Centro de Cirurgia de Epilepsia de Santa Catarina (CEPESC, Hospital Governador Celso Ramos, Florianópolis, SC, BrazilAbstract: Psychiatric disorders after traumatic brain injury (TBI are frequent. Researches in this area are important for the patients’ care and they may provide hints for the comprehension of primary psychiatric disorders. Here we approach epidemiology, diagnosis, associated factors and treatment of the main psychiatric disorders after TBI. Finally, the present situation of the knowledge in this field is discussed.Keywords: psychiatric disorders, traumatic brain injury, neuropsychiatry, diagnostic, epidemiology, pathophysiology

  2. Impaired Pituitary Axes Following Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Robert A. Scranton

    2015-07-01

    Full Text Available Pituitary dysfunction following traumatic brain injury (TBI is significant and rarely considered by clinicians. This topic has received much more attention in the last decade. The incidence of post TBI anterior pituitary dysfunction is around 30% acutely, and declines to around 20% by one year. Growth hormone and gonadotrophic hormones are the most common deficiencies seen after traumatic brain injury, but also the most likely to spontaneously recover. The majority of deficiencies present within the first year, but extreme delayed presentation has been reported. Information on posterior pituitary dysfunction is less reliable ranging from 3%–40% incidence but prospective data suggests a rate around 5%. The mechanism, risk factors, natural history, and long-term effect of treatment are poorly defined in the literature and limited by a lack of standardization. Post TBI pituitary dysfunction is an entity to recognize with significant clinical relevance. Secondary hypoadrenalism, hypothyroidism and central diabetes insipidus should be treated acutely while deficiencies in growth and gonadotrophic hormones should be initially observed.

  3. Altered calcium signaling following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    John Thomas Weber

    2012-04-01

    Full Text Available Cell death and dysfunction after traumatic brain injury (TBI is caused by a primary phase, related to direct mechanical disruption of the brain, and a secondary phase which consists of delayed events initiated at the time of the physical insult. Arguably, the calcium ion contributes greatly to the delayed cell damage and death after TBI. A large, sustained influx of calcium into cells can initiate cell death signaling cascades, through activation of several degradative enzymes, such as proteases and endonucleases. However, a sustained level of intracellular free calcium is not necessarily lethal, but the specific route of calcium entry may couple calcium directly to cell death pathways. Other sources of calcium, such as intracellular calcium stores, can also contribute to cell damage. In addition, calcium-mediated signal transduction pathways in neurons may be perturbed following injury. These latter types of alterations may contribute to abnormal physiology in neurons that do not necessarily die after a traumatic episode. This review provides an overview of experimental evidence that has led to our current understanding of the role of calcium signaling in death and dysfunction following TBI.

  4. Experimental model for civilian ballistic brain injury biomechanics quantification.

    Science.gov (United States)

    Zhang, Jiangyue; Yoganandan, Narayan; Pintar, Frank A; Guan, Yabo; Gennarelli, Thomas A

    2007-01-01

    Biomechanical quantification of projectile penetration using experimental head models can enhance the understanding of civilian ballistic brain injury and advance treatment. Two of the most commonly used handgun projectiles (25-cal, 275 m/s and 9 mm, 395 m/s) were discharged to spherical head models with gelatin and Sylgard simulants. Four ballistic pressure transducers recorded temporal pressure distributions at 308kHz, and temporal cavity dynamics were captured at 20,000 frames/second (fps) using high-speed digital video images. Pressures ranged from 644.6 to -92.8 kPa. Entry pressures in gelatin models were higher than exit pressures, whereas in Sylgard models entry pressures were lower or equivalent to exit pressures. Gelatin responded with brittle-type failure, while Sylgard demonstrated a ductile pattern through formation of micro-bubbles along projectile path. Temporary cavities in Sylgard models were 1.5-2x larger than gelatin models. Pressures in Sylgard models were more sensitive to projectile velocity and diameter increase, indicating Sylgard was more rate sensitive than gelatin. Based on failure patterns and brain tissue rate-sensitive characteristics, Sylgard was found to be an appropriate simulant. Compared with spherical projectile data, full-metal jacket (FMJ) projectiles produced different temporary cavity and pressures, demonstrating shape effects. Models using Sylgard gel and FMJ projectiles are appropriate to enhance understanding and mechanisms of ballistic brain injury.

  5. Incorporating Human Body Mass in Standards of Helmet Impact Protection against Traumatic Brain Injury

    CERN Document Server

    Blackman, Eric G

    2009-01-01

    Impact induced traumatic brain injury (ITBI) describes brain injury from head impact not necessarily accompanied by skull fracture. For sufficiently abrupt head impact decelerations, ITBI results from brain tissue stress incurred as the brain crashes into the inside of the skull wall, displacing the surrounding cerebral spinal fluid (CSF). Proper helmet cushioning can damp the impact force and reduce ITBI. But force is mass times acceleration and commonly used helmet blunt impact standards are based only on acceleration thresholds. Here I show how this implies that present standards overestimate the minimum acceleration onset for ITBI by implicitly assuming that the brain is mechanically decoupled from the body. I quantify how an arbitrary orientation of the body with respect to impact direction increases the effective mass that should be used in calculating the required damping force and injury threshold accelerations. I suggest a practical method to incorporate the body mass and impact angle into ITBI helme...

  6. Pathophysiology and Treatment of Severe Traumatic Brain Injuries in Children.

    Science.gov (United States)

    Allen, Kimberly A

    2016-02-01

    Traumatic brain injuries (TBIs) in children are a major cause of morbidity and mortality worldwide. Severe TBIs account for 15,000 admissions annually and a mortality rate of 24% in children in the United States. The purpose of this article is to explore pathophysiologic events, examine monitoring techniques, and explain current treatment modalities and nursing care related to caring for children with severe TBI. The primary injury of a TBI is because of direct trauma from an external force, a penetrating object, blast waves, or a jolt to the head. Secondary injury occurs because of alterations in cerebral blood flow, and the development of cerebral edema leads to necrotic and apoptotic cellular death after TBI. Monitoring focuses on intracranial pressure, cerebral oxygenation, cerebral edema, and cerebrovascular injuries. If abnormalities are identified, treatments are available to manage the negative effects caused to the cerebral tissue. The mainstay treatments are hyperosmolar therapy; temperature control; cerebrospinal fluid drainage; barbiturate therapy; decompressive craniectomy; analgesia, sedation, and neuromuscular blockade; and antiseizure prophylaxis.

  7. Role of Lipids in Brain Injury and Diseases.

    Science.gov (United States)

    Adibhatla, Rao Muralikrishna; Hatcher, J F

    2007-08-01

    Lipid metabolism is of particular interest due to its high concentration in CNS. The importance of lipids in cell signaling and tissue physiology is demonstrated by many CNS disorders and injuries that involve deregulated metabolism. The long suffering lipid field is gaining reputation and respect as evidenced through the Center of Biomedical Research Excellence in Lipidomics and Pathobiology (COBRE), Lipid MAPS (Metabolites And Pathways Strategy) Consortium sponsored by NIH, European initiatives for decoding the lipids through genomic approaches, and Genomics of Lipid-associated Disorder (GOLD) project initiated by Austrian government. This review attempts to provide an overview of the lipid imbalances associated with neurological disorders (Alzheimer's, Parkinson's; Niemann-Pick; Multiple sclerosis, Huntington, amyotrophic lateral sclerosis, schizophrenia, bipolar disorders and epilepsy) and CNS injury (Stroke, traumatic brain injury; and spinal cord injury) and a few provocative thoughts. Lipidomic analyses along with RNA silencing will provide new insights into the role of lipid intermediates in cell signaling and hopefully open new avenues for prevention or treatment options.

  8. Chronic Traumatic Brain Injury in Amateur Boxers

    Directory of Open Access Journals (Sweden)

    M. Rahmati

    2008-04-01

    Full Text Available Introduction & objective: Despite of young and adolescence intent to the boxing sport, because of dominant aggression and direct blows contact to head, face and central nervous system, it is continuously criticize by different groups. The groups of sporting and physician conventions are distinguished boxing with physical and neuropsychological disorders and some groups believe that side effects of this sport are not more than other sports. For this base the aim of this study was to determine the chronic traumatic brain injury in a group amateur boxers.Materials & Methods: In a case-control study, three groups of sport men were considered, each group contained 20 randomly selected cases. The first group were amateur boxers with 4 years minimal activity(directly has been presented to the head blows, second group were amateur soccer players with 4 years minimal activity(has been presented to the not very severe head blows, third group were non athlete subjects .The groups were matched in weight, height, age and education .To understand brain disorder interview by medicine method has been used, then Wiskancin, Bonardele, Bender geshtalt, Kim karad visual memory, Benton and wechler memory (Alef type tests has been performed and EEG has got in the same hour and condition.Results: The homogeneity of between group variances was gained by the statistical method. Also between structural–visual abilities neuropsychological aspect in groups, significant difference has been gained (p= 0.000. In Kim karad visual memory test at the mild and long term visual memory deficit, significant differences between three groups was observed (P= 0.000, P=0.009 that least score has been belonged to the boxers. Also in boxers 6 abnormal EEGs is observed.Conclusion: It can be said that of four years amateur boxing can affect on boxers visual and memory perception and their spatial orientation. Additionally our study have showed that amateur boxing has a significant

  9. Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors.

    Science.gov (United States)

    Galgano, Michael; Toshkezi, Gentian; Qiu, Xuecheng; Russell, Thomas; Chin, Lawrence; Zhao, Li-Ru

    2016-11-22

    Traumatic brain injury presents in various forms ranging from mild alterations of consciousness to an unrelenting comatose state and death. In the most severe form of traumatic brain injury, the entirety of the brain is affected by a diffuse type of injury and swelling. Treatment modalities vary extensively based on the severity of the injury and range from daily cognitive therapy sessions to radical surgery such as bilateral decompressive craniectomies. Guidelines have been set forth regarding the optimal management of traumatic brain injury, but they must be taken in context of the situation and cannot be used in every individual circumstance. In this review article, we have summarized the current status of treatment for traumatic brain injury in both clinical practice and basic research. We have put forth a brief overview of the various subtypes of traumatic injuries, optimal medical management, as well as both the non-invasive and invasive monitoring modalities, in addition to the surgical interventions necessary in particular instances. We have overviewed the main achievements in searching for therapeutic strategies of traumatic brain injury in basic science. We have also discussed the future direction for developing traumatic brain injury treatment from an experimental perspective.

  10. White Matter Damage and Cognitive Impairment after Traumatic Brain Injury

    Science.gov (United States)

    Kinnunen, Kirsi Maria; Greenwood, Richard; Powell, Jane Hilary; Leech, Robert; Hawkins, Peter Charlie; Bonnelle, Valerie; Patel, Maneesh Chandrakant; Counsell, Serena Jane; Sharp, David James

    2011-01-01

    White matter disruption is an important determinant of cognitive impairment after brain injury, but conventional neuroimaging underestimates its extent. In contrast, diffusion tensor imaging provides a validated and sensitive way of identifying the impact of axonal injury. The relationship between cognitive impairment after traumatic brain injury…

  11. Mesenchymal Stem Cell Transplantation Attenuates Brain Injury After Neonatal Stroke

    NARCIS (Netherlands)

    van Velthoven, Cindy T. J.; Sheldon, R. Ann; Kavelaars, Annemieke; Derugin, Nikita; Vexler, Zinaida S.; Willemen, Hanneke L. D. M.; Maas, Mirjam; Heijnen, Cobi J.; Ferriero, Donna M.

    2013-01-01

    Background and Purpose-Brain injury caused by stroke is a frequent cause of perinatal morbidity and mortality with limited therapeutic options. Mesenchymal stem cells (MSC) have been shown to improve outcome after neonatal hypoxic-ischemic brain injury mainly by secretion of growth factors stimulati

  12. Pharmacological Neuroprotection after Perinatal Hypoxic-Ischemic Brain Injury

    NARCIS (Netherlands)

    Fan, Xiyong; Kavelaars, Annemieke; Heijnen, Cobi J.; Groenendaal, Floris; van Bel, Frank

    2010-01-01

    Perinatal hypoxia-ischemia (HI) is an important cause of neonatal brain injury. Recent progress in the search for neuroprotective compounds has provided us with several promising drugs to reduce perinatal HI-induced brain injury. In the early stage (first 6 hours after birth) therapies are concentra

  13. [Metallothionein-I/II in brain injury repair mechanism and its application in forensic medicine].

    Science.gov (United States)

    Li, Dong; Li, Ru-bo; Lin, Ju-li

    2013-10-01

    Metallothionein (MT) is a kind of metal binding protein. As an important member in metallothionein family, MT-I/II regulates metabolism and detoxication of brain metal ion and scavenges free radicals. It is capable of anti-inflammatory response and anti-oxidative stress so as to protect the brain tissue. During the repair process of brain injury, the latest study showed that MT-I/II could stimulate brain anti-inflammatory factors, growth factors, neurotrophic factors and the expression of the receptor, and promote the extension of axon of neuron, which makes contribution to the regeneration of neuron and has important effect on the recovery of brain injury. Based on the findings, this article reviews the structure, expression, distribution, adjustion, function, mechanism in the repair of brain injury of MT-I/II and its application prospect in forensic medicine. It could provide a new approach for the design and manufacture of brain injury drugs as well as for age estimation of the brain injury.

  14. Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

    OpenAIRE

    2012-01-01

    Microglia account for approximately 12% of the total cellular population in the mammalian brain. While neurons and astrocytes are considered the major cell types of the nervous system, microglia play a significant role in normal brain physiology by monitoring tissue for debris and pathogens and maintaining homeostasis in the parenchyma via phagocytic activity 1,2. Microglia are activated during a number of injury and disease conditions, including neurodegenerative disease, traumatic brain inj...

  15. Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    HuaHu; Wei-PingZhang; LeiZhang; ZhongChen; Er-QingWei

    2004-01-01

    Aquaporin-4 (AQP4) is one of the aquaporins (AQPs), a water channel family. In the brain, AQP4 is expressed in astroeyte foot processes, and plays an important role in water homeostasis and in the formation of brain edema. In our study, AQP4 expression in human brain specimens from patients with traumatic brain injury or different brain tumors was detected

  16. Outcome after Traumatic Brain Injury : Epidemiology, impact and assessment

    NARCIS (Netherlands)

    A.C. Scholten (Annemieke)

    2016-01-01

    markdownabstractInjuries are among the leading causes of death and disability in the world, often imposing great personal suffering and economic costs. An important severe injury that often affects young people is a traumatic brain injury (TBI). Over the past decades, the number of survivors of se

  17. Serious brain injury coexisting with multiple injuries caused by traffic accidents in 69 cases

    Institute of Scientific and Technical Information of China (English)

    张浚; 张鹤飞; 等

    1999-01-01

    Objective To explore the speciality,diagnosis,cure principle of serious brain injury coexisting with nultiple injuries caused by traffic accidents.Methods To analyze the clinic data of 69 cases of serious rain injury combined by oter parts of injuries caused by traffic accidents received from January 1998 to April 1999.Results This type of injury took up 11.5 percent of brain injuries in the same term and 33.6 percent of serious brain injuries.The specialities of the injury are that most of them were pedestrians crashed by vehicles.Coesisting injuries including chest injury and limb fractures accounted for a large part.The brain injury usally presented profound disturbance of consciousness,being dangerous and complicated,and a high ISS value.After treatment 13 cases died,9 cases was heavily crippled,11 cases lightly crippled,and 36 cases recovered.The death was usually caused by brain injury.Conclusions Road traffic accidents increased substantially every year.Most of them are related with violating drive rules and regulations.It is important to decrease the road traffic accidents by strengthening propaganda on traffic safety and traffic management.The main principles for salvage should emphasize the importance of pre-hospital emergency rescue and the accurate diagnosis rate,especially the distinction between coma and shock.The priority should be put on those injuries threatening to life.

  18. Relationship between trauma-induced coagulopathy and progressive hemorrhagic injury in patients with traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Jia Liu; Heng-Li Tian

    2016-01-01

    Progressive hemorrhagic injury (PHI) can be divided into coagulopathy-related PHI and normal coagulation PHI.Coagulation disorders after traumatic brain injuries can be included in trauma-induced coagulopathy (TIC).Some studies showed that TIC is associated with PHI and increases the rates of disability and mortality.In this review,we discussed some mechanisms in TIC,which is of great importance in the development of PHI,including tissue factor (TF) hypothesis,protein C pathway and thrombocytopenia.The main mechanism in the relation of TIC to PHI is hypocoagulability.We also reviewed some coagulopathy parameters and proposed some possible risk factors,predictors and therapies.

  19. Organotypic slice culture of embryonic brain tissue.

    Science.gov (United States)

    Daza, Ray A M; Englund, Chris; Hevner, Robert F

    2007-12-01

    INTRODUCTIONThis protocol describes how to dissect, assemble, and cultivate mouse embryonic (E) brain tissue from age E11.5 to E18.5 (days) for organotypic slice culture. These preparations can be used for a variety of assays and studies including coculture of different brain regions, cell migration assays, axon guidance assays, and DNA electroporation experiments. During electroporation, an electric current is applied to the surface of a specific target area of the brain slice in order to open holes in the plasma membrane and introduce a plasmid of coding DNA. The floating slice-on-membrane construct helps to preserve the structural integrity of the brain slices, while maintaining easy experimental access and optimal viability. Experiments can be monitored in living slices (e.g., with confocal imaging), and further studies can be completed using slices that have been fixed and cryosectioned at the end of the experiment. Any region of embryonic brain or spinal tissue can be used in this protocol.

  20. Genetic susceptibility to traumatic brain injury and apolipoprotein E gene

    Institute of Scientific and Technical Information of China (English)

    SUN Xiao-chuan; JIANG Yong

    2008-01-01

    @@ Traumatic brain injury (TBI) is defined as an injury caused by a blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain. It is a common emergency and severe case in neurosurgery field. Nowadays, there are more and more evidences showing that TBI, which is apparently similar in pathology and severity in the acute stage, may have different outcomes.

  1. Neonatal ischemic brain injury: what every radiologist needs to know

    Energy Technology Data Exchange (ETDEWEB)

    Badve, Chaitra A.; Khanna, Paritosh C.; Ishak, Gisele E. [Seattle Children' s Hospital, University of Washington Medical Center, Department of Radiology, Seattle, WA (United States)

    2012-05-15

    We present a pictorial review of neonatal ischemic brain injury and look at its pathophysiology, imaging features and differential diagnoses from a radiologist's perspective. The concept of perinatal stroke is defined and its distinction from hypoxic-ischemic injury is emphasized. A brief review of recent imaging advances is included and a diagnostic approach to neonatal ischemic brain injury is suggested. (orig.)

  2. The potential of neural transplantation for brain repair and regeneration following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Dong Sun

    2016-01-01

    Traumatic brain injury is a major health problem worldwide. Currently, there is no effective treatment to improve neural structural repair and functional recovery of patients in the clinic. Cell transplantation is a potential strategy to repair and regenerate the injured brain. This review article summarized recent de-velopment in cell transplantation studies for post-traumatic brain injury brain repair with varying types of cell sources. It also discussed the potential of neural transplantation to repair/promote recovery of the injured brain following traumatic brain injury.

  3. Inhomogeneous Deformation of Brain Tissue During Tension Tests

    CERN Document Server

    Rashid, Badar; Gilchrist, Michael D; 10.1016/j.commatsci.2012.05.030

    2013-01-01

    Mechanical characterization of brain tissue has been investigated extensively by various research groups over the past fifty years. These properties are particularly important for modelling Traumatic Brain Injury (TBI). In this research, we present the design and calibration of a High Rate Tension Device (HRTD) capable of performing tests up to a maximum strain rate of 90/s. We use experimental and numerical methods to investigate the effects of inhomogeneous deformation of porcine brain tissue during tension at different specimen thicknesses (4.0-14.0 mm), by performing tension tests at a strain rate of 30/s. One-term Ogden material parameters (mu = 4395.0 Pa, alpha = -2.8) were derived by performing an inverse finite element analysis to model all experimental data. A similar procedure was adopted to determine Young's modulus (E= 11200 Pa) of the linear elastic regime. Based on this analysis, brain specimens of aspect ratio (diameter/thickness) S < 1.0 are required to minimise the effects of inhomogeneous...

  4. Symptom Complaints Following Combat-Related Traumatic Brain Injury: Relationship to Traumatic Brain Injury Severity and Posttraumatic Stress Disorder

    Science.gov (United States)

    2009-08-01

    being less competent (Sawchyn, Mateer, & Suffi eld, 2005 ). Mild TBI has also been associated with greater emotional distress ( Leininger , Kreutzer...brain injury . Brain Injury , 23 , 83 – 91 . Leininger , B.E. , Kreutzer , J.S. , & Hill , M.R . ( 1991 ). Comparison of minor and severe

  5. Neuroprotective Strategies after Repetitive Mild Traumatic Brain Injury

    Science.gov (United States)

    2011-06-01

    performance in the HBOT groups improved sig- nificantly and was highly correlated with increased ipsilat- eral hippocampal blood volume ( cerebrovascular ...Oxygen Therapy Induces Cerebrovascular Changes and Improves Complex Learning/Memory in a Rat Open Head Bonk Chronic Brain Contusion Model. Undersea...injury. Dynamic brain trauma includes direct injury where trauma is directly imposed on the brain (e.g., non- accidental trauma, contact sports, falls

  6. Traumatic Brain Injury and Delayed Sequelae: A Review - Traumatic Brain Injury and Mild Traumatic Brain Injury (Concussion) are Precursors to Later-Onset Brain Disorders, Including Early-Onset Dementia

    OpenAIRE

    Kiraly, Michael A.; Kiraly, Stephen J.

    2007-01-01

    Brain injuries are too common. Most people are unaware of the incidence of and horrendous consequences of traumatic brain injury (TBI) and mild traumatic brain injury (MTBI). Research and the advent of sophisticated imaging have led to progression in the understanding of brain pathophysiology following TBI. Seminal evidence from animal and human experiments demonstrate links between TBI and the subsequent onset of premature, psychiatric syndromes and neurodegenerative diseases, including Alzh...

  7. Significance of prevertebral soft tissue measurement in cervical spine injuries

    Energy Technology Data Exchange (ETDEWEB)

    Dai Liyang E-mail: lydai@etang.com

    2004-07-01

    Objective: The objective of this study was to evaluate the diagnostic value of prevertebral soft tissue swelling in cervical spine injuries. Materials and methods: A group of 107 consecutive patients with suspected injuries of the cervical vertebrae were reviewed retrospectively to identify the presence of prevertebral soft tissue swelling and to investigate the association of prevertebral soft tissue swelling with the types and degrees of cervical spine injuries. Results: Prevertebral soft tissue swelling occurred in 47 (43.9%) patients. Of the 47 patients, 38 were found with bony injury and nine were without. The statistic difference was significant (P<0.05). No correlation was demonstrated between soft tissue swelling and either the injured level of the cervical vertebrae or the degree of the spinal cord injury (P>0.05). Anterior element injuries in the cervical vertebrae had widening of the prevertebral soft tissue more than posterior element injuries (P<0.05). Conclusion: The diagnostic value of prevertebral soft tissue swelling for cervical spine injuries is significant, but the absence of this sign does not mean that further image evaluation can be spared.

  8. Iatrogenic traumatic brain injury during tooth extraction.

    Science.gov (United States)

    Troxel, Mark

    2015-01-01

    An 8 yr old spayed female Yorkshire terrier was referred for evaluation of progressive neurological signs after a routine dental prophylaxis with tooth extractions. The patient was circling to the left and blind in the right eye with right hemiparesis. Neurolocalization was to the left forebrain. MRI revealed a linear tract extending from the caudal oropharynx, through the left retrobulbar space and frontal lobe, into the left parietal lobe. A small skull fracture was identified in the frontal bone through which the linear tract passed. Those findings were consistent with iatrogenic trauma from slippage of a dental elevator during extraction of tooth 210. The dog was treated empirically with clindamycin. The patient regained most of its normal neurological function within the first 4 mo after the initial injury. Although still not normal, the dog has a good quality of life. Traumatic brain injury is a rarely reported complication of extraction. Care must be taken while performing dental cleaning and tooth extraction, especially of the maxillary premolar and molar teeth to avoid iatrogenic damage to surrounding structures.

  9. Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury.

    Science.gov (United States)

    Durham, William J; Foreman, Jack P; Randolph, Kathleen M; Danesi, Christopher P; Spratt, Heidi; Masel, Brian D; Summons, Jennifer R; Singh, Charan K; Morrison, Melissa; Robles, Claudia; Wolfram, Cindy; Kreber, Lisa A; Urban, Randall J; Sheffield-Moore, Melinda; Masel, Brent E

    2017-01-15

    Individuals with a history of traumatic brain injury (TBI) are at increased risk for a number of disorders, including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. However, mediators of the long-term morbidity are uncertain. We conducted a multi-site, prospective trial in chronic TBI patients (∼18 years post-TBI) living in long-term 24-h care environments and local controls without a history of head injury. Inability to give informed consent was exclusionary for participation. A total of 41 individuals (17 moderate-severe TBI, 24 controls) were studied before and after consumption of a standardized breakfast to determine if concentrations of amino acids, cytokines, C-reactive protein, and insulin are potential mediators of long-term TBI morbidity. Analyte concentrations were measured in serum drawn before (fasting) and 1 h after meal consumption. Mean ages were 44 ± 15 and 49 ± 11 years for controls and chronic TBI patients, respectively. Chronic TBI patients had significantly lower circulating concentrations of numerous individual amino acids, as well as essential amino acids (p = 0.03) and large neutral amino acids (p = 0.003) considered as groups, and displayed fundamentally altered cytokine-amino acid relationships. Many years after injury, TBI patients exhibit abnormal metabolic responses and altered relationships between circulating amino acids, cytokines, and hormones. This pattern is consistent with TBI, inducing a chronic disease state in patients. Understanding the mechanisms causing the chronic disease state could lead to new treatments for its prevention.

  10. Altered expression of metabotropic glutamate receptor 1 alpha after acute diffuse brain injury Effect of the competitive antagonist 1-aminoindan-1, 5-dicarboxylic acid

    Institute of Scientific and Technical Information of China (English)

    Fei Cao; Mantao Chen; Gu Li; Ke Ye; Xin Huang; Xiujue Zheng

    2012-01-01

    The diffuse brain injury model was conducted in Sprague-Dawley rats, according to Marmarou's free-fall attack. The water content in brain tissue, expression of metabotropic glutamate receptor 1α mRNA and protein were significantly increased after injury, reached a peak at 24 hours, and then gradually decreased. After treatment with the competitive antagonist of metabotropic glutamate receptor 1α, (RS)-1-aminoindan-1, 5-dicarboxylic acid, the water content of brain tissues decreased between 12-72 hours after injury, and neurological behaviors improved at 2 weeks. These experimental findings suggest that the 1-aminoindan-1, 5-dicarboxylic acid may result in marked neuroprotection against diffuse brain injury.

  11. Extracellular Brain pH and Outcome following Severe Traumatic Brain Injury.

    Science.gov (United States)

    Gupta, Arun K; Zygun, David A; Johnston, Andrew J; Steiner, Luzius A; Al-Rawi, Pippa G; Chatfield, Dot; Shepherd, Edna; Kirkpatrick, Peter J; Hutchinson, Peter J; Menon, David K

    2004-06-01

    The ability to measure brain tissue chemistry has led to valuable information regarding pathophysiological changes in patients with traumatic brain injury (TBI). Over the last few years, the focus has been on monitoring changes in brain tissue oxygen to determine thresholds of ischemia that affect outcome. However, the variability of this measurement suggests that it may not be a robust method. We have therefore investigated the relationship of brain tissue pH (pH(b)) and outcome in patients with TBI. We retrospectively analyzed prospectively collected data of 38 patients admitted to the Neurosciences Critical Care Unit with TBI between 1998 and 2003, and who had a multiparameter tissue gas sensor inserted into the brain. All patients were managed using an evidence-based protocol targeting CPP > 70 mm Hg. Physiological variables were averaged over 4 min and analyzed using a generalized least squares random effects model to determine the temporal profile of pH(b) and its association with outcome. Median (IQR) minimum pH(b) was 7.00 (6.89, 7.08), median (IQR) maximum pH(b) was 7.25 (7.18, 7.33), and median (IQR) patient averaged pH(b) was 7.13 (7.07, 7.17). pH(b) was significantly lower in those who did not survive their hospital stay compared to those that survived. In addition, those with unfavorable neurological outcome had lower pH(b) values than those with favorable neurological outcome. pH(b) differentiated between survivors and non-survivors. Measurement of pH(b) may be a useful indicator of outcome in patients with TBI.

  12. Clinical neurorestorative progress in traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Huang H

    2015-03-01

    Full Text Available Huiling Huang,1 Lin Chen,2,3 Hongyun Huang4–61Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Huanhu Hospital, Tianjin Neurosurgical Institute, Tianjin, People's Republic of China; 2Medical Center, Tsinghua University, Beijing, People's Republic of China; 3Tsinghua University Yuquan Hospital, Beijing, People's Republic of China; 4General Hospital of Chinese people's Armed Police Forces, 5Beijing Rehabilitation Hospital of Capital Medical University, Beijing, People's Republic of China; 6Beijing Hongtianji Neuroscience Academy, Beijing, People's Republic of ChinaAbstract: Traumatic brain injury (TBI is a leading cause of death and disability from trauma to the central nervous system. Besides the surgical interventions and symptomatic management, the conventional therapies for TBI and its sequelae are still limited. Recently emerging evidence suggests that some neurorestorative treatments appear to have a potential therapeutic role for TBI and improving the patient's quality of life. The current clinical neurorestorative strategies available in TBI include pharmacological treatments (recombinant human interleukin-1 receptor antagonist, amantadine, lithium, and valproate, the neuromodulation treatments (repetitive transcranial magnetic stimulation, transcranial direct current stimulation, and low-level laser therapy, cell transplantation (bone marrow stromal cells and umbilical cord stromal cells, and combined neurorehabilitation. In this review, we summarize the recent clinical neurorestorative progress in the management of neurodegeneration as well as cognitive and motor deficits after TBI; indeed further clinical trials are required to provide more robust evidence.Keywords: brain trauma, neurorestorative treatment, cell transplantation, clinical study

  13. Physical Mechanisms of Soft Tissue Injury from Penetrating Ballistic Impact

    Science.gov (United States)

    2012-11-30

    2008; 64(6):1420-1426. 18. Gryth D, Rocksen D, Persson JK, Arborelius UP, Drobin D, Bursell J, Olsson LG, Kjellstrom BT. Severe lung contusion and...elastic tissues such as lungs and muscle, where the tissue tends to spring back into place with little damage from temporary stretch, most tissue...in a study comparing penetrating thoracic wounds caused by stab injuries to those caused by gunshot injuries, the occurrence of lung

  14. Opioid Abuse After Traumatic Brain Injury: Evaluation Using Rodet Models

    Science.gov (United States)

    2014-07-01

    dependence development using both precipitated and spontaneous withdrawal. Key findings to date: • There was no difference in baseline nociception ( pain ...analgesia studies demonstrate that moderate brain injury does not result in an altered pain state or diminished response to oxycodone analgesia, the... pain medications. There is significant overlap in anatomical brain regions involved in reward pathways associated with addiction and the brain regions

  15. Microglia and Inflammation: Impact on Developmental Brain Injuries

    Science.gov (United States)

    Chew, Li-Jin; Takanohashi, Asako; Bell, Michael

    2006-01-01

    Inflammation during the perinatal period has become a recognized risk factor for developmental brain injuries over the past decade or more. To fully understand the relationship between inflammation and brain development, a comprehensive knowledge about the immune system within the brain is essential. Microglia are resident immune cells within the…

  16. Chronic Traumatic Encephalopathy: The Neuropathological Legacy of Traumatic Brain Injury.

    Science.gov (United States)

    Hay, Jennifer; Johnson, Victoria E; Smith, Douglas H; Stewart, William

    2016-05-23

    Almost a century ago, the first clinical account of the punch-drunk syndrome emerged, describing chronic neurological and neuropsychiatric sequelae occurring in former boxers. Thereafter, throughout the twentieth century, further reports added to our understanding of the neuropathological consequences of a career in boxing, leading to descriptions of a distinct neurodegenerative pathology, termed dementia pugilistica. During the past decade, growing recognition of this pathology in autopsy studies of nonboxers who were exposed to repetitive, mild traumatic brain injury, or to a single, moderate or severe traumatic brain injury, has led to an awareness that it is exposure to traumatic brain injury that carries with it a risk of this neurodegenerative disease, not the sport or the circumstance in which the injury is sustained. Furthermore, the neuropathology of the neurodegeneration that occurs after traumatic brain injury, now termed chronic traumatic encephalopathy, is acknowledged as being a complex, mixed, but distinctive pathology, the detail of which is reviewed in this article.

  17. Sports-related brain injuries: connecting pathology to diagnosis.

    Science.gov (United States)

    Pan, James; Connolly, Ian D; Dangelmajer, Sean; Kintzing, James; Ho, Allen L; Grant, Gerald

    2016-04-01

    Brain injuries are becoming increasingly common in athletes and represent an important diagnostic challenge. Early detection and management of brain injuries in sports are of utmost importance in preventing chronic neurological and psychiatric decline. These types of injuries incurred during sports are referred to as mild traumatic brain injuries, which represent a heterogeneous spectrum of disease. The most dramatic manifestation of chronic mild traumatic brain injuries is termed chronic traumatic encephalopathy, which is associated with profound neuropsychiatric deficits. Because chronic traumatic encephalopathy can only be diagnosed by postmortem examination, new diagnostic methodologies are needed for early detection and amelioration of disease burden. This review examines the pathology driving changes in athletes participating in high-impact sports and how this understanding can lead to innovations in neuroimaging and biomarker discovery.

  18. Properdin in complement activation and tissue injury.

    Science.gov (United States)

    Lesher, Allison M; Nilsson, Bo; Song, Wen-Chao

    2013-12-15

    The plasma protein properdin is the only known positive regulator of complement activation. Although regarded as an initiator of the alternative pathway of complement activation at the time of its discovery more than a half century ago, the role and mechanism of action of properdin in the complement cascade has undergone significant conceptual evolution since then. Despite the long history of research on properdin, however, new insight and unexpected findings on the role of properdin in complement activation, pathogen infection and host tissue injury are still being revealed by ongoing investigations. In this article, we provide a brief review on recent studies that shed new light on properdin biology, focusing on the following three topics: (1) its role as a pattern recognition molecule to direct and trigger complement activation, (2) its context-dependent requirement in complement activation on foreign and host cell surfaces, and (3) its involvement in alternative pathway complement-mediated immune disorders and considerations of properdin as a potential therapeutic target in human diseases.

  19. Traumatic Brain Injury and Delayed Sequelae: A Review - Traumatic Brain Injury and Mild Traumatic Brain Injury (Concussion are Precursors to Later-Onset Brain Disorders, Including Early-Onset Dementia

    Directory of Open Access Journals (Sweden)

    Michael A. Kiraly

    2007-01-01

    Full Text Available Brain injuries are too common. Most people are unaware of the incidence of and horrendous consequences of traumatic brain injury (TBI and mild traumatic brain injury (MTBI. Research and the advent of sophisticated imaging have led to progression in the understanding of brain pathophysiology following TBI. Seminal evidence from animal and human experiments demonstrate links between TBI and the subsequent onset of premature, psychiatric syndromes and neurodegenerative diseases, including Alzheimer's disease (AD and Parkinson's disease (PD. Objectives of this summary are, therefore, to instill appreciation regarding the importance of brain injury prevention, diagnosis, and treatment, and to increase awareness regarding the long-term delayed consequences following TBI.

  20. Neural stem cell transplantation with Nogo-66 receptor gene silencing to treat severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Dong Wang; Jianjun Zhang; Jingjian Ma; Yuan Mu; Yinghui Zhuang

    2011-01-01

    Inhibition of neurite growth, which is mediated by the Nogo-66 receptor (NgR), affects nerve regeneration following neural stem cell (NSC) transplantation. The present study utilized RNA interference to silence NgR gene expression in NSCs, which were subsequently transplanted into rats with traumatic brain injury. Following transplantation of NSCs transfected with small interfering RNA,typical neural cell-like morphology was detected in injured brain tissues, and was accompanied by absence of brain tissue cavity, increased growth-associated protein 43 mRNA and protein expression,and improved neurological function compared with NSC transplantation alone. Results demonstrated that NSC transplantation with silenced NgR gene promoted functional recovery following brain injury.

  1. DARPA challenge: developing new technologies for brain and spinal injuries

    Science.gov (United States)

    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.

  2. Developmental traumatic brain injury decreased brain derived neurotrophic factor expression late after injury.

    Science.gov (United States)

    Schober, Michelle Elena; Block, Benjamin; Requena, Daniela F; Hale, Merica A; Lane, Robert H

    2012-06-01

    Pediatric traumatic brain injury (TBI) is a major cause of acquired cognitive dysfunction in children. Hippocampal Brain Derived Neurotrophic Factor (BDNF) is important for normal cognition. Little is known about the effects of TBI on BDNF levels in the developing hippocampus. We used controlled cortical impact (CCI) in the 17 day old rat pup to test the hypothesis that CCI would first increase rat hippocampal BDNF mRNA/protein levels relative to SHAM and Naïve rats by post injury day (PID) 2 and then decrease BDNF mRNA/protein by PID14. Relative to SHAM, CCI did not change BDNF mRNA/protein levels in the injured hippocampus in the first 2 days after injury but did decrease BDNF protein at PID14. Surprisingly, BDNF mRNA decreased at PID 1, 3, 7 and 14, and BDNF protein decreased at PID 2, in SHAM and CCI hippocampi relative to Naïve. In conclusion, TBI decreased BDNF protein in the injured rat pup hippocampus 14 days after injury. BDNF mRNA levels decreased in both CCI and SHAM hippocampi relative to Naïve, suggesting that certain aspects of the experimental paradigm (such as craniotomy, anesthesia, and/or maternal separation) may decrease the expression of BDNF in the developing hippocampus. While BDNF is important for normal cognition, no inferences can be made regarding the cognitive impact of any of these factors. Such findings, however, suggest that meticulous attention to the experimental paradigm, and possible inclusion of a Naïve group, is warranted in studies of BDNF expression in the developing brain after TBI.

  3. Traumatic Brain Injury in Rats Induces Lung Injury and Systemic Immune Suppression

    NARCIS (Netherlands)

    Vermeij, Jan-Dirk; Aslami, Hamid; Fluiter, Kees; Roelofs, Joris J.; van den Bergh, Walter M.; Juffermans, Nicole P.; Schultz, Marcus J.; Van der Sluijs, Koen; van de Beek, Diederik; van Westerloo, David J.

    2013-01-01

    Traumatic brain injury (TBI) is frequently complicated by acute lung injury, which is predictive for poor outcome. However, it is unclear whether lung injury develops independently or as a result of mechanical ventilation after TBI. Further, TBI is strongly associated with the development of pneumon

  4. Traumatic brain injury: Age at injury influences dementia risk after TBI

    OpenAIRE

    Johnson, Victoria E.; Stewart, William

    2015-01-01

    Traumatic brain injury (TBI) is increasingly recognized as a risk factor for dementia. New data provide further support for this association and demonstrate the influence of age at injury and injury severity on dementia risk after TBI, revealing that even mild TBI increases dementia risk in those aged ≥65 years.

  5. Cellular and Tissue Injury During Nonfreezing Cold Injury and Frostbite

    Science.gov (United States)

    1993-09-30

    Injuries - Rewarming Damages. 3 Biological, Angiological and Clinical Aspects. In "Disaster Medicine, Volume 3" (R. Frey and P. Safar, Ed.). Springer- Verlag...Kulka, J.P. Vasomotor microcirculatory insufficiency: observation of nonfreezing cold injury of the mouse ear. Angiology 12, 491-506 (1961). 38

  6. Exercise to enhance neurocognitive function after traumatic brain injury.

    Science.gov (United States)

    Fogelman, David; Zafonte, Ross

    2012-11-01

    Vigorous exercise has long been associated with improved health in many domains. Results of clinical observation have suggested that neurocognitive performance also is improved by vigorous exercise. Data derived from animal model-based research have been emerging that show molecular and neuroanatomic mechanisms that may explain how exercise improves cognition, particularly after traumatic brain injury. This article will summarize the current state of the basic science and clinical literature regarding exercise as an intervention, both independently and in conjunction with other modalities, for brain injury rehabilitation. A key principle is the factor of timing of the initiation of exercise after mild traumatic brain injury, balancing potentially favorable and detrimental effects on recovery.

  7. An Animal-to-Human Scaling Law for Blast-Induced Traumatic Brain Injury Risk Assessment

    Science.gov (United States)

    2014-10-28

    injury biomechanics (13–15, 17), the peak intra- cranial pressure was chosen as a characteristic metric of blast intensity transmitted to the brain tissue...Management, and Rehabilitation ( Springer , Berlin), pp 1–13. 7. Magnuson J, Leonessa F, Ling GSF (2012) Neuropathology of explosive blast traumatic brain...Front Neurol 3:70. 17. Sundaramurthy A, et al. (2012) Blast-induced biomechanical loading of the rat: An experimental and anatomically accurate

  8. Association of HIF- expression and cell apoptosis after traumatic brain injury in the rat

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To explore the expression of hypoxia inducible factor-1α (HIF-1~) and the correlation between HIF-1α and apoptosis after traumatic brain injury.Methods: Using experimental traumatic brain injury in the rats, the expression of HIF-1α was studied by immunohisto-chemistry in cerebral tissue, apoptotic cell death was evaluated with TUNEL (transferase-mediated XdUTP nick end labeling ), and double-labeled immunohistochemistry and TUNEL methods were used to investigate the relationship between HIF-1α and apoptosis.Results: There was remarkable difference in the expression of HIF-1α between the experimental groups and the control groups (P < 0.01), in the experimental groups,the expression of HIF-1α at 48 hours was highest; the evidence of apoptotic cell death after experimental traumatic brain injury was found by TUNEL; the apoptotic percentage increased or decreased according to the changes of the positive expression of HIF-1α (r = 0.99).Conclusions: The results suggest that secondary brain ischemia plays a crucial role in apoptotic cell death after traumatic brain injury; HIF-1α can prompt apoptotic cell death after experimental traumatic brain injury.e expres

  9. Application of minimally invasive surgery in traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Liu Baiyun

    2014-12-01

    Full Text Available This article aims to expound the essence of minimally invasive surgery as well as when and how to use it in craniocerebral trauma surgery according to the characteristics of the disease. In neurosurgery, the importance of tissue protection should be from the inside to the outside, i.e. brain→dura→skull→scalp. In this article, I want to share my opinion and our team’s experience in terms of selecting surgical approaches and incision, surgical treatment of the skull, dura handling, intracranial operation and placement of drainage based on the above theory. I hope this will be helpful for trauma surgeons. Key words: Traumatic brain injuries; Large craniectomy; Surgical procedures, minimally invasive

  10. Growth Factors for the Treatment of Ischemic Brain Injury (Growth Factor Treatment

    Directory of Open Access Journals (Sweden)

    Amara Larpthaveesarp

    2015-04-01

    Full Text Available In recent years, growth factor therapy has emerged as a potential treatment for ischemic brain injury. The efficacy of therapies that either directly introduce or stimulate local production of growth factors and their receptors in damaged brain tissue has been tested in a multitude of models for different Central Nervous System (CNS diseases. These growth factors include erythropoietin (EPO, vascular endothelial growth factor (VEGF, brain-derived neurotrophic factor (BDNF, and insulin-like growth factor (IGF-1, among others. Despite the promise shown in animal models, the particular growth factors that should be used to maximize both brain protection and repair, and the therapeutic critical period, are not well defined. We will review current pre-clinical and clinical evidence for growth factor therapies in treating different causes of brain injury, as well as issues to be addressed prior to application in humans.

  11. Growth factors for the treatment of ischemic brain injury (growth factor treatment).

    Science.gov (United States)

    Larpthaveesarp, Amara; Ferriero, Donna M; Gonzalez, Fernando F

    2015-04-30

    In recent years, growth factor therapy has emerged as a potential treatment for ischemic brain injury. The efficacy of therapies that either directly introduce or stimulate local production of growth factors and their receptors in damaged brain tissue has been tested in a multitude of models for different Central Nervous System (CNS) diseases. These growth factors include erythropoietin (EPO), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), and insulin-like growth factor (IGF-1), among others. Despite the promise shown in animal models, the particular growth factors that should be used to maximize both brain protection and repair, and the therapeutic critical period, are not well defined. We will review current pre-clinical and clinical evidence for growth factor therapies in treating different causes of brain injury, as well as issues to be addressed prior to application in humans.

  12. Correlating learning and memory improvements to long-term potentiation in patients with brain injury

    Institute of Scientific and Technical Information of China (English)

    Xingfu Peng; Qian Yu

    2008-01-01

    patients clinically present with various manifestations,such as paralysis and sensory disability,which closely correlate to injured regions.In addition,learning and memory abilities decrease in brain injury patients and LTP decreases following brain injury.Brain tissue injury will lead to brain functional deficits. Hippocampal LTP is very sensitive.Difficulties in LTP induction are apparent even prior to morphological changes in brain tissue.There are no specific treatments for learning and memory functional deficits following brain injury.At present,behavioral and compensative therapies are the typical forms of rehabilitation.These results indicate that rehabilitation promotes learning and memory functional recovery in brain injury patients by speeding up LTP formation in the hippocampal CA3 region.CONCLUSION:Rehabilitation intervention increases LTP formation in the hippocampal CA3 region and recovers learning and memory functions in brain injury patients.

  13. How to use PRICE treatment for soft tissue injuries.

    Science.gov (United States)

    Norton, Cormac

    2016-08-24

    Rationale and key points This article assists nurses to use the acronym PRICE (protection, rest, ice, compression and elevation) to guide the treatment of patients with uncomplicated soft tissue injuries to their upper or lower limbs. » Treatment of soft tissue injuries to limbs is important to reduce complications following injury, alleviate pain and ensure normal limb function is restored promptly. » Nurses should have an understanding of the rationale and evidence base supporting PRICE treatment of soft tissue injuries. » Providing accurate information to patients and carers about the management of soft tissue injuries and anticipated recovery time is an important aspect of treatment. » Further research is required to develop best practice in the treatment of soft tissue injuries. Reflective activity 'How to' articles can help you update your practice and ensure it remains evidence based. Apply this article to your practice. Reflect on and write a short account of: 1. How this article might change your practice when managing patients with soft tissue injuries to upper or lower limbs. 2. Positive elements of your current practice and those that could be enhanced. Subscribers can upload their reflective accounts at: rcni.com/portfolio.

  14. Injury and repair in perinatal brain injury: Insights from non-invasive MR perfusion imaging.

    Science.gov (United States)

    Wintermark, Pia

    2015-03-01

    Injury to the developing brain remains an important complication in critically ill newborns, placing them at risk for future neurodevelopment impairments. Abnormal brain perfusion is often a key mechanism underlying neonatal brain injury. A better understanding of how alternations in brain perfusion can affect normal brain development will permit the development of therapeutic strategies that prevent and/or minimize brain injury and improve the neurodevelopmental outcome of these high-risk newborns. Recently, non-invasive MR perfusion imaging of the brain has been successfully applied to the neonatal brain, which is known to be smaller and have lower brain perfusion compared to older children and adults. This article will present an overview of the potential role of non-invasive perfusion imaging by MRI to study maturation, injury, and repair in perinatal brain injury and demonstrate why this perfusion sequence is an important addition to current neonatal imaging protocols, which already include different sequences to assess the anatomy and metabolism of the neonatal brain.

  15. Imatinib treatment reduces brain injury in a murine model of traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Enming Joe Su

    2015-10-01

    Full Text Available Current therapies for Traumatic brain injury (TBI focus on stabilizing individuals and on preventing further damage from the secondary consequences of TBI. A major complication of TBI is cerebral edema, which can be caused by the loss of blood brain barrier (BBB integrity. Recent studies in several CNS pathologies have shown that activation of latent platelet derived growth factor-CC (PDGF-CC within the brain can promote BBB permeability through PDGF receptor α (PDGFRα signaling, and that blocking this pathway improves outcomes. In this study we examine the efficacy for the treatment of TBI of an FDA approved antagonist of the PDGFRα, Imatinib. Using a murine model we show that Imatinib treatment, begun 45 minutes after TBI and given twice daily for 5 days, significantly reduces BBB dysfunction. This is associated with significantly reduced lesion size 24 hours, 7 days, and 21 days after TBI, reduced cerebral edema, determined from apparent diffusion co-efficient (ADC measurements, and with the preservation of cognitive function. Finally, analysis of CSF from human TBI patients suggests a possible correlation between high PDGF-CC levels and increased injury severity. Thus, our data suggests a novel strategy for the treatment of TBI with an existing FDA approved antagonist of the PDGFRα.

  16. Brain response to traumatic brain injury in wild-type and interleukin-6 knockout mice: a microarray analysis.

    Science.gov (United States)

    Poulsen, Christian Bjørn; Penkowa, Milena; Borup, Rehannah; Nielsen, Finn Cilius; Cáceres, Mario; Quintana, Albert; Molinero, Amalia; Carrasco, Javier; Giralt, Mercedes; Hidalgo, Juan

    2005-01-01

    Traumatic injury to the brain is one of the leading causes of injury-related death or disability. Brain response to injury is orchestrated by cytokines, such as interleukin (IL)-6, but the full repertoire of responses involved is not well known. We here report the results obtained with microarrays in wild-type and IL-6 knockout mice subjected to a cryolesion of the somatosensorial cortex and killed at 0, 1, 4, 8 and 16 days post-lesion. Overall gene expression was analyzed by using Affymetrix genechips/oligonucleotide arrays with approximately 12,400 probe sets corresponding to approximately 10,000 different murine genes (MG_U74Av2). A robust, conventional statistical method (two-way anova) was employed to select the genes significantly affected. An orderly pattern of gene responses was clearly detected, with genes being up- or down-regulated at specific timings consistent with the processes involved in the initial tissue injury and later regeneration of the parenchyma. IL-6 deficiency showed a dramatic effect in the expression of many genes, especially in the 1 day post-lesion timing, which presumably underlies the poor capacity of IL-6 knockout mice to cope with brain damage. The results highlight the importance of IL-6 controlling the response of the brain to injury as well as the suitability of microarrays for identifying specific targets worthy of further study.

  17. Soft Tissue Injuries in Hungarian and Austrian Clinical Diagnostic Reports

    Directory of Open Access Journals (Sweden)

    Fogarasi-Nuber Katalin

    2013-04-01

    Full Text Available Introduction: In addition to providing first aid, primary treating doctors are required to describe and register injuries acquired in accidents and assaults. They should do this with the highest possible accuracy, as this official document is often the only documentary evidence of soft tissue injuries in case a lawsuit is filed later. Characteristics of injuries may disappear faster with the healing process of the soft tissue, making it impossible for forensic experts to deduce the weapon involved. Consequently, terminological accuracy is a prerequisite for the appropriate reconstruction of the type and severity of injuries. This study aims at analysing reports on soft tissue injuries in Hungary and Austria from the terminological point of view. It is meant to reveal inaccuracies in the use of noun phrases impairing objective and accurate forensic assessment.

  18. Evaluation of Axonal Strain as a Predictor for Mild Traumatic Brain Injuries Using Finite Element Modeling.

    Science.gov (United States)

    Giordano, Chiara; Kleiven, Svein

    2014-11-01

    Finite element (FE) models are often used to study the biomechanical effects of traumatic brain injury (TBI). Measures based on mechanical responses, such as principal strain or invariants of the strain tensor, are used as a metric to predict the risk of injury. However, the reliability of inferences drawn from these models depends on the correspondence between the mechanical measures and injury data, as well as the establishment of accurate thresholds of tissue injury. In the current study, a validated anisotropic FE model of the human head is used to evaluate the hypothesis that strain in the direction of fibers (axonal strain) is a better predictor of TBI than maximum principal strain (MPS), anisotropic equivalent strain (AESM) and cumulative strain damage measure (CSDM). An analysis of head kinematics-based metrics, such as head injury criterion (HIC) and brain injury criterion (BrIC), is also provided. Logistic regression analysis is employed to compare binary injury data (concussion/no concussion) with continuous strain/kinematics data. The threshold corresponding to 50% of injury probability is determined for each parameter. The predictive power (area under the ROC curve, AUC) is calculated from receiver operating characteristic (ROC) curve analysis. The measure with the highest AUC is considered to be the best predictor of mTBI. Logistic regression shows a statistical correlation between all the mechanical predictors and injury data for different regions of the brain. Peaks of axonal strain have the highest AUC and determine a strain threshold of 0.07 for corpus callosum and 0.15 for the brainstem, in agreement with previously experimentally derived injury thresholds for reversible axonal injury. For a data set of mild TBI from the national football league, the strain in the axonal direction is found to be a better injury predictor than MPS, AESM, CSDM, BrIC and HIC.

  19. Tissue tracking: applications for brain MRI classification

    Science.gov (United States)

    Melonakos, John; Gao, Yi; Tannenbaum, Allen

    2007-03-01

    Bayesian classification methods have been extensively used in a variety of image processing applications, including medical image analysis. The basic procedure is to combine data-driven knowledge in the likelihood terms with clinical knowledge in the prior terms to classify an image into a pre-determined number of classes. In many applications, it is difficult to construct meaningful priors and, hence, homogeneous priors are assumed. In this paper, we show how expectation-maximization weights and neighboring posterior probabilities may be combined to make intuitive use of the Bayesian priors. Drawing upon insights from computer vision tracking algorithms, we cast the problem in a tissue tracking framework. We show results of our algorithm on the classification of gray and white matter along with surrounding cerebral spinal fluid in brain MRI scans. We show results of our algorithm on 20 brain MRI datasets along with validation against expert manual segmentations.

  20. Brain Networks Subserving Emotion Regulation and Adaptation after Mild Traumatic Brain Injury

    NARCIS (Netherlands)

    van der Horn, Harm J.; Liemburg, Edith J.; Aleman, Andre; Spikman, Jacoba M.; van der Naalt, Joukje

    2016-01-01

    The majority of patients with traumatic brain injury (TBI) sustain a mild injury (mTBI). One out of 4 patients experiences persistent complaints, despite their often normal neuropsychological test results and the absence of structural brain damage on conventional neuroimaging. Susceptibility to deve

  1. Opioid Abuse after Traumatic Brain Injury: Evaluation Using Rodent Models

    Science.gov (United States)

    2013-07-01

    rats induces structural changes in brain regions associated with reward/risk circuitry including the nucleus accumbens, amygdala, hippocampus , and...to injury, animals underwent surgical implantation of a chronic indwelling venous catheter under isoflurane anesthesia with morphine pretreatment. A

  2. Spreading depolarisations and outcome after traumatic brain injury

    DEFF Research Database (Denmark)

    Hartings, Jed A; Bullock, M Ross; Okonkwo, David O

    2011-01-01

    Pathological waves of spreading mass neuronal depolarisation arise repeatedly in injured, but potentially salvageable, grey matter in 50-60% of patients after traumatic brain injury (TBI). We aimed to ascertain whether spreading depolarisations are independently associated with unfavourable...

  3. Better Sleep May Signal Recovery from Brain Injury

    Science.gov (United States)

    ... useful tool for assessing their recovery after traumatic brain injury," said study author Nadia Gosselin. She's an assistant professor in the department of psychology at the University of Montreal. "We found that ...

  4. Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System

    Data.gov (United States)

    U.S. Department of Health & Human Services — The Federal Interagency Traumatic Brain Injury Research (FITBIR) informatics system is an extensible, scalable informatics platform for TBI relevant imaging,...

  5. Neurogenic fever after traumatic brain injury: an epidemiological study

    OpenAIRE

    Thompson, H; Pinto-Martin, J; Bullock, M.

    2003-01-01

    Objectives: To determine the incidence of neurogenic fever (NF) in a population of patients in the acute phase following severe traumatic brain injury (TBI); to identify factors associated with the development of NF following severe TBI in adults.

  6. Kids' Mild Brain Injury Can Have Long-Term Effects

    Science.gov (United States)

    ... Brain Injury Can Have Long-Term Effects Early head trauma linked to psychiatric, financial issues as adults, study ... HealthDay News) -- Young people who suffer even mild head trauma are more likely to have serious issues later ...

  7. Defense Centers of Excellence for Psychological Health & Traumatic Brain Injury

    Science.gov (United States)

    ... Sign up Search: Defense Centers of Excellence For Psychological Health & Traumatic Brain Injury U.S. Department of Defense ... Reports Program Evaluation DoD/VA PH & TBI Registry Psychological Health About Psychological Health Psychological Health Resources About ...

  8. Effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    陈志刚; 卢亦成; 朱诚; 张光霁; 丁学华; 江基尧

    2003-01-01

    Objective: To observe the effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury (TBI).Methods: An acute experimental closed TBI model in rats was induced by a fluid-percussion brain injury model. At five and sixty minutes after TBI, the animals were intraperitoneally injected by ganglioside GM1 (30 mg/kg) or the same volume of saline. At the 6th hour after TBI, effects of ganglioside GM1 or saline on changes of mean arterial pressure (MAP), contents of water, lactic acid (LA) and lipid peroxidation (LPO) in the injured cerebral tissues were observed.Results: After TBI, MAP decreased and contents of water, LA and LPO increased in brain injury group; however, MAP was back to normal levels and contents of water, LA and LPO decreased in ganglioside GM1 treated group, compared with those in brain injury group (P0.05) was observed.Conclusions: Ganglioside GM1 does have obvious neuroprotective effect on early TBI.

  9. Metallic gold reduces TNFalpha expression, oxidative DNA damage and pro-apoptotic signals after experimental brain injury

    DEFF Research Database (Denmark)

    Pedersen, Mie Ostergaard; Larsen, Agnete; Pedersen, Dan Sonne;

    2009-01-01

    -45 microm in size or the vehicle (placebo) were implanted in the cortical tissue followed by a cortical freeze-lesioning. At 1-2 weeks post-injury, brains were analyzed by using immunohistochemistry and markers of inflammation, oxidative stress and apoptosis. This study shows that gold treatment......Brain injury represents a major health problem and may result in chronic inflammation and neurodegeneration. Due to antiinflammatory effects of gold, we have investigated the cerebral effects of metallic gold particles following a focal brain injury (freeze-lesion) in mice. Gold particles 20...

  10. Cooking breakfast after a brain injury

    Directory of Open Access Journals (Sweden)

    Annick N. Tanguay

    2014-09-01

    Full Text Available Acquired brain injury (ABI often compromises the ability to carry out instrumental activities of daily living such as cooking. ABI patients’ difficulties with executive functions and memory result in less independent and efficient meal preparation. Accurately assessing safety and proficiency in cooking is essential for successful community reintegration following ABI, but in vivo assessment of cooking by clinicians is time-consuming, costly, and difficult to standardize. Accordingly, we examined the usefulness of a computerized meal preparation task (the Breakfast Task; Craik & Bialystok, 2006 as an indicator of real life meal preparation skills. Twenty-two ABI patients and 22 age-matched controls completed the Breakfast Task and the Rehabilitation Activities of Daily Living Survey (RADLS; Salmon, 2003. Patients also prepared actual meals, and were rated by members of the clinical team. As expected, the ABI patients had significant difficulty on all aspects of the Breakfast Task (failing to have all their foods ready at the same time, over- and under-cooking foods, setting fewer places at the table, and so on relative to controls. Surprisingly, however, patients’ Breakfast Task performance was not correlated with their in vivo meal preparation. These results indicate caution when endeavoring to replace traditional evaluation methods with computerized tasks for the sake of expediency.

  11. Traumatic brain injury: Changing concepts and approaches

    Institute of Scientific and Technical Information of China (English)

    Andrew Maas

    2016-01-01

    Traumatic brain injury (TBI) represents a huge global medical and public health problem across all ages and in all populations.In this review,we discussed the changing concepts and approaches.Globally,the incidence is increasing and in high income countries epidemiologic patterns are changing with consequences for prevention campaigns.TBI should not be viewed as an event,but as a progressive and chronic disease with lifetime consequences.In the clinical field,precision approaches to treatment are being developed,which require more accurate disease phenotyping.Recent advances in genomics,neuroimaging and biomarker development offer great opportunities to develop improved phenotyping and better disease characterization.In clinical research,randomized controlled clinical trials are being complemented by large data collections in broad TBI populations in comparative effectiveness designs.Global collaborations are being developed among funding agencies,research organizations and researchers.Only by combining efforts and collaboration will we be able to advance the field by providing long-needed evidence to support practice recommendations and to improve treatment.

  12. /sup 31/P NMR characterization of graded traumatic brain injury in rats

    Energy Technology Data Exchange (ETDEWEB)

    Vink, R.; McIntosh, T.K.; Yamakami, I.; Faden, A.I.

    1988-01-01

    Irreversible tissue injury following central nervous system trauma is believed to result from both mechanical disruption at the time of primary insult, and more delayed autodestructive processes. These delayed events are associated with various biochemical changes, including alterations in phosphate energy metabolism and intracellular pH. Using /sup 31/P NMR, we have monitored the changes in phosphorus energy metabolism and intracellular pH in a single hemisphere of the rat brain over an 8-h period following graded, traumatic, fluid percussion-induced brain injury. Following trauma the ratio of phosphocreatine to inorganic phosphate (PCr/Pi) declined in each injury group. This decline was transitory with low injury (1.0 +/- 0.5 atm), biphasic with moderate (2.1 +/- 0.4 atm) and high (3.9 +/- 0.9 atm) injury, and sustained following severe injury (5.9 +/- 0.7 atm). The initial PCr/Pi decline in the moderate and high injury groups was associated with intracellular acidosis; however, the second decline occurred in the absence of any pH changes. Alterations in ATP occurred only in severely injured animals and such changes were associated with marked acidosis and 100% mortality rate. After 4h, the posttraumatic PCr/Pi ratio correlated linearly with the severity of injury. We suggest that a reduced posttraumatic PCr/Pi ratio may be indicative of altered mitochondrial energy production and may predict a reduced capacity of the cell to recover from traumatic injury.

  13. Prehospital Tranexamic Acid Use for Traumatic Brain Injury

    Science.gov (United States)

    2015-10-01

    incidence of post - traumatic stress disorder and suicide .112 Efforts to treat TBI in the field include avoiding hypotension and secondary brain injury...378-384. 19 Harhangi BS, Kompanje JO, Leebeek FWG, et al. Coagulation disorders after traumatic brain injury. Acta Neurochir. 2008;150;165-175...K, Xu X-M. MicroRNA in central nervous system trauma and degenerative disorders . Physiol Genomics. 2011;43:571-580. 37. Hoyt DB. Post hoc ergo

  14. Psychotherapy after acquired brain injury: Is less more?

    Directory of Open Access Journals (Sweden)

    Rudi Coetzer

    2014-02-01

    Full Text Available This paper considers the challenges and dilemmas facing psychotherapists working with neurological patients, and in particular those who work in the context of under-resourced brain injury rehabilitation healthcare systems. Through the subjective process of reflective practice integral to clinical supervision, the author attempts to identify five core aspects of psychotherapy intended to augment post-acute long- term rehabilitation programmes and interventions after acquired brain injury.

  15. Fluid-percussion–induced traumatic brain injury model in rats

    OpenAIRE

    2010-01-01

    Traumatic brain injury (TBI) is a major cause of mortality and morbidity. Various attempts have been made to replicate clinical TBI using animal models. The fluid-percussion model (FP) is one of the oldest and most commonly used models of experimentally induced TBI. Both central (CFP) and lateral (LFP) variations of the model have been used. Developed initially for use in larger species, the standard FP device was adapted more than 20 years ago to induce consistent degrees of brain injury in ...

  16. Traumatic Brain Injury: Hope Through Research

    Science.gov (United States)

    ... dura. Collectively, these three membranes form the meninges. brain death - an irreversible cessation of measurable brain function. Broca's ... Education Fact Sheets Hope Through Research Know Your Brain Preventing ... and Death of a Neuron Order Publications CONTACT US Contact ...

  17. Retinochoroidal changes after severe brain impact injury in rabbits

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To investigate retinochoroidal changes and establisheye damage model after brain impact injury.Methods: An eye damage model after brain impact injury was established by striking the frontoparietal zone in rabbits with BIM-Ⅱ bioimpact machine. Seventeen rabbits were killed at 4 different intervals after injury. The pathological characteristics of the retinal and choroid damages were observed.Results: All the rabbits had severe brain injury with subarachnoid hemorrhage and brain contusion. The eye damage occurred in all of the 17 rabbits. Hemorrhage in optic nerve sheaths was observed and retinal edema and bleeding was discovered with ophthalmoscope. Histopathologic study displayed subarachnoid hemorrhage in the retrobulbar portion of the retinal nerve, general choroid blood vessel dilatation, retinal nerve fibre swelling within 6 hours after injury, and flat retinal detachment with subretinal proteinoid exudation, and degeneration and disappearance of the outer segment of the optic cell over 6 hours after injury.Conclusions: The pathological characteristic of the eye damage at early stage following brain impact injury is local circulation disturbance. At late stage, it features in retinal detachment, and optic cellular degeneration and necrosis.

  18. Transcranial amelioration of inflammation and cell death after brain injury

    Science.gov (United States)

    Roth, Theodore L.; Nayak, Debasis; Atanasijevic, Tatjana; Koretsky, Alan P.; Latour, Lawrence L.; McGavern, Dorian B.

    2014-01-01

    Traumatic brain injury (TBI) is increasingly appreciated to be highly prevalent and deleterious to neurological function. At present, no effective treatment options are available, and little is known about the complex cellular response to TBI during its acute phase. To gain insights into TBI pathogenesis, we developed a novel murine closed-skull brain injury model that mirrors some pathological features associated with mild TBI in humans and used long-term intravital microscopy to study the dynamics of the injury response from its inception. Here we demonstrate that acute brain injury induces vascular damage, meningeal cell death, and the generation of reactive oxygen species (ROS) that ultimately breach the glial limitans and promote spread of the injury into the parenchyma. In response, the brain elicits a neuroprotective, purinergic-receptor-dependent inflammatory response characterized by meningeal neutrophil swarming and microglial reconstitution of the damaged glial limitans. We also show that the skull bone is permeable to small-molecular-weight compounds, and use this delivery route to modulate inflammation and therapeutically ameliorate brain injury through transcranial administration of the ROS scavenger, glutathione. Our results shed light on the acute cellular response to TBI and provide a means to locally deliver therapeutic compounds to the site of injury.

  19. Modelling Brain Tissue using Magnetic Resonance Imaging

    DEFF Research Database (Denmark)

    Dyrby, Tim Bjørn

    2008-01-01

    Diffusion MRI, or diffusion weighted imaging (DWI), is a technique that measures the restricted diffusion of water molecules within brain tissue. Different reconstruction methods quantify water-diffusion anisotropy in the intra- and extra-cellular spaces of the neural environment. Fibre tracking...... tractography. Although probabilistic tractography currently holds great promise as a powerful non-invasive connectivity-measurement tool, its accuracy and limitations remain to be evaluated. Probabilistic tractography was assessed post mortem in an in vitro environment. Postmortem DWI benefits from...... environment differs from that of in vivo both due to a lowered environmental temperature and due to the fixation process itself. We argue that the perfusion fixation procedure employed in this thesis ensures that the postmortem tissue is as close to that of in vivo as possible. Different fibre reconstruction...

  20. Effect of hyperbaric oxygenation treatment on expression of NF-κB p50 in the rat brain tissue after traumatic brain injury%高压氧干预对大鼠创伤性脑损伤后脑组织NF-κB(p50)表达的影响

    Institute of Scientific and Technical Information of China (English)

    杨柏林; 王欢; 彭军; 徐其明; 余超

    2014-01-01

    Objective To observe the effect of hyperbaric oxygenation treatment ( HBOT) on expression of NF-κB( p50) in the rat brain tissue after traumatic brain injury ( TBI) and discuss its mechanism .Methods Thirty-five Sprague-Dawley rats were divided into sham operation control group(5 rats), TBI group(15 rats) and HBOT group(15 rats).Based on the Feeney’s model of modified Allen’s method, experimental animals were treated with HBOT .The animals were sacrificed at the 8th hour, and on days 1,3,5,8,re-spectively.The expression of protein NF-κB was determined by Westernblotting .Results The expression of NF-κB was significantly higher in traumatic group than that in control group at the time of 8 hour and 1,3,5and 8 days after injury (P<0.05).The level of NF-κB reached peak on the 3th day, and maintained a high status from 5 to 8 days.Compared with traumatic group, the NF-κB level was significantly lower in the HBOT group (P<0.05).Conclusion HBOT can weaken NF-κB expression in traumatic brain tissue and inhibit effectively inflammatory response , which provides theoretical basis for treating severe traumatic brain injury .%目的:观察高压氧干预(hyperbaric oxygenation treatment, HBOT)对大鼠创伤性脑损伤(traumatic brain injury, TBI)后NF-κB(p50)表达的影响,并探讨其机制。方法将35只SD大鼠完全随机分为假手术对照组(Con组)5只、创伤组(TBI)15只、高压氧干预组(HBOT)15只。采用Allen’s改良法制造大鼠自由落体重型脑损伤模型,Con组仅切开头皮去骨窗,TBI组给予撞击损伤,HBOT组于创伤后给予高压氧治疗。利用Western-blot法分别于伤后8 h及1、3、5、8 d检测脑组织NF-κB的表达。结果与Con 组比,TBI 组各时点脑组织 NF-κB 表达均升高( P <0.05),损伤后3 d 达高峰(0.7267±0.0305),5~8 d 仍维持较高水平(0.5567±0.0603)。 HBOT 组各时点 NF-κB 表达水平均较 TBI

  1. Intravenous Fluid Therapy in Traumatic Brain Injury and Decompressive Craniectomy

    Science.gov (United States)

    Alvis-Miranda, Hernando Raphael; Castellar-Leones, Sandra Milena; Moscote-Salazar, Luis Rafael

    2014-01-01

    The patient with head trauma is a challenge for the emergency physician and for the neurosurgeon. Currently traumatic brain injury constitutes a public health problem. Knowledge of the various supportive therapeutic strategies in the pre-hospital and pre-operative stages is essential for optimal care. The immediate rapid infusion of large volumes of crystalloids to restore blood volume and blood pressure is now the standard treatment of patients with combined traumatic brain injury (TBI) and hemorrhagic shock (HS). The fluid in patients with brain trauma and especially in patients with brain injur y is a critical issue. In this context we present a review of the literature about the history, physiology of current fluid preparations, and a discussion regarding the use of fluid therapy in traumatic brain injury and decompressive craniectomy. PMID:27162857

  2. Intravenous Fluid Therapy in Traumatic Brain Injury and Decompressive Craniectomy

    Directory of Open Access Journals (Sweden)

    Hernando Raphael Alvis-Miranda

    2014-01-01

    Full Text Available The patient with head trauma is a challenge for the emergency physician and for the neurosurgeon. Currently traumatic brain injury constitutes a public health problem. Knowledge of the various supportive therapeutic strategies in the pre-hospital and pre-operative stages is essential for optimal care. The immediate rapid infusion of large volumes of crystalloids to restore blood volume and blood pressure is now the standard treatment of patients with combined traumatic brain injury (TBI and hemorrhagic shock (HS. The fluid in patients with brain trauma and especially in patients with brain injur y is a critical issue. In this context we present a review of the literature about the history, physiology of current fluid preparations, and a discussion regarding the use of fluid therapy in traumatic brain injury and decompressive craniectomy.

  3. Development of an Ontology for Rehabilitation: Traumatic Brain Injury

    Science.gov (United States)

    Grove, Michael J.

    2013-01-01

    Traumatic Brain Injury (TBI) rehabilitation interventions are very heterogeneous due to injury characteristics and pathology, patient demographics, healthcare settings, caregiver variability, and individualized, multi-discipline treatment plans. Consequently, comparing and generalizing the effectiveness of interventions is limited largely due to…

  4. Ethical Issues in Neuroprognostication after Severe Pediatric Brain Injury.

    Science.gov (United States)

    Kirschen, Matthew P; Walter, Jennifer K

    2015-09-01

    Neurologic outcome prediction, or neuroprognostication, after severe brain injury in children is a challenging task and has many ethical dimensions. Neurologists and intensivists are frequently asked by families to predict functional recovery after brain injury to help guide medical decision making despite limited outcome data. Using two clinical cases of children with severe brain injury from different mechanisms: hypoxic-ischemic injury secondary to cardiac arrest and traumatic brain injury, this article first addresses the importance of making a correct diagnosis in a child with a disorder of consciousness and then discusses some of the clinical challenges with deducing an accurate and timely outcome prediction. We further explore the ethical obligations of physicians when supporting parental decision making. We highlight the need to focus on how to elicit family values for a brain injured child, how to manage prognostic uncertainty, and how to effectively communicate with families in these challenging situations. We offer guidance for physicians when they have diverging views from families on aggressiveness of care or feel pressured to prognosticate with in a "window of opportunity" for limiting or withdrawing life sustaining therapies. We conclude with a discussion of the potential influence of emerging technologies, specifically advanced functional neuroimaging, on neurologic outcome prediction after severe brain injury.

  5. Traumatic Brain Injury Screening: Preliminary Findings in a US Army Brigade Combat Team

    Science.gov (United States)

    2009-01-01

    traumatic brain injury TRAUMATIC BRAIN INJURY ( TBI ) is often dis-cussed as a common injury of the war in... Traumatic Brain Injury Screening 17 TABLE 1 Screening results∗ Injury status Injured with TBI 907 (22.8) Injured without TBI 385 (9.7) Not injured 2681...remember the injury 335 (36.9) Total with TBI 907 (100) ∗Values represent n (%). TBI indicates traumatic brain

  6. The Role of Cytokines and Inflammatory Cells in Perinatal Brain Injury

    Directory of Open Access Journals (Sweden)

    Ryan M. McAdams

    2012-01-01

    Full Text Available Perinatal brain injury frequently complicates preterm birth and leads to significant long-term morbidity. Cytokines and inflammatory cells are mediators in the common pathways associated with perinatal brain injury induced by a variety of insults, such as hypoxic-ischemic injury, reperfusion injury, toxin-mediated injury, and infection. This paper examines our current knowledge regarding cytokine-related perinatal brain injury and specifically discusses strategies for attenuating cytokine-mediated brain damage.

  7. Concussion and Mild Traumatic Brain Injury: An Annotated Bibliography

    Science.gov (United States)

    2013-08-01

    induced mTBI has increased in recent years. Intracranial pressure monitoring is not always available in clinical care settings, and protocols need to... intracranial pressure , shear stress concentration, and relative motion between the brain and skull do indeed cause surface contusion, concussion, diffuse axonal injury, as well as acute subdural hematoma. ...civilian hospital for mild head injury. Follow-up 1-month post-injury, allowed for PCS evaluation. The analyses (odds ratios) suggest that elevated

  8. Changes in T lymphocyte subsets after severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Yulu Miao; Mingxia Zhang; Yulin Nie; Wan Zhao; Bin Huang; Zhengming Jiang; Shaoxiong Yu; Zhibin Huang; Hongjin Fu

    2007-01-01

    BACKGROUND: Besides local changes of cranial parenchymal cells, hemorrhage, etc., severe traumatic brain injuries also cause the changes of total body fluid and various functions, and the changes of lymphocytes and T lymphocyte subsets should be paid more attention to.OBJECTIVE: To reveal the changing laws of T lymphocyte subsets after severe traumatic brain injury, and compare with mild to moderate brain injury.DESIGN: A comparative observation.SETTINGS: Department of Neurosurgery, Longgang District Buji People's Hospital of Shenzhen City;Central Laboratory of Shenzhen Hospital of Prevention and Cure for Chronic Disease.PARTICIPANTS: All the subjects were selected from the Department of Neurosurgery, Longgang District Buji People's Hospital of Shenzhen City from August 2002 to August 2005. Thirty patients with severe brain injury, whose Glasgow coma score (GCS) was ≤ 8 points, were taken as the experimental group, including 21 males and 9 females, aging 16 - 62 years. Meanwhile, 30 patients with mild traumatic brain injury were taken as the control group (GCS ranged 14 - 15 points), including 18 males and 12 females, aging 15 - 58 years. All the subjects were in admission at 6 hours after injury, without disease of major organs before injury.Informed consents were obtained from all the patients or their relatives.conditions of pulmonaryinfections were observed at 4 days after injury. The differences of measurement data were compared with the t test.MAIN OUTCOME MEASURES: Changes of T lymphocytes subsets at 1 - 14 days after severe and mild or moderate traumatic injury.RESULTS: Finally, 28 and 25 patients with mild to moderate traumatic brain injury, whereas 25 and 21 patients with severe traumatic brain injury were analyzed at 7 and 14 days respectively, and the missed ones CD3, CD4, CD8, CD4/CD8 began to decrease, whereas CD8 increased in the experimental group, which were very significantly different from those in the control group (t =2.77 - 3.26, P < 0

  9. Targeting different pathophysiological events after traumatic brain injury in mice: Role of melatonin and memantine.

    Science.gov (United States)

    Kelestemur, Taha; Yulug, Burak; Caglayan, Ahmet Burak; Beker, Mustafa Caglar; Kilic, Ulkan; Caglayan, Berrak; Yalcin, Esra; Gundogdu, Reyhan Zeynep; Kilic, Ertugrul

    2016-01-26

    The tissue damage that emerges during traumatic brain injury (TBI) is a consequence of a variety of pathophysiological events, including free radical generation and over-activation of N-methyl-d-aspartate-type glutamate receptors (NMDAR). Considering the complex pathophysiology of TBI, we hypothesized that combination of neuroprotective compounds, targeting different events which appear during injury, may be a more promising approach for patients. In this context, both NMDAR antagonist memantine and free radical scavenger melatonin are safe in humans and promising agents for the treatment of TBI. Herein, we examined the effects of melatonin administered alone or in combination with memantine on the activation of signaling pathways, injury development and DNA fragmentation. Both compounds reduced brain injury moderately and the density of DNA fragmentation significantly. Notably, melatonin/memantine combination decreased brain injury and DNA fragmentation significantly, which was associated with reduced p38 and ERK-1/2 phosphorylation. As compared with melatonin and memantine groups, SAPK/JNK-1/2 phosphorylation was also reduced in melatonin/memantine combined animals. In addition, melatonin, memantine and their combination decreased iNOS activity significantly. Here, we provide evidence that melatonin/memantine combination protects brain from traumatic injury, which was associated with decreased DNA fragmentation, p38 phosphorylation and iNOS activity.

  10. [Guidelines for the management of severe traumatic brain injury. Part 3. Surgical management of severe traumatic brain injury (Options)].

    Science.gov (United States)

    Potapov, A A; Krylov, V V; Gavrilov, A G; Kravchuk, A D; Likhterman, L B; Petrikov, S S; Talypov, A E; Zakharova, N E; Solodov, A A

    2016-01-01

    Traumatic brain injury (TBI) is one of the main causes of mortality and severe disability in young and middle age patients. Patients with severe TBI, who are in coma, are of particular concern. Adequate diagnosis of primary brain injuries and timely prevention and treatment of secondary injury mechanisms markedly affect the possibility of reducing mortality and severe disability. The present guidelines are based on the authors' experience in developing international and national recommendations for the diagnosis and treatment of mild TBI, penetrating gunshot wounds of the skull and brain, severe TBI, and severe consequences of brain injury, including a vegetative state. In addition, we used the materials of international and national guidelines for the diagnosis, intensive care, and surgical treatment of severe TBI, which were published in recent years. The proposed recommendations for surgical treatment of severe TBI in adults are addressed primarily to neurosurgeons, neurologists, neuroradiologists, anesthesiologists, and intensivists who are routinely involved in treating these patients.

  11. High-Performance Bioinstrumentation for Real-Time Neuroelectrochemical Traumatic Brain Injury Monitoring

    Science.gov (United States)

    Papadimitriou, Konstantinos I.; Wang, Chu; Rogers, Michelle L.; Gowers, Sally A. N.; Leong, Chi L.; Boutelle, Martyn G.; Drakakis, Emmanuel M.

    2016-01-01

    Traumatic brain injury (TBI) has been identified as an important cause of death and severe disability in all age groups and particularly in children and young adults. Central to TBIs devastation is a delayed secondary injury that occurs in 30–40% of TBI patients each year, while they are in the hospital Intensive Care Unit (ICU). Secondary injuries reduce survival rate after TBI and usually occur within 7 days post-injury. State-of-art monitoring of secondary brain injuries benefits from the acquisition of high-quality and time-aligned electrical data i.e., ElectroCorticoGraphy (ECoG) recorded by means of strip electrodes placed on the brains surface, and neurochemical data obtained via rapid sampling microdialysis and microfluidics-based biosensors measuring brain tissue levels of glucose, lactate and potassium. This article progresses the field of multi-modal monitoring of the injured human brain by presenting the design and realization of a new, compact, medical-grade amperometry, potentiometry and ECoG recording bioinstrumentation. Our combined TBI instrument enables the high-precision, real-time neuroelectrochemical monitoring of TBI patients, who have undergone craniotomy neurosurgery and are treated sedated in the ICU. Electrical and neurochemical test measurements are presented, confirming the high-performance of the reported TBI bioinstrumentation. PMID:27242477

  12. Statistical analysis plan for the Erythropoietin in Traumatic Brain Injury trial: a randomised controlled trial of erythropoietin versus placebo in moderate and severe traumatic brain injury.

    LENUS (Irish Health Repository)

    Presneill, Jeffrey

    2014-01-01

    The Erythropoietin in Traumatic Brain Injury (EPO-TBI) trial aims to determine whether the administration of erythropoietin to patients with moderate or severe traumatic brain injury improves patient-centred outcomes.

  13. Utility of the brain injury screening index in identifying female prisoners with a traumatic brain injury and associated cognitive impairment.

    OpenAIRE

    O'Sullivan, Michelle

    2015-01-01

    An estimated 60.25% of offenders have a history of traumatic brain injury (TBI). There is currently no established valid or reliable screening tool for identifying female prisoners with a TBI and associated cognitive impairment available in the UK. Using a cross-sectional design, this study aimed to investigate the retest reliability and construct validity of the Brain Injury Screening Index (BISI). Convergent validity was explored using self-report measures of mood and neurodisability, as we...

  14. Neurological consequences of traumatic brain injuries in sports.

    Science.gov (United States)

    Ling, Helen; Hardy, John; Zetterberg, Henrik

    2015-05-01

    Traumatic brain injury (TBI) is common in boxing and other contact sports. The long term irreversible and progressive aftermath of TBI in boxers depicted as punch drunk syndrome was described almost a century ago and is now widely referred as chronic traumatic encephalopathy (CTE). The short term sequelae of acute brain injury including subdural haematoma and catastrophic brain injury may lead to death, whereas mild TBI, or concussion, causes functional disturbance and axonal injury rather than gross structural brain damage. Following concussion, symptoms such as dizziness, nausea, reduced attention, amnesia and headache tend to develop acutely but usually resolve within a week or two. Severe concussion can also lead to loss of consciousness. Despite the transient nature of the clinical symptoms, functional neuroimaging, electrophysiological, neuropsychological and neurochemical assessments indicate that the disturbance of concussion takes over a month to return to baseline and neuropathological evaluation shows that concussion-induced axonopathy may persist for years. The developing brains in children and adolescents are more susceptible to concussion than adult brain. The mechanism by which acute TBI may lead to the neurodegenerative process of CTE associated with tau hyperphosphorylation and the development of neurofibrillary tangles (NFTs) remains speculative. Focal tau-positive NFTs and neurites in close proximity to focal axonal injury and foci of microhaemorrhage and the predilection of CTE-tau pathology for perivascular and subcortical regions suggest that acute TBI-related axonal injury, loss of microvascular integrity, breach of the blood brain barrier, resulting inflammatory cascade and microglia and astrocyte activation are likely to be the basis of the mechanistic link of TBI and CTE. This article provides an overview of the acute and long-term neurological consequences of TBI in sports. Clinical, neuropathological and the possible pathophysiological

  15. Treatment for delayed brain injury after pituitary irradiation

    Energy Technology Data Exchange (ETDEWEB)

    Fujii, Takashi; Misumi, Shuzoh; Shibasaki, Takashi; Tamura, Masaru; Kunimine, Hideo; Hayakawa, Kazushige; Niibe, Hideo; Miyazaki, Mizuho; Miyagi, Osamu.

    1988-03-01

    Treatment for delayed brain injury after pituitary irradiation is discussed. Six cases with delayed brain injury were treated with a combination of dexamethasone or betamethasone, with heparin, glycerol, dextran 40 and some vasodilators. Two cases with temporal lobe syndrome were treated in the early stages of brain injury for a period of over 12 months were almost completely cured, another two cases with chiasma syndrome were treated in the relatively late stages, showed a partial improvement. One case which was irradiated 120 GY during 13 years did not improve. The final case treated with steroids for a short period also resulted in failure and the patient underwent an operation for the removal of the necrotic mass three years after the radiotherapy. Steroid therapy started in the early stages of brain injury after irradiation for over the 12 months is thought to be effective. Heparin therapy was also effective in one out of three cases, but in one of the cases subarachnoid hemorrhage from a traumatic aneurysm occurred during the therapy. In an acute phase, showing edematous change of the injured brain, the administration of glycerol is also thought to be useful. But the effectiveness of the other medicines containing some vasodilators was obscure or doubtful. We propose the following : (1) A meticulous observation is essential for the patients who received high doses of irradiation to diagnose brain injury in the early reversible stage. (2) Steroids should be given immediately in this reversible stage of brain injury before the irreversible ''necrosis'' occurs. (3) Steroids should be maintained for a long period over 12 months. (4) Heparin therapy is also thought to be effective, but careful precautions to avoid hemorrhagic complications before the therapy should be scheduled. This recommended plan may also be used for the treatment of brain injuries after cranial irradiation for other intracranial tumors.

  16. Trial of Oral Metoclopramide on Diurnal Bruxism of Brain Injury

    Science.gov (United States)

    Yi, Ho Sung; Seo, Mi Ri

    2013-01-01

    Bruxism is a diurnal or nocturnal parafunctional activity that includes tooth clenching, bracing, gnashing, and grinding. The dopaminergic system seems to be the key pathophysiology of bruxism and diminution of dopaminergic transmission at the prefrontal cortex seems to induce it. We report two patients with diurnal bruxism in whom a bilateral frontal lobe injury resulted from hemorrhagic stroke or traumatic brain injury. These patients' bruxism was refractory to bromocriptine but responded to low-dose metoclopramide therapy. We propose that administering low doses of metoclopramide is possibly a sound method for treating bruxism in a brain injury patient with frontal lobe hypoperfusion on positron emission tomography imaging. PMID:24466522

  17. [Penetrating head and brain injuries with nonmetal foreign bodies].

    Science.gov (United States)

    Potapov, A A; Okhlopkov, V A; Latyshev, Ya A; Serova, N K; Eolchiyan, S A

    2014-01-01

    Penetrating brain injuries (PBI) are common in neurosurgical practice. Most of them are civil or war-time missile and blast injuries. This type of trauma is widely presented in neurosurgical publication, textbooks and clinical evidence-based guidelines. At the same time, PBI by non-metallic foreign bodies are very rare. All the data are limited to case reports and small series of cases. Moreover, there are no clinical consideration on diagnosis, treatment, complication, outcome and prognosis of PBI by non-metallic penetrating brain injuries. In this review all the data are summarized to provide recommendations on the diagnosis and treatment of PBI by non-metallic foreign bodies.

  18. Sodium nitrite protects against kidney injury induced by brain death and improves post-transplant function.

    Science.gov (United States)

    Kelpke, Stacey S; Chen, Bo; Bradley, Kelley M; Teng, Xinjun; Chumley, Phillip; Brandon, Angela; Yancey, Brett; Moore, Brandon; Head, Hughston; Viera, Liliana; Thompson, John A; Crossman, David K; Bray, Molly S; Eckhoff, Devin E; Agarwal, Anupam; Patel, Rakesh P

    2012-08-01

    Renal injury induced by brain death is characterized by ischemia and inflammation, and limiting it is a therapeutic goal that could improve outcomes in kidney transplantation. Brain death resulted in decreased circulating nitrite levels and increased infiltrating inflammatory cell infiltration into the kidney. Since nitrite stimulates nitric oxide signaling in ischemic tissues, we tested whether nitrite therapy was beneficial in a rat model of brain death followed by kidney transplantation. Nitrite, administered over 2 h of brain death, blunted the increased inflammation without affecting brain death-induced alterations in hemodynamics. Kidneys were transplanted after 2 h of brain death and renal function followed over 7 days. Allografts collected from nitrite-treated brain-dead rats showed significant improvement in function over the first 2 to 4 days after transplantation compared with untreated brain-dead animals. Gene microarray analysis after 2 h of brain death without or with nitrite therapy showed that the latter significantly altered the expression of about 400 genes. Ingenuity Pathway Analysis indicated that multiple signaling pathways were affected by nitrite, including those related to hypoxia, transcription, and genes related to humoral immune responses. Thus, nitrite therapy attenuates brain death-induced renal injury by regulating responses to ischemia and inflammation, ultimately leading to better post-transplant kidney function.

  19. Intranasal epidermal growth factor treatment rescues neonatal brain injury

    Science.gov (United States)

    Scafidi, Joseph; Hammond, Timothy R.; Scafidi, Susanna; Ritter, Jonathan; Jablonska, Beata; Roncal, Maria; Szigeti-Buck, Klara; Coman, Daniel; Huang, Yuegao; McCarter, Robert J.; Hyder, Fahmeed; Horvath, Tamas L.; Gallo, Vittorio

    2014-02-01

    There are no clinically relevant treatments available that improve function in the growing population of very preterm infants (less than 32 weeks' gestation) with neonatal brain injury. Diffuse white matter injury (DWMI) is a common finding in these children and results in chronic neurodevelopmental impairments. As shown recently, failure in oligodendrocyte progenitor cell maturation contributes to DWMI. We demonstrated previously that the epidermal growth factor receptor (EGFR) has an important role in oligodendrocyte development. Here we examine whether enhanced EGFR signalling stimulates the endogenous response of EGFR-expressing progenitor cells during a critical period after brain injury, and promotes cellular and behavioural recovery in the developing brain. Using an established mouse model of very preterm brain injury, we demonstrate that selective overexpression of human EGFR in oligodendrocyte lineage cells or the administration of intranasal heparin-binding EGF immediately after injury decreases oligodendroglia death, enhances generation of new oligodendrocytes from progenitor cells and promotes functional recovery. Furthermore, these interventions diminish ultrastructural abnormalities and alleviate behavioural deficits on white-matter-specific paradigms. Inhibition of EGFR signalling with a molecularly targeted agent used for cancer therapy demonstrates that EGFR activation is an important contributor to oligodendrocyte regeneration and functional recovery after DWMI. Thus, our study provides direct evidence that targeting EGFR in oligodendrocyte progenitor cells at a specific time after injury is clinically feasible and potentially applicable to the treatment of premature children with white matter injury.

  20. Delayed mGluR5 activation limits neuroinflammation and neurodegeneration after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Byrnes Kimberly R

    2012-02-01

    Full Text Available Abstract Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5 activation by (RS-2-chloro-5-hydroxyphenylglycine (CHPG decreases microglial activation and release of associated pro-inflammatory factors in vitro, which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. Methods One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolylethynylpyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Results Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Conclusion Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors

  1. Microdialysis study of cefotaxime cerebral distribution in patients with acute brain injury.

    Science.gov (United States)

    Dahyot-Fizelier, Claire; Frasca, Denis; Grégoire, Nicolas; Adier, Christophe; Mimoz, Olivier; Debaene, Bertrand; Couet, William; Marchand, Sandrine

    2013-06-01

    Central nervous system (CNS) antibiotic distribution was described mainly from cerebrospinal fluid data, and only few data exist on brain extracellular fluid concentrations. The aim of this study was to describe brain distribution of cefotaxime (2 g/8 h) by microdialysis in patients with acute brain injury who were treated for a lung infection. Microdialysis probes were inserted into healthy brain tissue of five critical care patients. Plasma and unbound brain concentrations were determined at steady state by high-performance liquid chromatography. In vivo recoveries were determined individually using retrodialysis by drug. Noncompartmental and compartmental pharmacokinetic analyses were performed. Unbound cefotaxime brain concentrations were much lower than corresponding plasma concentrations, with a mean cefotaxime unbound brain-to-plasma area under the curve ratio equal to 26.1 ± 12.1%. This result was in accordance with the brain input-to-brain output clearances ratio (CL(in,brain)/CL(out,brain)). Unbound brain concentrations were then simulated at two dosing regimens (4 g every 6 h or 8 h), and the time over the MICs (T>MIC) was estimated for breakpoints of susceptible and resistant Streptococcus pneumoniae strains. T>MIC was higher than 90% of the dosing interval for both dosing regimens for susceptible strains and only for 4 g every 6 h for resistant ones. In conclusion, brain distribution of cefotaxime was well described by microdialysis in patients and was limited.

  2. Sub-Chronic Neuropathological and Biochemical Changes in Mouse Visual System after Repetitive Mild Traumatic Brain Injury

    OpenAIRE

    Radouil Tzekov; Clint Dawson; Megan Orlando; Benoit Mouzon; Jon Reed; James Evans; Gogce Crynen; Michael Mullan; Fiona Crawford

    2016-01-01

    Repetitive mild traumatic brain injury (r-mTBI) results in neuropathological and biochemical consequences in the human visual system. Using a recently developed mouse model of r-mTBI, with control mice receiving repetitive anesthesia alone (r-sham) we assessed the effects on the retina and optic nerve using histology, immunohistochemistry, proteomic and lipidomic analyses at 3 weeks post injury. Retina tissue was used to determine retinal ganglion cell (RGC) number, while optic nerve tissue w...

  3. Opioid Abuse after Traumatic Brain Injury: Evaluation Using Rodent Models

    Science.gov (United States)

    2015-09-01

    nociception ( pain threshold) between the sham controls and the brain-injured subjects in either the spinally or supra-spinally mediated measures of acute pain ...brain injury does not result in an altered pain state or diminished response to oxycodone analgesia and the dependence studies show withdrawal is not...of persons who are prescribed opioid pain medications. There is significant overlap in anatomical brain regions involved in reward pathways

  4. Biomarkers and acute brain injuries: interest and limits.

    Science.gov (United States)

    Mrozek, Ségolène; Dumurgier, Julien; Citerio, Giuseppe; Mebazaa, Alexandre; Geeraerts, Thomas

    2014-04-24

    For patients presenting with acute brain injury (such as traumatic brain injury, subarachnoid haemorrhage and stroke), the diagnosis and identification of intracerebral lesions and evaluation of the severity, prognosis and treatment efficacy can be challenging. The complexity and heterogeneity of lesions after brain injury are most probably responsible for this difficulty. Patients with apparently comparable brain lesions on imaging may have different neurological outcomes or responses to therapy. In recent years, plasmatic and cerebrospinal fluid biomarkers have emerged as possible tools to distinguish between the different pathophysiological processes. This review aims to summarise the plasmatic and cerebrospinal fluid biomarkers evaluated in subarachnoid haemorrhage, traumatic brain injury and stroke, and to clarify their related interests and limits for diagnosis and prognosis. For subarachnoid haemorrhage, particular interest has been focused on the biomarkers used to predict vasospasm and cerebral ischaemia. The efficacy of biomarkers in predicting the severity and outcome of traumatic brain injury has been stressed. The very early diagnostic performance of biomarkers and their ability to discriminate ischaemic from haemorrhagic stroke were studied.

  5. A prospective study to evaluate a new residential community reintegration programme for severe chronic brain injury: the Brain Integration Programme.

    NARCIS (Netherlands)

    Geurtsen, G.J.; Martina, J.D.; Heugten, C.M. van; Geurts, A.C.H.

    2008-01-01

    PURPOSE: To assess the effectiveness of a residential community reintegration programme for participants with chronic sequelae of severe acquired brain injury that hamper community functioning. DESIGN: Prospective cohort study. SUBJECTS: Twenty-four participants with acquired brain injury (traumatic

  6. Biomarkers of brain injury in the premature infant

    Directory of Open Access Journals (Sweden)

    Martha V. Douglas-Escobar

    2013-01-01

    Full Text Available The term encephalopathy of prematurity encompasses not only the acute brain injury (such as intraventricular hemorrhage but also complex disturbance on the infant’s subsequent brain development. In premature infants, the most frequent recognized source of brain injury is intraventricular hemorrhage (IVH and periventricular leukomalacia (PVL. Furthermore 20-25% infants with birth weigh less than 1,500 g will have IVH and that proportion increases to 45% if the birth weight is less than 500-750 g. In addition, nearly 60% of very low birth weight newborns will have hypoxic-ischemic injury. Therefore permanent lifetime neurodevelopmental disabilities are frequent in premature infants. Innovative approach to prevent or decrease brain injury in preterm infants requires discovery of biomarkers able to discriminate infants at risk for injury, monitor the progression of the injury and assess efficacy of neuroprotective clinical trials. In this article, we will review biomarkers studied in premature infants with IVH, Post-hemorrhagic ventricular dilation (PHVD and PVL including: S100b, Activin A, erythropoietin, chemokine CCL 18, GFAP and NFL will also be examined. Some of the most promising biomarkers for IVH are S100β and Activin. The concentrations of TGF-β1, MMP-9 and PAI-1 in cerebrospinal fluid could be used to discriminate patients that will require shunt after post-hemorrhagic ventricular dilation. Neonatal brain injury is frequent in premature infants admitted to the neonatal intensive care and we hope to contribute to the awareness and interest in clinical validation of established as well as novel neonatal brain injury biomarkers.

  7. Biomarkers of brain injury in the premature infant.

    Science.gov (United States)

    Douglas-Escobar, Martha; Weiss, Michael D

    2012-01-01

    The term "encephalopathy of prematurity" encompasses not only the acute brain injury [such as intraventricular hemorrhage (IVH)] but also complex disturbance on the infant's subsequent brain development. In premature infants, the most frequent recognized source of brain injury is IVH and periventricular leukomalacia (PVL). Furthermore 20-25% infants with birth weigh less than 1,500 g will have IVH and that proportion increases to 45% if the birth weight is less than 500-750 g. In addition, nearly 60% of very low birth weight newborns will have hypoxic-ischemic injury. Therefore permanent lifetime neurodevelopmental disabilities are frequent in premature infants. Innovative approach to prevent or decrease brain injury in preterm infants requires discovery of biomarkers able to discriminate infants at risk for injury, monitor the progression of the injury, and assess efficacy of neuroprotective clinical trials. In this article, we will review biomarkers studied in premature infants with IVH, Post-hemorrhagic ventricular dilation (PHVD), and PVL including: S100b, Activin A, erythropoietin, chemokine CCL 18, GFAP, and NFL will also be examined. Some of the most promising biomarkers for IVH are S100β and Activin. The concentrations of TGF-β1, MMP-9, and PAI-1 in cerebrospinal fluid could be used to discriminate patients that will require shunt after PHVD. Neonatal brain injury is frequent in premature infants admitted to the neonatal intensive care and we hope to contribute to the awareness and interest in clinical validation of established as well as novel neonatal brain injury biomarkers.

  8. Therapeutic effect of nimodipine on experimental brain injury

    Institute of Scientific and Technical Information of China (English)

    杨树源; 王增光

    2003-01-01

    Objective: To study the therapeutic effect of nimodipine on experimental brain injury.Methods: Experimental and control rabbits were subjected to a closed head injury. In one group nimodipine was given intravenously and the effect evaluated by electron microscopy, brain water content, calcium levels, transcranial Doppler, and intracranial pressure monitoring.Results: In rabbits treated with nimodipine the level of neuronal cytosolic free calcium was markedly decreased. There were less cellular damage and less spasm of the middle cerebral artery seen on electron microscopy. No difference regarding intracranial pressure changes between the two groups was noted. Conclusions: Nimodipine has a protective action on brain injury by blocking a series of pathological reactions induced by neuronal calcium overload, and by reducing the spasm of brain vessels and improving cerebral blood flow.

  9. Autophagy in acute brain injury: feast, famine, or folly?

    Science.gov (United States)

    Smith, Craig M; Chen, Yaming; Sullivan, Mara L; Kochanek, Patrick M; Clark, Robert S B

    2011-07-01

    In the central nervous system, increased autophagy has now been reported after traumatic brain and spinal cord injury, cerebral ischemia, intracerebral hemorrhage, and seizures. This increase in autophagy could be physiologic, converting damaged or dysfunctional proteins, lipids, and/or organelles to their amino acid and fatty acid components for recycling. On the other hand, this increase in autophagy could be supraphysiologic, perhaps consuming and eliminating functional proteins, lipids, and/or organelles as well. Whether an increase in autophagy is beneficial (feast) or detrimental (famine) in brain likely depends on both the burden of intracellular substrate targeted for autophagy and the capacity of the cell's autophagic machinery. Of course, increased autophagy observed after brain injury could also simply be an epiphenomenon (folly). These divergent possibilities have clear ramifications for designing therapeutic strategies targeting autophagy after acute brain injury and are the subject of this review. This article is part of a Special Issue entitled "Autophagy and protein degradation in neurological diseases."

  10. Burn Injury: A Challenge for Tissue Engineers

    Directory of Open Access Journals (Sweden)

    Yerneni LK

    2009-01-01

    Full Text Available Ever since man invented fire he has been more frequently burning himself by this creation than by the naturally occurring bushfires. It is estimated that over 1.152 million people in India suffer from burn injuries requiring treatment every year and majority of them are women aged between 16-40 years and most of them occur in the kitchen. The treatment for burns basically involves autologous skin grafting, which originated in India more than two thousand years ago (Sushruta Samhita, is still the gold standard for the wound resurfacing, although, autografting is difficult where graftable donor sites are limited. Although, Cadaver skin, porcine or bovine xenografts are used alternatively over the past thirty years, modern approaches like the Bioengineering of skin substitutes emerged during the past 20 years as advanced wound management technologies with no social impediment. They can be broadly categorized as Acellular and Cellular biotechnological products. The acellular products like Alloderm (LifeCell Corporation, Integra (Integra Life Sciences act like template and depend on natural regeneration, while the cellular ones are either ‘Off-the-Shelf’ products like Apligraf (Organogenesis Inc and Orcel (Ortec International have allogenic elements and ‘home grown’ autologous cell products like Cultured Epithelial Autograft (CEA and epidermal-dermal composite skin use synthetic or natural non-human matrices. The CEA is based on the ex-vivo epidermal stem cell-expansion and our laboratory has been engaged in CEA technique development with innovative cost-effective approach and yielded promising preliminary clinical success. The basic methodological approach in CEA technique which is still clinically adopted by several developed countries involves the use of growth arrested mouse dermal fibroblasts as growth supportive matrix and is thus considered a drawback as a whole. Additionally, there is no superior enough method available to augment the

  11. Management of facial soft tissue injuries in children.

    Science.gov (United States)

    Vasconez, Henry C; Buseman, Jason L; Cunningham, Larry L

    2011-07-01

    Pediatric facial trauma can present a challenge to even the more experienced plastic surgeon. Injuries to the head and neck may involve bone and soft tissues with an assortment of specialized organs and tissue elements involved. Because of the active nature of children, facial soft tissue injuries can be diverse and extensive as well as some of the more common injuries a plastic surgeon is asked to treat. In 2007, approximately 800,000 patients younger than 15 years presented to emergency departments around the country with significant open wounds of the head that required treatment.In this review, we present the different types and regions of pediatric soft tissue facial trauma, as well as treatment options and goals of plastic surgery wound management. Special aspects, such as bite wounds, burns, pediatric analgesia, and antibiotic therapy, are also discussed.

  12. TREATMENT OF SOFT TISSUE INJURY BY PUNCTURING CLEFT-POINTS

    Institute of Scientific and Technical Information of China (English)

    Xu Yunxiang; Chen Guizhen

    2001-01-01

    Objective: To observe the therapeutic effect of acupuncture of "Xi" (Cleft)-points in treatment of soft tissue injury. Methods: 335 cases of soft tissue injury patients were divided into Cleft-point group (264 cases) and Ashipoint group (control group, 71 cases) randomly. In Cleft-point group, the 16 Cleft-points were used in combination with Ahshi points. In control group, only local Ahshi-points were punctured. The treatment was conducted once every day, with 5 sessions being a therapeutic course. After 2 courses of treatment, the therapeutic effect was analyzed.Results: Results showed that the therapeutic effect of cleft-point group was significantly better than that of control group (P<0.05), particularly in treatment of acute soft tissue. Conclusion: Cleft-point acupuncture has a better therapeutic effect in treatment of soft tissue injury in comparison with Ashi-point.

  13. Changes in circulating inflammatory cells and the relationship to secondary brain injury in patients with craniocerebral injury

    Institute of Scientific and Technical Information of China (English)

    Xiaoping Tang; Renguo Luo; Tao Zhang; Yuanchuan Wang; Hua Peng; Ling Feng; Jian Qi; Wenguo Tang; Zhangyang Gou; Dingyong Yu

    2008-01-01

    BACKGROUND: Recent studies have indicated that reactive encephalitis plays an important role in secondary tissue damage after craniocerebral injury.OBJECTIVE: To observe changes in white blood cells (WBC) and polymorphonuclear neutrophils (PMN)in peripheral blood, and to determine their role in secondary brain insult in patients with craniocerebral injury.DESIGN, TIME AND SETTING: A case-control study at the Department of Neurosurgery of the Affiliated Hospital North Sichuan University of Medical Sciences between August 2007 and May 2008.PARTICIPANTS: Sixty-three patients, admitted within 24 hours after craniocerebral injury and who received no surgery, were included in the study. The cohort consisted of 41 males and 22 females, aged 9-72years, with an average age of 42 years. Ten healthy volunteers, selected from the Department of Neurosurgery, were designated as the control group.METHODS: WBC and PMN from the peripheral blood were measured 0, 24, 48, 72, and 168 hours after admission to hospital. The Glasgow coma scale, area of cerebral hemorrhage, and degree of brain edema were simultaneously determined. The Glasgow outcome scale was evaluated six months after injury. The relationship between changes in WBC and PMN were analyzed. Sixty-three patients were divided into 0, 24,48, 72, and 168 hours groups, with admission time to hospital as the determining factor. As controls, WBC and PMN of peripheral blood were also detected in 10 healthy volunteers.MAIN OUTCOME MEASURES: The main outcome measures were WBC and PMN counts in the peripheral blood at 0, 24, 48, 72, and 168 hours after admission to hospital, the mutual relationship between GCS, WBC and PMN, and changes in brain hemorrhage volume and edema size.RESULTS: WBC peaked at 24 hours after injury, and PMN peaked at 48 hours after injury (P < 0.01).These measures negatively correlated to the Glasgow coma scale (r = 0.657, -0.541, respectively, P < 0.05).In patients with Glasgow coma sale < 8, WBC and PMN were

  14. Strain and rate-dependent neuronal injury in a 3D in vitro compression model of traumatic brain injury

    Science.gov (United States)

    Bar-Kochba, Eyal; Scimone, Mark T.; Estrada, Jonathan B.; Franck, Christian

    2016-08-01

    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.

  15. Strain and rate-dependent neuronal injury in a 3D in vitro compression model of traumatic brain injury.

    Science.gov (United States)

    Bar-Kochba, Eyal; Scimone, Mark T; Estrada, Jonathan B; Franck, Christian

    2016-08-02

    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.

  16. Neuroprotection of lipoic acid treatment promotes angiogenesis and reduces the glial scar formation after brain injury.

    Science.gov (United States)

    Rocamonde, B; Paradells, S; Barcia, J M; Barcia, C; García Verdugo, J M; Miranda, M; Romero Gómez, F J; Soria, J M

    2012-11-01

    After trauma brain injury, a large number of cells die, releasing neurotoxic chemicals into the extracellular medium, decreasing cellular glutathione levels and increasing reactive oxygen species that affect cell survival and provoke an enlargement of the initial lesion. Alpha-lipoic acid is a potent antioxidant commonly used as a treatment of many degenerative diseases such as multiple sclerosis or diabetic neuropathy. Herein, the antioxidant effects of lipoic acid treatment after brain cryo-injury in rat have been studied, as well as cell survival, proliferation in the injured area, gliogenesis and angiogenesis. Thus, it is shown that newborn cells, mostly corresponded with blood vessels and glial cells, colonized the damaged area 15 days after the lesion. However, lipoic acid was able to stimulate the synthesis of glutathione, decrease cell death, promote angiogenesis and decrease the glial scar formation. All those facts allow the formation of new neural tissue. In view of the results herein, lipoic acid might be a plausible pharmacological treatment after brain injury, acting as a neuroprotective agent of the neural tissue, promoting angiogenesis and reducing the glial scar formation. These findings open new possibilities for restorative strategies after brain injury, stroke or related disorders.

  17. Complement and Immunoregulation in Tissue Injury

    Science.gov (United States)

    2015-12-01

    rheumatoid arthritis . N Engl J Med 350(25): 2546-2548. 26. Hill, D. A., D. Artis. (2010). Intestinal bacteria and the regulation of immune cell...the rat intestinal epithelium. Gut 42(4): 530-537. 9. Carden, D. L. and D. N. Granger (2000). Pathophysiology of ischaemia-reperfusion injury. J Pathol

  18. NMR imaging of cell phone radiation absorption in brain tissue

    OpenAIRE

    Gultekin, David H.; Moeller, Lothar

    2012-01-01

    A method is described for measuring absorbed electromagnetic energy radiated from cell phone antennae into ex vivo brain tissue. NMR images the 3D thermal dynamics inside ex vivo bovine brain tissue and equivalent gel under exposure to power and irradiation time-varying radio frequency (RF) fields. The absorbed RF energy in brain tissue converts into Joule heat and affects the nuclear magnetic shielding and the Larmor precession. The resultant temperature increase is measured by the resonance...

  19. Hyperbaric oxygen therapy ameliorates local brain metabolism, brain edema and inflammatory response in a blast-induced traumatic brain injury model in rabbits.

    Science.gov (United States)

    Zhang, Yongming; Yang, Yanyan; Tang, Hong; Sun, Wenjiang; Xiong, Xiaoxing; Smerin, Daniel; Liu, Jiachuan

    2014-05-01

    Many studies suggest that hyperbaric oxygen therapy (HBOT) can provide some clinically curative effects on blast-induced traumatic brain injury (bTBI). The specific mechanism by which this occurs still remains unknown, and no standardized time or course of hyperbaric oxygen treatment is currently used. In this study, bTBI was produced by paper detonators equivalent to 600 mg of TNT exploding at 6.5 cm vertical to the rabbit's head. HBO (100% O2 at 2.0 absolute atmospheres) was used once, 12 h after injury. Magnetic resonance spectroscopy was performed to investigate the impact of HBOT on the metabolism of local injured nerves in brain tissue. We also examined blood-brain barrier (BBB) integrity, brain water content, apoptotic factors, and some inflammatory mediators. Our results demonstrate that hyperbaric oxygen could confer neuroprotection and improve prognosis after explosive injury by promoting the metabolism of local neurons, inhibiting brain edema, protecting BBB integrity, decreasing cell apoptosis, and inhibiting the inflammatory response. Furthermore, timely intervention within 1 week after injury might be more conducive to improving the prognosis of patients with bTBI.

  20. Human neuronal apoptosis secondary to traumatic brain injury and the regulative role of apoptosis-related genes

    Institute of Scientific and Technical Information of China (English)

    杨树源; 雪亮

    2004-01-01

    Objective: To observe human neuronal apoptosis secondary to traumatic brain injury, and to elucidate its regulative mechanism and the change of expression of apoptosis-related genes.Methods: Specimens of brain were collected from cases of traumatic brain injury in humans. The histological and cellular morphology was examined by light and electron microscopy. The extent of DNA injury to cortical neurons was detected by using TUNEL. By in situ hybridisation and immunohistochemistry the mRNA changes and protein expression of Bcl-2, Bax, p53, and caspase 3 p20 subunit were observed.Results: Apoptotic neurons appeared following traumatic brain injury, peaked at 24 hours and lasted for 7 days. In normal brain tissue activated caspase 3 was rare,but a short time after trauma it became activated. The activity peaked at 20-28 hours and remained higher than normal for 5-7 days. There was no expression of Bcl-2 mRNA and Bcl-2 protein in normal brain tissue but 8 hours after injury their expression became evident and then increased, peaked at 2-3 days and remained higher than normal for 5-7 days. The primary expression of Bax-mRNA and Bax protein was high in normal brain tissue. At 20-28 hours they increased and remained high for 2-3 days; on the 7th days they returned to a normal level. In normal brain tissue, p53mRNA and P53 were minimally expressed.Increased expression was detected at the 8th hour, and decreased at 20-28 hours but still remained higher than normal on the 5th day.Conclusions: Following traumatic injury to the human brain, apoptotic neurons appear around the focus of trauma. The mRNA and protein expression of Bcl-2, Bax and p53 and the activity of caspase 3 enzyme are increased.

  1. Mechanical Loading of Neurons and Astrocytes with Application to Blast Traumatic Brain Injury

    Science.gov (United States)

    2010-01-01

    traumatic brain injury ( TBI ). Neurons and astrocytes are susceptible to damage mechanisms arising from various...further developments may be pursued to unravel the key mechanical pathways potentially involved in TBI . 1. INTRODUCTION Traumatic brain injury ... injury mechanisms at the cellular level. This is especially important when studying traumatic brain injury ( TBI ). Neurons and astrocytes

  2. Social competence at 2 years following child traumatic brain injury.

    Science.gov (United States)

    Anderson, Vicki; Beauchamp, Miriam Helen; Yeates, Keith Owen; Crossley, Louise; Ryan, Nicholas Peter; Hearps, Stephen J C; Catroppa, Cathy

    2017-02-08

    Children with traumatic brain injury (TBI) are at risk of social impairment, but research is yet to document the trajectory of these skills post-injury and factors that may predict social problems. The study addressed these gaps in knowledge, reporting on findings from a prospective, longitudinal follow-up study which investigated social outcomes post injury and explored factors contributing to these outcomes at 2 years post-injury. The sample included 113 children, 74 with TBI and 39 typically developing (TD) controls. TBI participants were recruited on presentation to hospital. Parents rated pre-injury function at that time and all children underwent magnetic resonance imaging (MRI) scan. Participants were followed up at 2 years post-injury. Outcomes were social adjustment, social participation, social relationships, and social cognition. Predictors of social outcomes examined included brain lesion characteristics, child cognition (6 months post-TBI) and behavior and environmental factors (pre-injury and 2 years). Reduced social adjustment (p=.011) and social participation (pchildren with TBI compared to TD controls. Poor social adjustment was predicted by externalizing behaviour problems and younger age at injury. Reduced social participation was linked to internalizing behavior problems. Greater lesion volume, lower socioeconomic status and family burden contributed to poorer social relationships, while age at injury predicted social cognition. Within the TBI group, 23% of children exhibited social impairment: younger age at injury, greater pre-injury and current behavior problems and family dysfunction, poorer IQ, processing speed, and empathy were linked to impairment. Further follow-up is required to track social recovery and the influences of cognition, brain, and environment over time.

  3. Role of Melatonin in Traumatic Brain Injury and Spinal Cord Injury

    Directory of Open Access Journals (Sweden)

    Mehar Naseem

    2014-01-01

    Full Text Available Brain and spinal cord are implicated in incidences of two of the most severe injuries of central nervous system (CNS. Traumatic brain injury (TBI is a devastating neurological deficit involving primary and secondary injury cascades. The primary and secondary mechanisms include complex consequences of activation of proinflammatory cytokines, cerebral edema, upregulation of NF-κβ, disruption of blood-brain barrier (BBB, and oxidative stress. Spinal cord injury (SCI includes primary and secondary injury cascades. Primary injury leads to secondary injury in which generation of free radicals and oxidative or nitrative damage play an important pathophysiological role. The indoleamine melatonin is a hormone secreted or synthesized by pineal gland in the brain which helps to regulate sleep and wake cycle. Melatonin has been shown to be a versatile hormone having antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. It has a special characteristic of crossing BBB. Melatonin has neuroprotective role in the injured part of the CNS after TBI and SCI. A number of studies have successfully shown its therapeutic value as a neuroprotective agent in the treatment of neurodegenerative diseases. Here in this review we have compiled the literature supporting consequences of CNS injuries, TBI and SCI, and the protective role of melatonin in it.

  4. Development of a new biomechanical indicator for primary blast-induced brain injury

    Institute of Scientific and Technical Information of China (English)

    Feng Zhu; Cliff C.Chou; King H.Yang; Albert I.King

    2015-01-01

    Primary blast-induced traumatic brain injury (bTBI) has been observed at the boundary of brain tissue and cerebrospinal fluid (CSF).Such injury can hardly be explained by using the theory of compressive wave propagation,since both the solid and fluid materials have similar compressibility and thus the intracranial pressure (ICP) has a continuous distribution across the boundary.Since they have completely different shear properties,it is hypothesized the injury at the interface is caused by shear wave.In the present study,a preliminary combined numerical and theoretical analysis was conducted based on the theory of shear wave propagation]reflection.Simulation results show that higher lateral acceleration of brain tissue particles is concentrated in the boundary region.Based on this finding,a new biomechanical vector,termed as strain gradient,was suggested for primary bTBI.The subsequent simple theoretical analysis reveals that this parameter is proportional to the value of lateral acceleration.At the boundary of lateral ventricles,high spatial strain gradient implies that the brain tissue in this area (where neuron cells may be contained) undergo significantly different strains and large velocity discontinuity,which may result in mechanical damage of the neuron cells.

  5. Correlation of brain-derived neurotrophic factor to cognitive impairment following traumatic brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    Dezhi Kang; Zhang Guo

    2008-01-01

    BACKGROUND: In vitro and in vivo studies have confirmed that brain-derived neurotrophic factor (BDNF) can promote survival and differentiation of cholinergic, dopaminergic and motor neurons, and axonal regeneration. BDNF has neuroprotective effects on the nervous system. OBJECTIVE: To explore changes in BDNF expression and cognitive function in rats after brain injury DESIGN, TIME AND SETTING: The neuropathology experiment was performed at the Second Research Room, Department of Neurosurgery, Fujian Medical University (China) from July 2007 to July 2008. MATERIALS: A total of 72 healthy, male, Sprague Dawley, rats were selected for this study. METHODS: Rat models of mild and moderate traumatic brain injury were created by percussion, according to Feeney's method (n = 24, each group). A bone window was made in rats from the sham operation group (n = 24), but no attack was conducted. MAIN OUTCOME MEASURES: At days 1,2, 4 and 7 following injury, BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was examined by immunohistochemistry (streptavidin-biotin-peroxidase complex method). Changes in rat cognitive function were assessed by the walking test, balance-beam test and memory function detection. RESULTS: Cognitive impairment was aggravated at day 2, and recovered to normal at days 3 and 7 in rats from the mild and moderate traumatic brain injury groups. BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was increased at 1 day, decreased at day 2, and then gradually increased in the mild and moderate traumatic brain injury groups. BDNF expression was greater in rats from the moderate traumatic brain injury group than in the sham operation and mild traumatic brain injury groups (P < 0.05). CONCLUSION: BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain is correlated to cognitive impairment after traumatic brain injury. BDNF has a protective effect on cognitive function in rats

  6. Hemodynamic and morphologic responses in mouse brain during acute head injury imaged by multispectral structured illumination

    Science.gov (United States)

    Volkov, Boris; Mathews, Marlon S.; Abookasis, David

    2015-03-01

    Multispectral imaging has received significant attention over the last decade as it integrates spectroscopy, imaging, tomography analysis concurrently to acquire both spatial and spectral information from biological tissue. In the present study, a multispectral setup based on projection of structured illumination at several near-infrared wavelengths and at different spatial frequencies is applied to quantitatively assess brain function before, during, and after the onset of traumatic brain injury in an intact mouse brain (n=5). For the production of head injury, we used the weight drop method where weight of a cylindrical metallic rod falling along a metal tube strikes the mouse's head. Structured light was projected onto the scalp surface and diffuse reflected light was recorded by a CCD camera positioned perpendicular to the mouse head. Following data analysis, we were able to concurrently show a series of hemodynamic and morphologic changes over time including higher deoxyhemoglobin, reduction in oxygen saturation, cell swelling, etc., in comparison with baseline measurements. Overall, results demonstrates the capability of multispectral imaging based structured illumination to detect and map of brain tissue optical and physiological properties following brain injury in a simple noninvasive and noncontact manner.

  7. The role of autophagic and lysosomal pathways in ischemic brain injury******

    Institute of Scientific and Technical Information of China (English)

    Zhaohua Gu; Nan Shi; Qian Zhang; Wei Zhang; Meizhen Zhao; Xiaojiang Sun; Yinyi Sun; Kangyong Liu; Fen Wang; Ting Zhang; Qiang Li; Liwei Shen; Ling Zhou; Liang Dong

    2013-01-01

    Autophagy is involved in neural cel death after cerebral ischemia. Our previous studies showed that rapamycin-induced autophagy decreased the rate of apoptosis, but the rate of apoptosis was creased after the autophagy inhibitor, 3-methyladenine, was used. In this study, a suture-occluded method was performed to generate a rat model of brain ischemia. Under a transmission electron microscope, autophagic bodies and autophagy lysosomes were markedly accumulated in neurons at 4 hours post brain ischemic injury, with their numbers gradual y reducing over time. Western blotting demonstrated that protein levels of light chain 3-II and cathepsin B were significantly in-creased within 4 hours of ischemic injury, but these levels were not persistently upregulated over time. Confocal microscopy showed that autophagy was mainly found in neurons with positive light chain 3 signal. Injection of rapamycin via tail vein promoted the occurrence of autophagy in rat brain tissue after cerebral ischemia and elevated light chain 3 and cathepsin B expression. However, in-jection of 3-methyladenine significantly diminished light chain 3-II and cathepsin B expression. Results verified that autophagic and lysosomal activity is increased in ischemic neurons. Abnormal components in cel s can be eliminated through upregulating cel autophagy or inhibiting autophagy after ischemic brain injury, resulting in a dynamic balance of substances in cel s. Moreover, drugs that interfere with autophagy may be potential therapies for the treatment of brain injury.

  8. Blast and the Consequences on Traumatic Brain Injury-Multiscale Mechanical Modeling of Brain

    Science.gov (United States)

    2011-02-17

    brain and spinal cord injury, is the largest contributor to a poor neurological outcome in survivors of brain and spinal cord trauma. Microscale...anatomical features of a 50th percentile male head, including the brain, falx and tentorium, cerebral spinal fluid (CSF), duramater, piamater, facial...discretized finite elements. (b) Sections of the head model; the right half of the head model is shown with the brain, the meningeal layers (dura

  9. Effect of ischemic preconditioning on expression of intracellular adhesion molecule-1 in brain tissues following traumatic brain injury in rats%缺血预处理对大鼠创伤性脑损伤后脑组织细胞间黏附分子-1表达的影响

    Institute of Scientific and Technical Information of China (English)

    朱克军; 黄洪; 储辉; 罗志勇; 徐志明; 俞航; 张世明

    2014-01-01

    目的 探讨缺血预处理(ischemic precoudition,IPC)对大鼠创伤性脑损伤(traumatic brain injury,TBI)后脑组织细胞间黏附分子-1(intracellular adhesion molecule-1,ICAM-1)表达的影响. 方法 雄性SD大鼠60只,体重220 ~250 g,按随机数字表法分为假手术组、TBI组和IPC组,每组20只.短暂夹闭双侧颈总动脉制备脑IPC模型,采用Feeney自由落体撞击法制作TBI模型,假手术组仅行右侧顶部开窗而无TBI.分别于TBI后6,72 h处死10只大鼠,取损伤脑组织,计算脑组织湿/干重比(W/D)值,采用免疫组化法测定ICAM-1表达水平,光镜观察病理学结果. 结果 与假手术组比较,TBI组脑组织W/D值升高(6 h:4.2±0.4比2.7±0.4;72 h:5.0±0.1比3.1±0.2,P<0.05),脑组织ICAM-1表达上调(6 h:25.4 ±3.5比8.6±1.3;72 h:36.5 ±5.4比8.4±1.6,P<0.05);与TBI组比较,IPC组脑组织W/D值降低(6 h:3.5±0.6比4.2±0.4;72 h:3.7±0.4比5.0±0.1,P <0.05),脑组织ICAM-1表达下调(6 h:16.5±2.7比25.4 ±3.5;72 h:24.3 ±4.6比36.5 ±5.4,P<0.05).IPC组脑组织损伤程度轻于TBI组. 结论 IPC可以下调脑组织ICAM-1表达,从而减轻大鼠TBI.%Objective To investigate the effect of ischemic preconditioning (IPC) on expression of intracellular adhesion molecule-1 (ICAM-1) in brain tissues following traumatic brain injury (TBI) in rats.Methods Sixty male SD rats weighing 220-250 g were randomly divided into three groups (n =20 for each):sham operation group,TBI group,and IPC group.Cerebral IPC models were induced by transient occlusion of the bilateral common carotid arteries; TBI models were induced by Feeney's freefalling method; rats in sham operation group were only performed exposure of dura of the right parietal lobe.Ten rats were sacrificed respectively at 6 and 72 hours after TBI and injured brain tissues were harvested to estimate wet/dry weight (W/D) ratio for the brain,determine ICAM-1 expression by immunohistochemistry and perform microscopic examination.Results Brain W

  10. The Relationship between Mid-face Fractures and Brain Injuries

    Directory of Open Access Journals (Sweden)

    Khalighi Sigaroudi A.

    2012-03-01

    Full Text Available Statement of Problem: Although advances in technology have led to improvements in man’s life in different aspects, statistics show that the incidence of fractures is increasing in different regions of the body. Recent studies show that midface fractures are strongly associated with patient's death. The exact relationship between different types of facial fractures and brain injuries is still controversial. Purpose: To evaluate individuals with midface fractures from different causes and determine if there is any relationship between various midface fractures and brain injuries. Materials and Methods: In this descriptive cross-sectional retrospective study, we assessed the hospital charts of all the patients with midface fractures at the trauma center of Poursina hospital. The complete medical record of each patient was reviewed. The etiologic and demographic data, the type of midface fracture and brain injury, and Glasgow coma scale (GCS were assessed. The data were analyzed by, the Chi-square, and the Fisher’s exact tests. The statistical package SPSS was used for all the analyses.Results: Of all the patients 47% had brain injury. The Important significant correlations were as follows: Le Fort III with Brain Contusion ( p =0.0001, nasal orbital ethmoid fractures with subdural hematoma ( p =0.0001, frontal fracture with subdural hematoma ( p =0.0001. Zygomatic complex fracture with Brain Contusion ( p =0.009. Nasal fracture correlated with Brain Contusion ( p =0.0001. The zygomatic complex fracture was the most prevalent fracture.Conclusion: Different midface fracture patterns have the risk of brain injury simultaneously. So midface fractures need more attention. According to the results, more attention is needed to be paid to driving rules specially the use of helmet and seat belt.

  11. NMR imaging of cell phone radiation absorption in brain tissue.

    Science.gov (United States)

    Gultekin, David H; Moeller, Lothar

    2013-01-02

    A method is described for measuring absorbed electromagnetic energy radiated from cell phone antennae into ex vivo brain tissue. NMR images the 3D thermal dynamics inside ex vivo bovine brain tissue and equivalent gel under exposure to power and irradiation time-varying radio frequency (RF) fields. The absorbed RF energy in brain tissue converts into Joule heat and affects the nuclear magnetic shielding and the Larmor precession. The resultant temperature increase is measured by the resonance frequency shift of hydrogen protons in brain tissue. This proposed application of NMR thermometry offers sufficient spatial and temporal resolution to characterize the hot spots from absorbed cell phone radiation in aqueous media and biological tissues. Specific absorption rate measurements averaged over 1 mg and 10 s in the brain tissue cover the total absorption volume. Reference measurements with fiber optic temperature sensors confirm the accuracy of the NMR thermometry.

  12. Immunohistochemical detection of brain tissue in heated meat products.

    Science.gov (United States)

    Tersteeg, M H G; Koolmees, P A; van Knapen, F

    2002-05-01

    Immunohistochemical methods were used to determine whether brain tissue could be detected in test batches of meat products prepared with known levels of this tissue (0, 1, 5, 10, or 20% bovine brain tissue or 5% porcine brain tissue). Four different, commercially-available antibodies were examined: anti-Neurofilament (anti-NF), anti-MyelinBasicProtein (anti-MBP), anti-NeuronSpecificEnolase (anti-NSE) and anti-GlialFibrillaryAcidicProtein (anti-GFAP). Results obtained with the four antibodies differed with the heat treatment applied to the products (pasteurisation or sterilisation). The amount of immunoreaction product in the raw meat product varied with the antibody, even when the sample contained the same amount of brain tissue. The staining pattern also varied with the antibody. Overall, the anti-MBP antibody proved to be most useful in detecting brain tissue in finely comminuted heated meat products.

  13. Effects of isoflurane postconditioning on mitochondrial permeability transition pore in brain tissues of neonatal rats with hypoxic-ischemic brain injury%异氟醚后处理对缺血缺氧性脑损伤新生大鼠脑组织线粒体通透性转换孔的影响

    Institute of Scientific and Technical Information of China (English)

    纪国余; 薛杭; 于威威; 季海音; 杨雅婷; 赵平

    2014-01-01

    Objective To evaluate the effects of isoflurane postconditioning on mitochondrial permeability transition pore (mPTP) in brain tissues of neonatal rats with hypoxic-ischemic brain injury.Methods One hundred and twenty 7-day-old Sprague-Dawley rats,weighing 12-16 g,were randomly divided into 4 groups (n =30 each) using a random number table:sham operation group (group S),isoflurane group (group I),hypoxicischemic brain injury group (group HIBI),and hypoxic-ischemic brain injury + isoflurane postconditioning group (group HI).To establish hypoxic-ischemic brain injury model in the neonatal rats,the left common carotid artery ligation was carried out,and then the rats were exposed to 8% O2 + 92% N2 at 37 ℃ for 2 h in HIBI and HI groups.The rats inhaled 1.5 % isoflurane for 30 min after the model was established in group HI.The rats only inhaled 1.5% isoflurane for 30 min in group I.At 24 h after the model was established,10 rats taken out randomly in each group were sacrificed and brains were removed to detect mPTP opening.At 7 days after the model was established,the survival rate was recorded in the rest rats.The rats were then sacrificed and brains were removed and the right and left cerebral hemispheres were weighed separately,and the ratio between left/right cerebral hemispheres was calculated.The density of normal neurons in ventral posterior inferior thalamic nucleus and hippocampal CA3 region in the left and right cerebral hemispheres were measured and the ratios of the density of normal neurons in the left to right cerebral hemisphere were calculated.Results There was no significant difference in the survival rate between the four groups (P > 0.05).Compared with group S,the ratios of the density of normal neurons in the left to right cerebral hemisphere,weight of left cerebral hemisphere,and ratio between left/right cerebral hemispheres were significantly decreased,and mPTP opening was increased in group HIBI (P < 0.05),and no significant changes

  14. Expression and antioxidation of Nrf2/ARE pathway in traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Zhen-Guo Cheng; Guo-Dong Zhang; Peng-Qiang Shi; Bao-Shun Du

    2013-01-01

    Objective: To explore the expression of Nrf2/ARE pathway in hindbrain tissue after the traumatic brain injury (TBI) and its anti-oxidative stress effect in the secondary nerve injury. Methods:The mice with Nrf2 gene knockout were used for the establishment of brain injury model. The experimental animals were divided into four groups: (Nrf2+/+) sham-operation group, (Nrf2+/+) brain injury group, (Nrf2-/-) sham-operation group and (Nrf2-/-) brain injury group. The specimen 24 h after cerebral trauma was selected. Then RT-PCR method was adopted to detect the expression of Nrf2 mRNA in brain; Western blotting method was adopted to detect the levels of Nrf2, HO-1 and NQO1 proteins in brain; ELISA method was adopted to detect the oxidative stress indicators:protein carbonyls, 4-hydroxy-2-nonenal (4-HNE) and 8-hydroxy-2’-deoxyguanosine (8-OHdG). Results: The Nrf2 mRNA and protein of Nrf2-/- mice were not expressed, and the difference of the relative amount of Nrf2 mRNA between Nrf2+/+ TBI group and Nrf2+/+ sham-operation group was not statistically significant (P>0.05); the level of Nrf2 protein in Nrf2+/+ TBI group increased significantly compared with the Nrf2+/+ sham-operation group (P0.05); there was only a little amount of expression of protein carbonyls, 4-HNE and 8-OHdG proteins in brain tissues in the Nrf2+/+ and Nrf2-/- sham-operation groups, and the difference was not statistically significant (P>0.05); after brain injury, the three oxidative stress indicators were significantly up-regulated in the Nrf2+/+ and Nrf2-/-groups, and the up-regulation of the latter group was more significant (P<0.01). Conclusions:After TBI the Nrf2/ARE pathway is activated and the activity of Nrf2 transcription regulation increases. However, the regulation dose not occur in the gene transcription level and only could increase the Nrf2 protein level, while the mRNA expression level has no obvious change. The nerve cell protective effect of Nrf2/ARE pathway in TBI achieves through

  15. Brain injury and severe eating difficulties at admission

    DEFF Research Database (Denmark)

    Kjærsgaard, Annette; Kaae Kristensen, Hanne

    Objective: The objective of this pilot study was to explore and interpret the way that individuals with acquired brain injury, admitted to inpatient neurorehabilitation with severe eating difficulties, experienced eating nine to fifteen months after discharge. Methods: Four individuals with acqui......-of-life. The preliminary findings provide knowledge regarding the patient perspective of adapting to and developing new strategies for activities related to eating, however, further prospective, longitudinal research in a larger scale and with repeated interviews is needed.......Objective: The objective of this pilot study was to explore and interpret the way that individuals with acquired brain injury, admitted to inpatient neurorehabilitation with severe eating difficulties, experienced eating nine to fifteen months after discharge. Methods: Four individuals...... with acquired brain injury were interviewed via qualitative semi-structured interviews. An explorative study was conducted to study eating difficulties. Qualitative content analysis was used. Results: Four main themes emerged from the analysis: personal values related to eating, swallowing difficulties, eating...

  16. Neuromodulation of the conscious state following severe brain injuries.

    Science.gov (United States)

    Fridman, Esteban A; Schiff, Nicholas D

    2014-12-01

    Disorders of consciousness (DOC) following severe structural brain injuries globally affect the conscious state and the expression of goal-directed behaviors. In some subjects, neuromodulation with medications or electrical stimulation can markedly improve the impaired conscious state present in DOC. We briefly review recent studies and provide an organizing framework for considering the apparently widely disparate collection of medications and approaches that may modulate the conscious state in subjects with DOC. We focus on neuromodulation of the anterior forebrain mesocircuit in DOC and briefly compare mechanisms supporting recovery from structural brain injuries to those underlying facilitated emergence from unconsciousness produced by anesthesia. We derive some general principles for approaching the problem of restoration of consciousness after severe structural brain injuries, and suggest directions for future research.

  17. Ischemic postconditioning protects against ischemic brain injury by up-regulation of acid-sensing ion channel 2a

    Institute of Scientific and Technical Information of China (English)

    Wang-sheng Duanmu; Liu Cao; Jing-yu Chen; Hong-fei Ge; Rong Hu; Hua Feng

    2016-01-01

    Ischemic postconditioning renders brain tissue tolerant to brain ischemia, thereby alleviating ischemic brain injury. However, the exact mechanism of action is still unclear. In this study, a rat model of global brain ischemia was subjected to ischemic postconditioning treat-ment using the vessel occlusion method. After 2 hours of ischemia, the bilateral common carotid arteries were blocked immediately for 10 seconds and then perfused for 10 seconds. This procedure was repeated six times. Ischemic postconditioning was found to mitigate hippocampal CA1 neuronal damage in rats with brain ischemia, and up-regulate acid-sensing ion channel 2a expression at the mRNA and protein level. These ifndings suggest that ischemic postconditioning up-regulates acid-sensing ion channel 2a expression in the rat hippo-campus after global brain ischemia, which promotes neuronal tolerance to ischemic brain injury.

  18. Therapeutic potential of brain-derived neurotrophic factor (BDNF) and a small molecular mimics of BDNF for traumatic brain injury

    Science.gov (United States)

    Wurzelmann, Mary; Romeika, Jennifer; Sun, Dong

    2017-01-01

    Traumatic brain injury (TBI) is a major health problem worldwide. Following primary mechanical insults, a cascade of secondary injuries often leads to further neural tissue loss. Thus far there is no cure to rescue the damaged neural tissue. Current therapeutic strategies primarily target the secondary injuries focusing on neuroprotection and neuroregeneration. The neurotrophin brain-derived neurotrophic factor (BDNF) has significant effect in both aspects, promoting neuronal survival, synaptic plasticity and neurogenesis. Recently, the flavonoid 7,8-dihydroxyflavone (7,8-DHF), a small TrkB agonist that mimics BDNF function, has shown similar effects as BDNF in promoting neuronal survival and regeneration following TBI. Compared to BDNF, 7,8-DHF has a longer half-life and much smaller molecular size, capable of penetrating the blood-brain barrier, which makes it possible for non-invasive clinical application. In this review, we summarize functions of the BDNF/TrkB signaling pathway and studies examining the potential of BDNF and 7,8-DHF as a therapy for TBI.

  19. Therapeutic potential of brain-derived neurotrophic factor (BDNF) and a small molecular mimics of BDNF for traumatic brain injury.

    Science.gov (United States)

    Wurzelmann, Mary; Romeika, Jennifer; Sun, Dong

    2017-01-01

    Traumatic brain injury (TBI) is a major health problem worldwide. Following primary mechanical insults, a cascade of secondary injuries often leads to further neural tissue loss. Thus far there is no cure to rescue the damaged neural tissue. Current therapeutic strategies primarily target the secondary injuries focusing on neuroprotection and neuroregeneration. The neurotrophin brain-derived neurotrophic factor (BDNF) has significant effect in both aspects, promoting neuronal survival, synaptic plasticity and neurogenesis. Recently, the flavonoid 7,8-dihydroxyflavone (7,8-DHF), a small TrkB agonist that mimics BDNF function, has shown similar effects as BDNF in promoting neuronal survival and regeneration following TBI. Compared to BDNF, 7,8-DHF has a longer half-life and much smaller molecular size, capable of penetrating the blood-brain barrier, which makes it possible for non-invasive clinical application. In this review, we summarize functions of the BDNF/TrkB signaling pathway and studies examining the potential of BDNF and 7,8-DHF as a therapy for TBI.

  20. Brain Injury Risk from Primary Blast

    Science.gov (United States)

    2012-02-29

    injury has been studied extensively in air-containing organs such as the lungs , gastrointestinal tract, and ear due to their increased...veterans (Owens, 2008). Primary blast injury has been studied extensively in air-containing organs such as the lungs , gastrointestinal tract, and ear... contusions typically on or around the brainstem though there were no skull fractures for any blast intensity. Risk functions were developed that

  1. Ischemic preconditioning reduces ischemic brain injury by suppressing nuclear factor kappa B expression and neuronal apoptosis

    Institute of Scientific and Technical Information of China (English)

    Songsheng Shi; Weizhong Yang; Xiankun Tu; Chunmei Chen; Chunhua Wang

    2013-01-01

    Ischemic stroke induces a series of complex pathophysiological events including blood-brain barrier disruption, inflammatory response and neuronal apoptosis. Previous studies demonstrate that ischemic preconditioning attenuates ischemic brain damage via inhibiting blood-brain barrier disruption and the inflammatory response. Rats underwent transient (15 minutes) occlusion of the bilateral common carotid artery with 48 hours of reperfusion, and were subjected to permanent middle cerebral artery occlusion. This study explored whether ischemic preconditioning could reduce ischemic brain injury and relevant molecular mechanisms by inhibiting neuronal apoptosis. Results found that at 72 hours following cerebral ischemia, myeloperoxidase activity was enhanced, malondialdehyde levels increased, and neurological function was obviously damaged. Simultaneously, neuronal apoptosis increased, and nuclear factor-κB and cleaved caspase-3 expression was significantly increased in ischemic brain tissues. Ischemic preconditioning reduced the cerebral ischemia-induced inflammatory response, lipid peroxidation, and neurological function injury. In addition, ischemic preconditioning decreased nuclear factor-κB p65 and cleaved caspase-3 expression. These results suggested that ischemic preconditioning plays a protective effect against ischemic brain injury by suppressing the inflammatory response, reducing lipid peroxidation, and neuronal apoptosis via inhibition of nuclear factor-κB and cleaved caspase-3 expression.

  2. Why most traumatic brain injuries are not caused by linear acceleration but skull fractures are.

    Directory of Open Access Journals (Sweden)

    Svein eKleiven

    2013-11-01

    Full Text Available Injury statistics have found the most common accident situation to be an oblique impact. An oblique impact will give rise to both linear and rotational head kinematics. The human brain is most sensitive to rotational motion. The bulk modulus of brain tissue is roughly five to six orders of magnitude larger than the shear modulus so that for a given impact it tends to deform predominantly in shear. This gives a large sensitivity of the strain in the brain to rotational loading and a small sensitivity to linear kinematics. Therefore, rotational kinematics should be a better indicator of traumatic brain injury risk than linear acceleration. To illustrate the difference between radial and oblique impacts, perpendicular impacts through the center of gravity of the head and 45o oblique impacts were simulated. It is obvious that substantially higher strain levels in the brain are obtained for an oblique impact, compared to a corresponding perpendicular one, when impacted into the same padding using an identical impact velocity. It was also clearly illustrated that the radial impact causes substantially higher stresses in the skull with an associated higher risk of skull fractures, and traumatic brain injuries secondary to those.

  3. Human Traumatic Brain Injury Results in Oligodendrocyte Death and Increases the Number of Oligodendrocyte Progenitor Cells.

    Science.gov (United States)

    Flygt, Johanna; Gumucio, Astrid; Ingelsson, Martin; Skoglund, Karin; Holm, Jonatan; Alafuzoff, Irina; Marklund, Niklas

    2016-06-01

    Oligodendrocyte (OL) death may contribute to white matter pathology, a common cause of network dysfunction and persistent cognitive problems in patients with traumatic brain injury (TBI). Oligodendrocyte progenitor cells (OPCs) persist throughout the adult CNS and may replace dead OLs. OL death and OPCs were analyzed by immunohistochemistry of human brain tissue samples, surgically removed due to life-threatening contusions and/or focal brain swelling at 60.6 ± 75 hours (range 4-192 hours) postinjury in 10 severe TBI patients (age 51.7 ± 18.5 years). Control brain tissue was obtained postmortem from 5 age-matched patients without CNS disorders. TUNEL and CC1 co-labeling was used to analyze apoptotic OLs, which were increased in injured brain tissue (p number of single-labeled Olig2, A2B5, NG2, and PDGFR-α-positive cells, numbers of Olig2 and A2B5 co-labeled cells were increased in TBI samples (p < 0.05); this was inversely correlated with time from injury to surgery (r = -0.8, p < 0.05). These results indicate that severe focal human TBI results in OL death and increases in OPCs postinjury, which may influence white matter function following TBI.

  4. Glyburide - Novel Prophylaxis and Effective Treatment for Traumatic Brain Injury

    Science.gov (United States)

    2010-08-01

    hemorrhagic shock. 15. SUBJECT TERMS blast, traumatic brain injury, neurogenic pulmonary edema, mortality, caspase-3, beta- amylase precursor... function and on pat hophysiological mani festations (IgG, caspase-3 and β-APP immunolabeling), ind ependent of transthoracic mechani sms of blast injury...Glendale Heights, IL). The tool was modified by removing the piston that normally drives the fastener, making the tool function like a firearm and

  5. Neuroendocrine Abnormalities in Patients with Traumatic Brain Injury

    Science.gov (United States)

    1991-01-01

    is common in head trauma. INJURY MECHANISMS Hypothalamic Injury The supraoptic nucleus (SON) is the most vulnerable area of the hypothalamus because...pothaIlimus. but portlif esscls to the antenorpituitat) ma) escape injur). (C) oss stalk transvecion ma% causect rupture of the A gportal sessels ssth...via the systemic circulation to the adrenal gland, where it stimulates secretion of cortisol and aldosterone . Thus, when the brain is traumatized

  6. Optical spectroscopy for the detection of ischemic tissue injury

    Science.gov (United States)

    Demos, Stavros; Fitzgerald, Jason; Troppmann, Christoph; Michalopoulou, Andromachi

    2009-09-08

    An optical method and apparatus is utilized to quantify ischemic tissue and/or organ injury. Such a method and apparatus is non-invasive, non-traumatic, portable, and can make measurements in a matter of seconds. Moreover, such a method and apparatus can be realized through optical fiber probes, making it possible to take measurements of target organs deep within a patient's body. Such a technology provides a means of detecting and quantifying tissue injury in its early stages, before it is clinically apparent and before irreversible damage has occurred.

  7. The profile of head injuries and traumatic brain injury deaths in Kashmir

    Directory of Open Access Journals (Sweden)

    Tabish Amin

    2008-06-01

    Full Text Available Abstract This study was conducted on patients of head injury admitted through Accident & Emergency Department of Sher-i-Kashmir Institute of Medical Sciences during the year 2004 to determine the number of head injury patients, nature of head injuries, condition at presentation, treatment given in hospital and the outcome of intervention. Traumatic brain injury (TBI deaths were also studied retrospectively for a period of eight years (1996 to 2003. The traumatic brain injury deaths showed a steady increase in number from year 1996 to 2003 except for 1999 that showed decline in TBI deaths. TBI deaths were highest in age group of 21–30 years (18.8%, followed by 11–20 years age group (17.8% and 31–40 years (14.3%. The TBI death was more common in males. Maximum number of traumatic brain injury deaths was from rural areas as compared to urban areas. To minimize the morbidity and mortality resulting from head injury there is a need for better maintenance of roads, improvement of road visibility and lighting, proper mechanical maintenance of automobile and other vehicles, rigid enforcement of traffic rules, compulsory wearing of crash helmets by motor cyclist and scooterists and shoulder belt in cars and imparting compulsory road safety education to school children from primary education level. Moreover, appropriate medical care facilities (including trauma centres need to be established at district level, sub-divisional and block levels to provide prompt and quality care to head injury patients

  8. The profile of head injuries and traumatic brain injury deaths in Kashmir.

    Science.gov (United States)

    Yattoo, Gh; Tabish, Amin

    2008-01-01

    This study was conducted on patients of head injury admitted through Accident & Emergency Department of Sher-i-Kashmir Institute of Medical Sciences during the year 2004 to determine the number of head injury patients, nature of head injuries, condition at presentation, treatment given in hospital and the outcome of intervention. Traumatic brain injury (TBI) deaths were also studied retrospectively for a period of eight years (1996 to 2003).The traumatic brain injury deaths showed a steady increase in number from year 1996 to 2003 except for 1999 that showed decline in TBI deaths. TBI deaths were highest in age group of 21-30 years (18.8%), followed by 11-20 years age group (17.8%) and 31-40 years (14.3%). The TBI death was more common in males. Maximum number of traumatic brain injury deaths was from rural areas as compared to urban areas.To minimize the morbidity and mortality resulting from head injury there is a need for better maintenance of roads, improvement of road visibility and lighting, proper mechanical maintenance of automobile and other vehicles, rigid enforcement of traffic rules, compulsory wearing of crash helmets by motor cyclist and scooterists and shoulder belt in cars and imparting compulsory road safety education to school children from primary education level. Moreover, appropriate medical care facilities (including trauma centres) need to be established at district level, sub-divisional and block levels to provide prompt and quality care to head injury patients.

  9. Blast-induced traumatic brain injury: a new trend of blast injury research

    Institute of Scientific and Technical Information of China (English)

    Yan Zhao; Zheng-Guo Wang

    2015-01-01

    Blast injury has become the major life-and function-threatening injuries in recent warfares.There is increased research interest in the mental disorders caused by blast-induced traumatic brain injury (bTBI),which has been proved as one of the "signature wounds" in modern battlefield.We reviewed the recent progresses in bTBl-related researches and concluded that the new era of blast injury research has shifted from the traditional physical impairments to cognitive dysfunctional/mental disorders that are proved to be more related to the outcome of combat casualty care.

  10. Brain MRI volumetry in a single patient with mild traumatic brain injury.

    Science.gov (United States)

    Ross, David E; Castelvecchi, Cody; Ochs, Alfred L

    2013-01-01

    This letter to the editor describes the case of a 42 year old man with mild traumatic brain injury and multiple neuropsychiatric symptoms which persisted for a few years after the injury. Initial CT scans and MRI scans of the brain showed no signs of atrophy. Brain volume was measured using NeuroQuant®, an FDA-approved, commercially available software method. Volumetric cross-sectional (one point in time) analysis also showed no atrophy. However, volumetric longitudinal (two points in time) analysis showed progressive atrophy in several brain regions. This case illustrated in a single patient the principle discovered in multiple previous group studies, namely that the longitudinal design is more powerful than the cross-sectional design for finding atrophy in patients with traumatic brain injury.

  11. Activation of the Notch signaling pathway promotes neurovascular repair after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Qi-shan Ran; Yun-hu Yu; Xiao-hong Fu; Yuan-chao Wen

    2015-01-01

    The Notch signaling pathway plays a key role in angiogenesis and endothelial cell formation, but it remains unclear whether it is involved in vascular repair by endothelial progenitor cells after traumatic brain injury. Therefore, in the present study, we controlled the Notch signaling path-way using overexpression and knockdown constructs. Activation of the Notch signaling pathway by Notch1 or Jagged1 overexpression enhanced the migration, invasiveness and angiogenic ability of endothelial progenitor cells. Suppression of the Notch signaling pathway with Notch1 or Jagged1 siRNAs reduced the migratory capacity, invasiveness and angiogenic ability of endo-thelial progenitor cells. Activation of the Notch signaling pathwayin vivo in a rat model of mild traumatic brain injury promoted neurovascular repair. These ifndings suggest that the activation of the Notch signaling pathway promotes blood vessel formation and tissue repair after brain trauma.

  12. Biomarkers of traumatic injury are transported from brain to blood via the glymphatic system.

    Science.gov (United States)

    Plog, Benjamin A; Dashnaw, Matthew L; Hitomi, Emi; Peng, Weiguo; Liao, Yonghong; Lou, Nanhong; Deane, Rashid; Nedergaard, Maiken

    2015-01-14

    The nonspecific and variable presentation of traumatic brain injury (TBI) has motivated an intense search for blood-based biomarkers that can objectively predict the severity of injury. However, it is not known how cytosolic proteins released from traumatized brain tissue reach the peripheral blood. Here we show in a murine TBI model that CSF movement through the recently characterized glymphatic pathway transports biomarkers to blood via the cervical lymphatics. Clinically relevant manipulation of glymphatic activity, including sleep deprivation and cisternotomy, suppressed or eliminated TBI-induced increases in serum S100β, GFAP, and neuron specific enolase. We conclude that routine TBI patient management may limit the clinical utility of blood-based biomarkers because their brain-to-blood transport depends on glymphatic activity.

  13. Neuroinflammation in animal models of traumatic brain injury

    Science.gov (United States)

    Chiu, Chong-Chi; Liao, Yi-En; Yang, Ling-Yu; Wang, Jing-Ya; Tweedie, David; Karnati, Hanuma K.; Greig, Nigel H.; Wang, Jia-Yi

    2016-01-01

    Traumatic brain injury (TBI) is a leading cause of mortality and morbidity worldwide. Neuroinflammation is prominent in the short and long-term consequences of neuronal injuries that occur after TBI. Neuroinflammation involves the activation of glia, including microglia and astrocytes, to release inflammatory mediators within the brain, and the subsequent recruitment of peripheral immune cells. Various animal models of TBI have been developed that have proved valuable to elucidate the pathophysiology of the disorder and to assess the safety and efficacy of novel therapies prior to clinical trials. These models provide an excellent platform to delineate key injury mechanisms that associate with types of injury (concussion, contusion, and penetration injuries) that occur clinically for the investigation of mild, moderate, and severe forms of TBI. Additionally, TBI modeling in genetically engineered mice, in particular, has aided the identification of key molecules and pathways for putative injury mechanisms, as targets for development of novel therapies for human TBI. This Review details the evidence showing that neuroinflammation, characterized by the activation of microglia and astrocytes and elevated production of inflammatory mediators, is a critical process occurring in various TBI animal models, provides a broad overview of commonly used animal models of TBI, and overviews representative techniques to quantify markers of the brain inflammatory process. A better understanding of neuroinflammation could open therapeutic avenues for abrogation of secondary cell death and behavioral symptoms that may mediate the progression of TBI. PMID:27382003

  14. [Scandinavian guidelines for prehospital management of severe traumatic brain injury

    DEFF Research Database (Denmark)

    Sollid, S.; Sundstrom, T.; Kock-Jensen, C.

    2008-01-01

    Head trauma is the cause the death for many young persons. The number of fatalities can be reduced through systematic management. Prevention of secondary brain injury combined with the fastest possible transport to a neurosurgical unit, have been shown to effectively reduce mortality and morbidity....... Evidence-based guidelines already exist that focus on all steps in the process. In the present article members of the Scandinavian Neurotrauma Committee present recommendations on prehospital management of traumatic brain injury adapted to the infrastructure of the Nordic region Udgivelsesdato: 2008/6/26...

  15. Early Bifrontal Brain Injury: Disturbances in Cognitive Function Development

    Directory of Open Access Journals (Sweden)

    Christine Bonnier

    2010-01-01

    Full Text Available We describe six psychomotor, language, and neuropsychological sequential developmental evaluations in a boy who sustained a severe bifrontal traumatic brain injury (TBI at 19 months of age. Visuospatial, drawing, and writing skills failed to develop normally. Gradually increasing difficulties were noted in language leading to reading and spontaneous speech difficulties. The last two evaluations showed executive deficits in inhibition, flexibility, and working memory. Those executive abnormalities seemed to be involved in the other impairments. In conclusion, early frontal brain injury disorganizes the development of cognitive functions, and interactions exist between executive function and other cognitive functions during development.

  16. EphrinB3 restricts endogenous neural stem cell migration after traumatic brain injury.

    Science.gov (United States)

    Dixon, Kirsty J; Mier, Jose; Gajavelli, Shyam; Turbic, Alisa; Bullock, Ross; Turnley, Ann M; Liebl, Daniel J

    2016-11-01

    Traumatic brain injury (TBI) leads to a series of pathological events that can have profound influences on motor, sensory and cognitive functions. Conversely, TBI can also stimulate neural stem/progenitor cell proliferation leading to increased numbers of neuroblasts migrating outside their restrictive neurogenic zone to areas of damage in support of tissue integrity. Unfortunately, the factors that regulate migration are poorly understood. Here, we examine whether ephrinB3 functions to restrict neuroblasts from migrating outside the subventricular zone (SVZ) and rostral migratory stream (RMS). We have previously shown that ephrinB3 is expressed in tissues surrounding these regions, including the overlying corpus callosum (CC), and is reduced after controlled cortical impact (CCI) injury. Our current study takes advantage of ephrinB3 knockout mice to examine the influences of ephrinB3 on neuroblast migration into CC and cortex tissues after CCI injury. Both injury and/or ephrinB3 deficiency led to increased neuroblast numbers and enhanced migration outside the SVZ/RMS zones. Application of soluble ephrinB3-Fc molecules reduced neuroblast migration into the CC after injury and limited neuroblast chain migration in cultured SVZ explants. Our findings suggest that ephrinB3 expression in tissues surrounding neurogenic regions functions to restrict neuroblast migration outside the RMS by limiting chain migration.

  17. A Simplified Workflow for Protein Quantitation of Rat Brain Tissues Using Label-Free Proteomics and Spectral Counting.

    Science.gov (United States)

    Boutté, Angela M; Grant, Shonnette F; Dave, Jitendra R

    2016-01-01

    Mass spectrometry-based proteomics is an increasingly valuable tool for determining relative or quantitative protein abundance in brain tissues. A plethora of technical and analytical methods are available, but straightforward and practical approaches are often needed to facilitate reproducibility. This aspect is particularly important as an increasing number of studies focus on models of traumatic brain injury or brain trauma, for which brain tissue proteomes have not yet been fully described. This text provides suggested techniques for robust identification and quantitation of brain proteins by using molecular weight fractionation prior to mass spectrometry-based proteomics. Detailed sample preparation and generalized protocols for chromatography, mass spectrometry, spectral counting, and normalization are described. The rat cerebral cortex isolated from a model of blast-overpressure was used as an exemplary source of brain tissue. However, these techniques may be adapted for lysates generated from several types of cells or tissues and adapted by the end user.

  18. Misconceptions on neuropsychological rehabilitation and traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Alberto García- Molina

    2013-12-01

    Full Text Available There are many misconceptions about traumatic brain injuries, their recovery and outcome; misconceptions that have their origin in a lack of information influenced by the image that the media show of the brain damage. Development. Based on clinical experience, the authors of this essay sets out his personal view on some of the most frequent misconceptions in the field of neuropsychological rehabilitation of traumatic brain injury: 1 All deficits are evident; 2 The recovery depends mainly on the involvement of the patient: more effort, more rapid recovery; 3 Two years after traumatic brain injury there is no possibility of improvement and recovery; and 4 The “miracle” of recovery will occur when is found the appropriate professional or treatment. These and other beliefs may influence directly or indirectly on the recovery process and the expectations placed on it by the families and patients. Conclusions. Provide accurate, clear and honest information, at the right time, helps patients and their families to better understand the deficits, the course of recovery and to adapt to the new reality resulting from a traumatic brain injury.

  19. Hyperbaric oxygen therapy improves cognitive functioning after brain injury

    Institute of Scientific and Technical Information of China (English)

    Su Liu; Guangyu Shen; Shukun Deng; Xiubin Wang; Qinfeng Wu; Aisong Guo

    2013-01-01

    Hyperbaric oxygen therapy has been widely applied and recognized in the treatment of brain injury;however, the correlation between the protective effect of hyperbaric oxygen therapy and changes of metabolites in the brain remains unclear. To investigate the effect and potential mechanism of hyperbaric oxygen therapy on cognitive functioning in rats, we established traumatic brain injury models using Feeney’s free fal ing method. We treated rat models with hyperbaric oxygen therapy at 0.2 MPa for 60 minutes per day. The Morris water maze test for spatial navigation showed that the average escape latency was significantly prolonged and cognitive function decreased in rats with brain injury. After treatment with hyperbaric oxygen therapy for 1 and 2 weeks, the rats’ spatial learning and memory abilities were improved. Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was sig-nificantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy. Nissl staining and immunohistochemical staining showed that the number of nerve cells and Nissl bodies in the hippocampal CA3 region was significantly increased, and glial fibril ary acidic protein positive cells were decreased after a 2-week hyperbaric oxygen therapy treatment. Our findings indicate that hyperbaric oxygen therapy significantly im-proves cognitive functioning in rats with traumatic brain injury, and the potential mechanism is me-diated by metabolic changes and nerve cellrestoration in the hippocampal CA3 region.

  20. Hyperbaric oxygen therapy improves cognitive functioning after brain injury.

    Science.gov (United States)

    Liu, Su; Shen, Guangyu; Deng, Shukun; Wang, Xiubin; Wu, Qinfeng; Guo, Aisong

    2013-12-15

    Hyperbaric oxygen therapy has been widely applied and recognized in the treatment of brain injury; however, the correlation between the protective effect of hyperbaric oxygen therapy and changes of metabolites in the brain remains unclear. To investigate the effect and potential mechanism of hyperbaric oxygen therapy on cognitive functioning in rats, we established traumatic brain injury models using Feeney's free falling method. We treated rat models with hyperbaric oxygen therapy at 0.2 MPa for 60 minutes per day. The Morris water maze test for spatial navigation showed that the average escape latency was significantly prolonged and cognitive function decreased in rats with brain injury. After treatment with hyperbaric oxygen therapy for 1 and 2 weeks, the rats' spatial learning and memory abilities were improved. Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was significantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy. Nissl staining and immunohistochemical staining showed that the number of nerve cells and Nissl bodies in the hippocampal CA3 region was significantly increased, and glial fibrillary acidic protein positive cells were decreased after a 2-week hyperbaric oxygen therapy treatment. Our findings indicate that hyperbaric oxygen therapy significantly improves cognitive functioning in rats with traumatic brain injury, and the potential mechanism is mediated by metabolic changes and nerve cell restoration in the hippocampal CA3 region.

  1. Integrin suppresses neurogenesis and regulates brain tissue assembly in planarian regeneration.

    Science.gov (United States)

    Bonar, Nicolle A; Petersen, Christian P

    2017-03-01

    Animals capable of adult regeneration require specific signaling to control injury-induced cell proliferation, specification and patterning, but comparatively little is known about how the regeneration blastema assembles differentiating cells into well-structured functional tissues. Using the planarian Schmidtea mediterranea as a model, we identify β1-integrin as a crucial regulator of blastema architecture. β1-integrin(RNAi) animals formed small head blastemas with severe tissue disorganization, including ectopic neural spheroids containing differentiated neurons normally found in distinct organs. By mimicking aspects of normal brain architecture but without normal cell-type regionalization, these spheroids bore a resemblance to mammalian tissue organoids synthesized in vitro We identified one of four planarian integrin-alpha subunits inhibition of which phenocopied these effects, suggesting that a specific receptor controls brain organization through regeneration. Neoblast stem cells and progenitor cells were mislocalized in β1-integrin(RNAi) animals without significantly altered body-wide patterning. Furthermore, tissue disorganization phenotypes were most pronounced in animals undergoing brain regeneration and not homeostatic maintenance or regeneration-induced remodeling of the brain. These results suggest that integrin signaling ensures proper progenitor recruitment after injury, enabling the generation of large-scale tissue organization within the regeneration blastema.

  2. A mouse model of human repetitive mild traumatic brain injury

    OpenAIRE

    Kane, Michael J; Pérez, Mariana Angoa; Briggs, Denise I.; Viano, David C.; Kreipke, Christian W.; Kuhn, Donald M.

    2011-01-01

    A novel method for the study of repetitive mild traumatic brain injury (rmTBI) that models the most common form of head injury in humans is presented. Existing animal models of TBI impart focal, severe damage unlike that seen in repeated and mild concussive injuries, and few are configured for repetitive application. Our model is a modification of the Marmarou weight drop method and allows repeated head impacts to lightly anesthetized mice. A key facet of this method is the delivery of an imp...

  3. Brain-computer interface after nervous system injury.

    Science.gov (United States)

    Burns, Alexis; Adeli, Hojjat; Buford, John A

    2014-12-01

    Brain-computer interface (BCI) has proven to be a useful tool for providing alternative communication and mobility to patients suffering from nervous system injury. BCI has been and will continue to be implemented into rehabilitation practices for more interactive and speedy neurological recovery. The most exciting BCI technology is evolving to provide therapeutic benefits by inducing cortical reorganization via neuronal plasticity. This article presents a state-of-the-art review of BCI technology used after nervous system injuries, specifically: amyotrophic lateral sclerosis, Parkinson's disease, spinal cord injury, stroke, and disorders of consciousness. Also presented is transcending, innovative research involving new treatment of neurological disorders.

  4. Recent Research in Behind-Armor Blunt Trauma and Traumatic Brain Injury

    Science.gov (United States)

    2014-02-01

    biomechanics that may cause injury from blast impact. Rafaels et al. (8) used animal models in their research to suggest that blast TBI may also depend on...vasculature of neck primarily proposed by Cernak et al. (20). The blast wave generated from a shock front followed by blast overpressure can have...design of new or existing equipment used to mitigate blast exposures. El Sayed et al. (42) studied the biomechanical modeling of the brain tissue

  5. Vagal stimulation modulates inflammation through a ghrelin mediated mechanism in traumatic brain injury

    OpenAIRE

    Bansal, V; Ryu, SY; Lopez, N; Allexan, S; Krzyzaniak, M; Eliceiri, B; Baird, A.; Coimbra, R

    2012-01-01

    Traumatic brain injury (TBI) releases a cascade of inflammatory cytokines. Vagal nerve stimulation (VNS) and ghrelin have known anti-inflammatory effects; furthermore, ghrelin release is stimulated by acetylcholine. We hypothesized VNS decreases post-TBI inflammation through a ghrelin-mediated mechanism. TBI was created in five groups of mice: sham, TBI, TBI/ghrelin, TBI/VNS, and TBI/VNS/ghrelin receptor antagonist (GRa). Serum and tissue ghrelin, and serum TNF-αwere measured. Ghrelin increas...

  6. Traumatic Brain Injury and Peripheral Immune Suppression: Primer and Prospectus.

    Science.gov (United States)

    Hazeldine, Jon; Lord, Janet M; Belli, Antonio

    2015-01-01

    Nosocomial infections are a common occurrence in patients following traumatic brain injury (TBI) and are associated with an increased risk of mortality, longer length of hospital stay, and poor neurological outcome. Systemic immune suppression arising as a direct result of injury to the central nervous system (CNS) is considered to be primarily responsible for this increased incidence of infection, a view strengthened by recent studies that have reported novel changes in the composition and function of the innate and adaptive arms of the immune system post-TBI. However, our knowledge of the mechanisms that underlie TBI-induced immune suppression is equivocal at best. Here, after summarizing our current understanding of the impact of TBI on peripheral immunity and discussing CNS-mediated regulation of immune function, we propose roles for a series of novel mechanisms in driving the immune suppression that is observed post-TBI. These mechanisms, which have never been considered before in the context of TBI-induced immune paresis, include the CNS-driven emergence into the circulation of myeloid-derived suppressor cells and suppressive neutrophil subsets, and the release from injured tissue of nuclear and mitochondria-derived damage associated molecular patterns. Moreover, in an effort to further our understanding of the mechanisms that underlie TBI-induced changes in immunity, we pose throughout the review a series of questions, which if answered would address a number of key issues, such as establishing whether manipulating peripheral immune function has potential as a future therapeutic strategy by which to treat and/or prevent infections in the hospitalized TBI patient.

  7. Nonlinear Dynamic Theory of Acute Cell Injuries and Brain Ischemia

    Science.gov (United States)

    Taha, Doaa; Anggraini, Fika; Degracia, Donald; Huang, Zhi-Feng

    2015-03-01

    Cerebral ischemia in the form of stroke and cardiac arrest brain damage affect over 1 million people per year in the USA alone. In spite of close to 200 clinical trials and decades of research, there are no treatments to stop post-ischemic neuron death. We have argued that a major weakness of current brain ischemia research is lack of a deductive theoretical framework of acute cell injury to guide empirical studies. A previously published autonomous model based on the concept of nonlinear dynamic network was shown to capture important facets of cell injury, linking the concept of therapeutic to bistable dynamics. Here we present an improved, non-autonomous formulation of the nonlinear dynamic model of cell injury that allows multiple acute injuries over time, thereby allowing simulations of both therapeutic treatment and preconditioning. Our results are connected to the experimental data of gene expression and proteomics of neuron cells. Importantly, this new model may be construed as a novel approach to pharmacodynamics of acute cell injury. The model makes explicit that any pro-survival therapy is always a form of sub-lethal injury. This insight is expected to widely influence treatment of acute injury conditions that have defied successful treatment to date. This work is supported by NIH NINDS (NS081347) and Wayne State University President's Research Enhancement Award.

  8. Brain hemorrhage after electrical burn injury: Case report and probable mechanism

    Science.gov (United States)

    Axayacalt, Gutierrez Aceves Guillermo; Alejandro, Ceja Espinosa; Marcos, Rios Alanis; Inocencio, Ruiz Flores Milton; Alfredo, Herrera Gonzalez Jose

    2016-01-01

    Background: High-voltage electric injury may induce lesion in different organs. In addition to the local tissue damage, electrical injuries may lead to neurological deficits, musculoskeletal damage, and cardiovascular injury. Severe vascular damage may occur making the blood vessels involved prone to thrombosis and spontaneous rupture. Case Description: Here, we present the case of a 39-year-old male who suffered an electrical burn with high tension wire causing intracranial bleeding. He presented with an electrical burn in the parietal area (entry zone) and the left forearm (exit zone). The head tomography scan revealed an intraparenchimatous bleeding in the left parietal area. In this case, the electric way was the scalp, cranial bone, blood vessels and brain, upper limb muscle, and skin. The damage was different according to the dielectric property in each tissue. The injury was in the scalp, cerebral blood vessel, skeletal muscle, and upper limb skin. The main damage was in brain’s blood vessels because of the dielectric and geometric features that lead to bleeding, high temperature, and gas delivering. Conclusion: This is a report of a patient with an electric brain injury that can be useful to elucidate the behavior of the high voltage electrical current flow into the nervous system. PMID:27904757

  9. Oligodendrogenesis after Cerebral Ischaemia and Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Zheng Gang Zhang

    2013-08-01

    Full Text Available Stroke and traumatic brain injury (TBI damage white and grey matter. Loss of oligodendrocytes and their myelin, impairs axonal function. Remyelination involves oligodendrogenesis during which new myelinating oligodendrocytes are generated by differentiated oligodendrocyte progenitor cells (OPCs. This article briefly reviews the processes of oligodendrogenesis in adult rodent brains, and promising experimental therapies targeting the neurovascular unit that reduce oligodendrocyte damage and amplify endogenous oligodendrogenesis after stroke and TBI.

  10. Death Associated Protein Kinases: Molecular Structure and Brain Injury

    OpenAIRE

    Claire Thornton; Carina Mallard; Rajanikant Krishnamurthy; Syam Nair; Henrik Hagberg

    2013-01-01

    Perinatal brain damage underlies an important share of motor and neurodevelopmental disabilities, such as cerebral palsy, cognitive impairment, visual dysfunction and epilepsy. Clinical, epidemiological, and experimental studies have revealed that factors such as inflammation, excitotoxicity and oxidative stress contribute considerably to both white and grey matter injury in the immature brain. A member of the death associated protein kinase (DAPk) family, DAPk1, has been implicated in cerebr...

  11. Melatonin treatment reduces astrogliosis and apoptosis in rats with traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Abdolreza Babaee

    2015-09-01

    Full Text Available Objective(s:Melatonin is known as an anti-inflammatory agent, and it has been proven to exert neuroprotection through inhibition of cell death (apoptosis in several models of brain injury.Secondary injury following the primary traumatic brain injury (TBI results in glial cells activation, especially astrocytes. In fact, astrocyte activation causes the production of pro-inflammatory cytokines that may lead to secondary injury. Since most TBI research studies have focused on injured neurons and paid little attention to glial cells, the aim of current study was to investigate the effects of melatonin against astrocytes activation (astrogliosis, as well as inhibition of apoptosis in brain tissue of male rats after TBI. Materials and Methods: The animals were randomly allocated into five groups: sham group, TBI+ vehicle group (1% ethanol in saline and TBI+ melatonin groups (5 mg/kg, 10 mg/kg and 20 mg/kg. All rats were intubated and then exposed to diffuse TBI, except for the sham group. Immunohistochemical methods were conducted using glial fibrillary acidic protein (GFAP marker and TUNEL assay to evaluate astrocyte reactivity and cell death, respectively. Results: The results showed that based on the number of GFAP positive astrocytes in brain cortex, astrogliosis was reduced significantly (P

  12. What Can I Do to Help Feel Better After a Mild Traumatic Brain Injury?

    Science.gov (United States)

    ... to Help Feel Better After a Mild Traumatic Brain Injury? Although most people recover after a concussion, how ... Potential Effects Prevention Severe TBI HEADS UP to Brain Injury Awareness Get Email Updates To receive email updates ...

  13. Potential risk factors for developing heterotopic ossification in patients with severe traumatic brain injury

    NARCIS (Netherlands)

    Kampen, P.J. van; Martina, J.D.; Vos, P.E.; Hoedemaekers, C.W.E.; Hendricks, H.T.

    2011-01-01

    BACKGROUND: Heterotopic ossification (HO) is a frequent complication after traumatic brain injury (TBI). The current preliminary study is intended to provide additional data on the potential roles that brain injury severity, concomitant orthopaedic trauma, and specific intensive care complicating ev

  14. Abnormal whole-brain functional networks in homogeneous acute mild traumatic brain injury.

    NARCIS (Netherlands)

    Shumskaya, E.; Andriessen, T.; Norris, D.G.; Vos, P.E.

    2012-01-01

    Objectives: To evaluate the whole-brain resting-state networks in a homogeneous group of patients with acute mild traumatic brain injury (MTBI) and to identify alterations in functional connectivity induced by MTBI. Methods: Thirty-five patients with acute MTBI and 35 healthy control subjects, mat

  15. MRI-DTI Tractography to Quantify Brain Connectivity in Traumatic Brain Injury

    Science.gov (United States)

    2009-04-01

    to Traumatic Brain Injury and Alzheimer Disease ”, 5-th International Annual Symposium of the Brain Mapping and Intraoperative Surgical Planning... Alzheimer Disease , Proc Intl Soc Mag Reson Med 15: 343, 2007. 9. Singh M and Jeong J-W, “ICA based multi-fiber tractography” Proceedings, 17-th

  16. Abnormal whole-brain functional networks in homogeneous acute mild traumatic brain injury.

    NARCIS (Netherlands)

    Shumskaya, A.N.; Andriessen, T.M.J.C.; Norris, D.G.; Vos, P.E.

    2012-01-01

    OBJECTIVES: To evaluate the whole-brain resting-state networks in a homogeneous group of patients with acute mild traumatic brain injury (MTBI) and to identify alterations in functional connectivity induced by MTBI. METHODS: Thirty-five patients with acute MTBI and 35 healthy control subjects, match

  17. Brain network dysregulation, emotion, and complaints after mild traumatic brain injury

    NARCIS (Netherlands)

    van der Horn, Harm J.; Liemburg, Edith J.; Scheenen, Myrthe E.; de Koning, Myrthe E.; Marsman, Jan-Bernard C.; Spikman, Jacoba M.; van der Naalt, Joukje

    2016-01-01

    ObjectivesTo assess the role of brain networks in emotion regulation and post-traumatic complaints in the sub-acute phase after non-complicated mild traumatic brain injury (mTBI). Experimental designFifty-four patients with mTBI (34 with and 20 without complaints) and 20 healthy controls (group-matc

  18. NINDS Traumatic Brain Injury Information Page

    Science.gov (United States)

    ... occupational therapy, speech/language therapy, physiatry (physical medicine), psychology/psychiatry, and social ... brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and ...

  19. Implementation of magnetic resonance elastography for the investigation of traumatic brain injuries

    Science.gov (United States)

    Boulet, Thomas

    Magnetic resonance elastography (MRE) is a potentially transformative imaging modality allowing local and non-invasive measurement of biological tissue mechanical properties. It uses a specific phase contrast MR pulse sequence to measure induced vibratory motion in soft material, from which material properties can be estimated. Compared to other imaging techniques, MRE is able to detect tissue pathology at early stages by quantifying the changes in tissue stiffness associated with diseases. In an effort to develop the technique and improve its capabilities, two inversion algorithms were written to evaluate viscoelastic properties from the measured displacements fields. The first one was based on a direct algebraic inversion of the differential equation of motion, which decouples under certain simplifying assumptions, and featured a spatio-temporal multi-directional filter. The second one relies on a finite element discretization of the governing equations to perform a direct inversion. Several applications of this technique have also been investigated, including the estimation of mechanical parameters in various gel phantoms and polymers, as well as the use of MRE as a diagnostic tools for brain disorders. In this respect, the particular interest was to investigate traumatic brain injury (TBI), a complex and diverse injury affecting 1.7 million Americans annually. The sensitivity of MRE to TBI was first assessed on excised rat brains subjected to a controlled cortical impact (CCI) injury, before execution of in vivo experiments in mice. MRE was also applied in vivo on mouse models of medulloblastoma tumors and multiple sclerosis. These studies showed the potential of MRE in mapping the brain mechanically and providing non-invasive in vivo imaging markers for neuropathology and pathogenesis of brain diseases. Furthermore, MRE can easily be translatable to clinical settings; thus, while this technique may not be used directly to diagnose different abnormalities in

  20. Glucocorticoids aggravate retrograde memory deficiency associated with traumatic brain injury in rats.

    Science.gov (United States)

    Chen, Xin; Zhang, Ke-Li; Yang, Shu-Yuan; Dong, Jing-Fei; Zhang, Jian-Ning

    2009-02-11

    Administration of glucocorticoid to patients with head injury has previously been demonstrated to impair memory. We hypothesize that glucocorticoids promote post-traumatic hippocampal apoptosis, resulting in retrograde memory deficiency associated with traumatic brain injury (TBI). In the present study, we tested this hypothesis by measuring spatial memory deficiency in rats subjected to fluid percussion injury (FPI) and receiving dexamethasone (DXM at 0.5-10 mg/kg) or methylprednisolone (MP at 5-30 mg/kg); we also examined neuronal apoptosis in hippocampus. Adult male Wistar rats were trained for the acquisition of spatial memory, then subjected to FPI and tested for spatial reference memory on post-injury days 7 and 14 using the Morris Water Maze. Brain tissue from injured rats was examined 24 h to 2 weeks after injury. The percent time in the goal quadrant, which measures spatial reference memory, was significantly lower in injured rats receiving either high-dose DXM or MP than in control groups. TUNEL-positive cells in hippocampus were first detected 24 h post-injury, plateauing at 48h. The number of TUNEL-positive cells was significantly higher in injured rats treated with either DXM or MP. The data suggest that glucocorticoid therapy for TBI may increase neuronal apoptosis in hippocampus and, as a result, aggravate retrograde memory deficits induced by TBI.

  1. Pathophysiology Associated with Traumatic Brain Injury: Current Treatments and Potential Novel Therapeutics.

    Science.gov (United States)

    Pearn, Matthew L; Niesman, Ingrid R; Egawa, Junji; Sawada, Atsushi; Almenar-Queralt, Angels; Shah, Sameer B; Duckworth, Josh L; Head, Brian P

    2016-07-06

    Traumatic brain injury (TBI) is one of the leading causes of death of young people in the developed world. In the United States alone, 1.7 million traumatic events occur annually accounting for 50,000 deaths. The etiology of TBI includes traffic accidents, falls, gunshot wounds, sports, and combat-related events. TBI severity ranges from mild to severe. TBI can induce subtle changes in molecular signaling, alterations in cellular structure and function, and/or primary tissue injury, such as contusion, hemorrhage, and diffuse axonal injury. TBI results in blood-brain barrier (BBB) damage and leakage, which allows for increased extravasation of immune cells (i.e., increased neuroinflammation). BBB dysfunction and impaired homeostasis contribute to secondary injury that occurs from hours to days to months after the initial trauma. This delayed nature of the secondary injury suggests a potential therapeutic window. The focus of this article is on the (1) pathophysiology of TBI and (2) potential therapies that include biologics (stem cells, gene therapy, peptides), pharmacological (anti-inflammatory, antiepileptic, progrowth), and noninvasive (exercise, transcranial magnetic stimulation). In final, the review briefly discusses membrane/lipid rafts (MLR) and the MLR-associated protein caveolin (Cav). Interventions that increase Cav-1, MLR formation, and MLR recruitment of growth-promoting signaling components may augment the efficacy of pharmacologic agents or already existing endogenous neurotransmitters and neurotrophins that converge upon progrowth signaling cascades resulting in improved neuronal function after injury.

  2. Timing of long bone fracture fixation in severe traumatic brain injury.

    Science.gov (United States)

    Jamjoom, Bakur A; Jamjoom, Abdulhakim B

    2012-04-01

    We present a review of the published evidence on the optimal timing for long bone fracture fixation in severe traumatic brain injury (TBI); a matter that remains under debate. Fifteen retrospective articles (level II-3 evidence) were considered suitable for the review. We conclude that the published evidence does not provide a definitive answer to the optimal timing of long bone fracture surgery in severe TBI, and a randomized controlled trial is required. We recommend a safe strategy that combines damage control surgery with a period of monitoring of intracranial pressure, cerebral perfusion pressure, and if available brain tissue oxygen until the patient is considered fit for the fracture fixation.

  3. Crash Simulator: Brain-and-Spine Injury Mechanics

    Science.gov (United States)

    Ivancevic, Vladimir G.; Reid, Darryn J.

    2015-11-01

    Recently, the first author has proposed a new coupled loading-rate hypothesis as a unique cause of both brain and spinal injuries, which states that they are both caused by a Euclidean jolt, an impulsive loading that strikes head and spine (or, any other part of the human body)- in several coupled degrees-of-freedom simultaneously. Injury never happens in a single direction only, nor is it ever caused by a static force. It is always an impulsive translational plus rotational force. The Euclidean jolt causes two basic forms of brain, spine and other musculo-skeletal injuries: (i) localized translational dislocations; and (ii) localized rotational disclinations. In the present Chapter, we first review this unique mechanics of a general human mechanical injury, and then describe how it can be predicted and controlled by a crash simulator toolbox. This rigorous Matlab toolbox has been developed using an existing thirdparty toolbox DiffMan, for accurately solving differential equations on smooth manifolds and mechanical Lie groups. The present crash simulator toolbox performs prediction/control of brain and spinal injuries within the framework of the Euclidean group SE(3) of rigid motions in our natural 3-dimensional space.

  4. Human plasma DNP level after severe brain injury

    Institute of Scientific and Technical Information of China (English)

    GAO Yi-lu; XIN Hui-ning; FENG Yi; FAN Ji-wei

    2006-01-01

    Objective: To determine the relationship between DNP level after human severe brain injury and hyponatremia as well as isorrhea.Methods: The peripheral venous plasma as control was collected from 8 volunteers. The peripheral venous plasma from 14 severe brain injury patients were collected in the 1, 3, 7 days after injury. Radioimmunoassay was used to detect the DNP concentration. Meanwhile, daily plasma and urine electrolytes, osmotic pressure as well as 24 h liquid intake and output volume were detected.Results: The normal adult human plasma DNP level was 62. 46 pg/ml ± 27. 56 pg/ml. In the experimental group, the plasma DNP levels were higher from day 1 today 3 in 8 of the 14 patients than those in the control group (P1 =0.05, P3 =0.03). Negative fluid balance occurred in 8 patients and hyponatremia in 7 patients. The increase of plasma DNP level was significantly correlated with the development of a negative fluid balance (r=-0.69,P<0.01) and hyponatremia (x2 =4.38, P<0.05).Conclusions: The increase of plasma DNP level is accompanied by the enhancement of natriuretic and diuretic responses in severe brain-injured patients, which is associated with the development of a negative fluid balance and hyponatremia after brain injury.

  5. Assessment of Cerebral Hemodynamics in Traumatic Brain Injury

    Science.gov (United States)

    2006-11-01

    haemorrhage, and 6 with subarach- noid hemorrhage from ruptured aneurysm . There were 4 cases of cerebral contusions and a single case of traumatic...B. Goldstein, 2003: Significance of Intracranial Pressure Pulse Morphology in Pediatric Traumatic Brain Injury. IEEE, 2491-2494. Anile, C., H. D

  6. Intervention Strategies for Serving Students with Traumatic Brain Injury

    Science.gov (United States)

    Arroyos-Jurado, Elsa; Savage, Todd A.

    2008-01-01

    As school-age children are at the highest risk for sustaining a traumatic brain injury (TBI), educational professionals working in school settings will encounter students dealing with the after-effects of a TBI. These effects can influence students' ability to navigate the behavioral, social, and academic demands of the classroom. This article…

  7. Evaluation of a Health Education Programme about Traumatic Brain Injury

    Science.gov (United States)

    Garcia, Jane Mertz; Sellers, Debra M.; Hilgendorf, Amy E.; Burnett, Debra L.

    2014-01-01

    Objective: Our aim was to evaluate a health education programme (TBIoptions: Promoting Knowledge) designed to increase public awareness and understanding about traumatic brain injury (TBI) through in-person (classroom) and computer-based (electronic) learning environments. Design: We used a pre-post survey design with randomization of participants…

  8. [Neuroendocrine dysfunctions and their consequences following traumatic brain injury].

    Science.gov (United States)

    Czirják, Sándor; Rácz, Károly; Góth, Miklós

    2012-06-17

    Posttraumatic hypopituitarism is of major public health importance because it is more prevalent than previously thought. The prevalence of hypopituitarism in children with traumatic brain injury is unknown. Most cases of posttraumatic hypopituitarism remain undiagnosed and untreated in the clinical practice, and it may contribute to the severe morbidity seen in patients with traumatic brain injury. In the acute phase of brain injury, the diagnosis of adrenal insufficiency should not be missed. Determination of morning serum cortisol concentration is mandatory, because adrenal insufficiency can be life threatening. Morning serum cortisol lower than 200 nmol/L strongly suggests adrenal insufficiency. A complete hormonal investigation should be performed after one year of the trauma. Isolated growth hormone deficiency is the most common deficiency after traumatic brain injury. Sports-related chronic repetitive head trauma (because of boxing, kickboxing, football and ice hockey) may also result in hypopituitarism. Close co-operation between neurosurgeons, endocrinologists, rehabilitation physicians and representatives of other disciplines is important to provide better care for these patients.

  9. Clinimetrics and functional outcome one year after traumatic brain injury

    NARCIS (Netherlands)

    J.T.M. van Baalen (Bianca)

    2008-01-01

    textabstractThis thesis is based on the findings of the FuPro-TBI (Functional Prognosis in Traumatic Brain Injury) study, which was part of the national FuPro research programme which investigated the functional prognosis of four neurological disorders: multiple sclerosis (MS), stroke, amyotrofic l

  10. Death Associated Protein Kinases: Molecular Structure and Brain Injury

    Directory of Open Access Journals (Sweden)

    Claire Thornton

    2013-07-01

    Full Text Available Perinatal brain damage underlies an important share of motor and neurodevelopmental disabilities, such as cerebral palsy, cognitive impairment, visual dysfunction and epilepsy. Clinical, epidemiological, and experimental studies have revealed that factors such as inflammation, excitotoxicity and oxidative stress contribute considerably to both white and grey matter injury in the immature brain. A member of the death associated protein kinase (DAPk family, DAPk1, has been implicated in cerebral ischemic damage, whereby DAPk1 potentiates NMDA receptor-mediated excitotoxicity through interaction with the NR2BR subunit. DAPk1 also mediate a range of activities from autophagy, membrane blebbing and DNA fragmentation ultimately leading to cell death. DAPk mRNA levels are particularly highly expressed in the developing brain and thus, we hypothesize that DAPk1 may play a role in perinatal brain injury. In addition to reviewing current knowledge, we present new aspects of the molecular structure of DAPk domains, and relate these findings to interacting partners of DAPk1, DAPk-regulation in NMDA-induced cerebral injury and novel approaches to blocking the injurious effects of DAPk1.

  11. School-Based Traumatic Brain Injury and Concussion Management Program

    Science.gov (United States)

    Davies, Susan C.

    2016-01-01

    Traumatic brain injuries (TBIs), including concussions, can result in a constellation of physical, cognitive, emotional, and behavioral symptoms that affect students' well-being and performance at school. Despite these effects, school personnel remain underprepared identify, educate, and assist this population of students. This article describes a…

  12. Classroom Interventions for Students with Traumatic Brain Injuries

    Science.gov (United States)

    Bowen, Julie M.

    2005-01-01

    Students who have sustained a traumatic brain injury (TBI) return to the school setting with a range of cognitive, psychosocial, and physical deficits that can significantly affect their academic functioning. Successful educational reintegration for students with TBI requires careful assessment of each child's unique needs and abilities and the…

  13. Assisting Students with a Traumatic Brain Injury in School Interventions

    Science.gov (United States)

    Aldrich, Erin M.; Obrzut, John E.

    2012-01-01

    Traumatic brain injury (TBI) in children and adolescents can significantly affect their lives and educational needs. Deficits are often exhibited in areas such as attention, concentration, memory, executive function, emotional regulation, and behavioral functioning, but specific outcomes are not particular to any one child or adolescent with a…

  14. Decompressive Craniectomy and Traumatic Brain Injury: A Review

    Science.gov (United States)

    Alvis-Miranda, Hernando; Castellar-Leones, Sandra Milena; Moscote-Salazar, Luis Rafael

    2013-01-01

    Intracranial hypertension is the largest cause of death in young patients with severe traumatic brain injury. Decompressive craniectomy is part of the second level measures for the management of increased intracranial pressure refractory to medical management as moderate hypothermia and barbiturate coma. The literature lack of concepts is their indications. We present a review on the state of the art. PMID:27162826

  15. Death associated protein kinases: molecular structure and brain injury.

    Science.gov (United States)

    Nair, Syam; Hagberg, Henrik; Krishnamurthy, Rajanikant; Thornton, Claire; Mallard, Carina

    2013-07-04

    Perinatal brain damage underlies an important share of motor and neurodevelopmental disabilities, such as cerebral palsy, cognitive impairment, visual dysfunction and epilepsy. Clinical, epidemiological, and experimental studies have revealed that factors such as inflammation, excitotoxicity and oxidative stress contribute considerably to both white and grey matter injury in the immature brain. A member of the death associated protein kinase (DAPk) family, DAPk1, has been implicated in cerebral ischemic damage, whereby DAPk1 potentiates NMDA receptor-mediated excitotoxicity through interaction with the NR2BR subunit. DAPk1 also mediate a range of activities from autophagy, membrane blebbing and DNA fragmentation ultimately leading to cell death. DAPk mRNA levels are particularly highly expressed in the developing brain and thus, we hypothesize that DAPk1 may play a role in perinatal brain injury. In addition to reviewing current knowledge, we present new aspects of the molecular structure of DAPk domains, and relate these findings to interacting partners of DAPk1, DAPk-regulation in NMDA-induced cerebral injury and novel approaches to blocking the injurious effects of DAPk1.

  16. Hypofibrinogenemia in isolated traumatic brain injury in Indian patients

    Directory of Open Access Journals (Sweden)

    Chhabra Gaurav

    2010-12-01

    Full Text Available Coagulation abnormalities are common in patients with head injuries. However, the effect of brain injury on fibrinogen levels has not been well studied prospectively to assess coagulation abnormalities in patients with moderate and severe head injuries and correlate these abnormalities with the neurologic outcome. Consecutive patients with moderate (Glasgow Comma Scale (GCS,9-12 and severe (GCS≤8 head injuries were the subjects of this pilot study, All patients had coagulation parameters, including plasma fibrinogen levels measured. Clinical and computed tomography (CT scan findings and immediate clinical outcome were analyzed. Of the 100 patients enrolled, only seven (7% patients had hypofibrinogenemia (fibrinogen ≤200 mg/dL. The head injury was moderate in two patients and severe in five patients. Fibrinogen levels showed a progressively increasing trend in four patients (three with severe head injuries and one with moderate head injury. CT scan revealed subdural hematoma in five patients; extradural hematoma in one; and subarachnoid hemorrhage in another patient. Of the seven patients, two patients died during hospital. Large-scale prospective studies are needed to assess the fibrinogen level in patients with head injury and its impact on outcome.

  17. Suicide after traumatic brain injury: a population study

    DEFF Research Database (Denmark)

    Teasdale, T W; Engberg, A W

    2001-01-01

    OBJECTIVES: To determine the rates of suicide among patients who have had a traumatic brain injury. METHODS: From a Danish population register of admissions to hospital covering the years 1979-93 patients were selected who had had either a concussion (n=126 114), a cranial fracture (n=7560......), or a cerebral contusion or traumatic intracranial haemorrhage (n=11 766). All cases of deaths by the end of the study period were identified. RESULTS: In the three diagnostic groups there had been 750 (0.59%), 46 (0.61%), and 99 (0.84%) cases of suicide respectively. Standardised mortality ratios, stratified......). There was, however, no evidence of a specific risk period for suicide after injury. CONCLUSION: The increased risk of suicide among patients who had a mild traumatic brain injury may result from concomitant risk factors such as psychiatric conditions and psychosocial disadvantage. The greater risk among...

  18. Neuropathology of mild traumatic brain injury: relationship to neuroimaging findings.

    Science.gov (United States)

    Bigler, Erin D; Maxwell, William L

    2012-06-01

    Neuroimaging identified abnormalities associated with traumatic brain injury (TBI) are but gross indicators that reflect underlying trauma-induced neuropathology at the cellular level. This review examines how cellular pathology relates to neuroimaging findings with the objective of more closely relating how neuroimaging findings reveal underlying neuropathology. Throughout this review an attempt will be made to relate what is directly known from post-mortem microscopic and gross anatomical studies of TBI of all severity levels to the types of lesions and abnormalities observed in contemporary neuroimaging of TBI, with an emphasis on mild traumatic brain injury (mTBI). However, it is impossible to discuss the neuropathology of mTBI without discussing what occurs with more severe injury and viewing pathological changes on some continuum from the mildest to the most severe. Historical milestones in understanding the neuropathology of mTBI are reviewed along with implications for future directions in the examination of neuroimaging and neuropathological correlates of TBI.

  19. Past, Present, and Future of Traumatic Brain Injury Research.

    Science.gov (United States)

    Hawryluk, Gregory W J; Bullock, M Ross

    2016-10-01

    Traumatic brain injury (TBI) is the greatest cause of death and severe disability in young adults; its incidence is increasing in the elderly and in the developing world. Outcome from severe TBI has improved dramatically as a result of advancements in trauma systems and supportive critical care, however we remain without a therapeutic which acts directly to attenuate brain injury. Recognition of secondary injury and its molecular mediators has raised hopes for such targeted treatments. Unfortunately, over 30 late-phase clinical trials investigating promising agents have failed to translate a therapeutic for clinical use. Numerous explanations for this failure have been postulated and are reviewed here. With this historical context we review ongoing research and anticipated future trends which are armed with lessons from past trials, new scientific advances, as well as improved research infrastructure and funding. There is great hope that these new efforts will finally lead to an effective therapeutic for TBI as well as better clinical management strategies.

  20. 78 FR 9929 - Current Traumatic Brain Injury State Implementation Partnership Grantees; Non-Competitive One...

    Science.gov (United States)

    2013-02-12

    ...-Competitive One-Year Extension Funds for Current Traumatic Brain Injury (TBI) State Implementation Partnership... Traumatic Brain Injury Act of 2008 (Pub. L. 110- 206). Under this authority, the HRSA TBI Program is charged... HUMAN SERVICES Health Resources and Services Administration Current Traumatic Brain Injury......

  1. Postdeployment Symptom Changes and Traumatic Brain Injury and/or Posttraumatic Stress Disorder in Men

    Science.gov (United States)

    2012-01-01

    traumatic brain injury ( TBI ) and posttraumatic stress disorder...stress disorder, TBI = traumatic brain injury . *Address all correspondence to Hilary J. Aralis, MS; Naval Health Research Center, Warfighter...both diagnoses. See Figure 1 for sampling details. Figure 1. Flow diagram outlining selection of final blast traumatic brain injury ( TBI ) and no TBI

  2. Triple Peripheral Nerve Injury Accompanying to Traumatic Brain Injury: A Case Report

    Directory of Open Access Journals (Sweden)

    Ižlknur Can

    2014-02-01

    Full Text Available Secondary injuries especially extremity fractures may be seen concurrently with traumatic brain injury (TBI. Peripheral nerve damages may accompany to these fractures and may be missed out, especially in acute stage. In this case report; damage of radial, ulnar and median nerves which was developed secondarily to distal humerus fracture that could not be detected in acute stage, in a patient who had motor vehicle accident (MVA. 29-year-old male patient was admitted with weakness in the right upper extremity. 9 months ago, he had traumatic brain injury because of MVA, and fracture of distal humerus was detected in follow-ups. Upon the suspect of the peripheral nerve injury, the diagnosis was confirmed with ENMG. The patient responded well to the rehabilitation program treatment. In a TBI patient, it must be kept in mind that there might be a secondary trauma and therefore peripheral nerve lesions may accompany to TBI.

  3. OCT-based in vivo tissue injury mapping

    Science.gov (United States)

    Baran, Utku; Li, Yuandong; Wang, Ruikang K.

    2016-03-01

    Tissue injury mapping (TIM) is developed by using a non-invasive in vivo optical coherence tomography to generate optical attenuation coefficient and microvascular map of the injured tissue. Using TIM, the infarct region development in mouse cerebral cortex during stroke is visualized. Moreover, we demonstrate the in vivo human facial skin structure and microvasculature during an acne lesion development. The results indicate that TIM may help in the study and the treatment of various diseases by providing high resolution images of tissue structural and microvascular changes.

  4. Penetrating Brain Injury after Suicide Attempt with Speargun

    Directory of Open Access Journals (Sweden)

    John Ross Williams

    2014-07-01

    Full Text Available Penetrating cranial injury by mechanisms other than are exceedingly rare, and so strategies and guidelines for the management of PBI are largely informed by data from higher-velocity penetrating injuries. Here we present a case of penetrating brain injury by the low velocity mechanism of a harpoon from an underwater fishing speargun in an attempted suicide by a 56-year-old Caucasian male. The case raised a number of interesting points in management of lower-velocity penetrating brain injury (LVPBI, including benefit in delaying foreign body removal to allow for tamponade; the importance of history taking in establishing the social/legal significance of the events surrounding the injury; the use of cerebral angiogram in all cases of PBI; advantages of using DECT to reduce artifact when available; and antibiotic prophylaxis in the context of idiosyncratic histories of usage of penetrating objects before coming in contact with the intracranial environment. We present here the management of the case in full along with an extended discussion and review of existing literature regarding key points in management of LVPBI vs. higher velocity forms of intracranial injury.

  5. [Pathogenic variants of brain injuries and pharmalogic cerebroprotection performed on the model of brain condition during cardiovascular bypass surgery].

    Science.gov (United States)

    Tsygan, N V; Trashkov, A P

    2014-10-01

    Developed and approved a pathogenic grounded experimental model of brain condition during cardiovascular bypass surgery. Undertaken in Wistar rats research allowed to evaluate in detail effectiveness and safety of protracted cerebroprotective treatment. Advantages of this model are researches in laboratory animals with the aim to research condition of nerve tissue, not intensive procedures and consequently high reproducibility and possibility of complex evaluation of changes at every stage of research. Results of neurons, neuroglia and activation of neurotrophic mechanisms prove that simulation of brain condition during cardiovascular bypass surgery is accompanied with acute and delayed brain injuries. Use of Cytoflavin under pharmalogic cerebroprotection had prolonged multimodal and neuroprotactive effect, leading to improvement of neurotrophic protection from the first days.

  6. Early CT signs of progressive hemorrhagic injury following acute traumatic brain injury

    Energy Technology Data Exchange (ETDEWEB)

    Tong, Wu-song; Zheng, Ping; Xu, Jun-fa; Guo, Yi-jun; Zeng, Jing-song; Yang, Wen-jin; Li, Gao-yi; He, Bin; Yu, Hui [Pudong New Area People' s Hospital, Department of Neurosurgery, Shanghai (China)

    2011-05-15

    Since progressive hemorrhagic injury (PHI) was introduced in neurosurgical literatures, several studies have been performed, the results of which have influenced doctors but do not define guidelines for the best treatment of PHI. PHI may be confirmed by a serial computerized tomography (CT) scan, and it has been shown to be associated with a fivefold increase in the risk of clinical worsening and is a significant cause of morbidity and mortality as well. So, early detection of PHI is practically important in a clinical situation. To analyze the early CT signs of progressive hemorrhagic injury following acute traumatic brain injury (TBI) and explore their clinical significances, PHI was confirmed by comparing the first and repeated CT scans. Data were analyzed and compared including times from injury to the first CT and signs of the early CT scan. Logistic regression analysis was used to show the risk factors related to PHI. A cohort of 630 TBI patients was evaluated, and there were 189 (30%) patients who suffered from PHI. For patients with their first CT scan obtained as early as 2 h post-injury, there were 116 (77.25%) cases who suffered from PHI. The differences between PHIs and non-PHIs were significant in the initial CT scans showing fracture, subarachnoid hemorrhage (SAH), brain contusion, epidural hematoma (EDH), subdural hematoma (SDH), and multiple hematoma as well as the times from injury to the first CT scan (P < 0.01). Logistic regression analysis showed that early CT scans (EDH, SDH, SAH, fracture, and brain contusion) were predictors of PHI (P < 0.01). For patients with the first CT scan obtained as early as 2 h post-injury, a follow-up CT scan should be performed promptly. If the initial CT scan shows SAH, brain contusion, and primary hematoma with brain swelling, an earlier and dynamic CT scan should be performed for detection of PHI as early as possible and the medical intervention would be enforced in time. (orig.)

  7. Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats

    Directory of Open Access Journals (Sweden)

    Huang Yen

    2011-09-01

    Full Text Available Abstract Background Perinatal brain injury is the leading cause of subsequent neurological disability in both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy (HIE. Glutamate transporter GLT1, expressed mainly in mature astrocytes, is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE. Methods We used a neonatal rat model of HIE by unilateral ligation of carotid artery and subsequent exposure to 8% oxygen for 2 hrs on postnatal day 7 (P7 rats. Neonatal rats were administered three dosages of an antibiotic, ceftriaxone, 48 hrs prior to experimental HIE. Neurobehavioral tests of treated rats were assessed. Brain sections from P14 rats were examined with Nissl and immunohistochemical stain, and TUNEL assay. GLT1 protein expression was evaluated by Western blot and immunohistochemistry. Results Pre-treatment with 200 mg/kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus, restored myelination in the external capsule of P14 rats, and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. Conclusion These results suggest that pre-treatment of infants at risk for HIE with ceftriaxone may reduce subsequent brain injury.

  8. Lateral fluid percussion injury of the brain induces CCL20 inflammatory chemokine expression in rats

    Directory of Open Access Journals (Sweden)

    Das Mahasweta

    2011-10-01

    Full Text Available Abstract Background Traumatic brain injury (TBI evokes a systemic immune response including leukocyte migration into the brain and release of pro-inflammatory cytokines; however, the mechanisms underlying TBI pathogenesis and protection are poorly understood. Due to the high incidence of head trauma in the sports field, battlefield and automobile accidents identification of the molecular signals involved in TBI progression is critical for the development of novel therapeutics. Methods In this report, we used a rat lateral fluid percussion impact (LFPI model of TBI to characterize neurodegeneration, apoptosis and alterations in pro-inflammatory mediators at two time points within the secondary injury phase. Brain histopathology was evaluated by fluoro-jade (FJ staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL assay, polymerase chain reaction (qRT PCR, enzyme linked immunosorbent assay (ELISA and immunohistochemistry were employed to evaluate the CCL20 gene expression in different tissues. Results Histological analysis of neurodegeneration by FJ staining showed mild injury in the cerebral cortex, hippocampus and thalamus. TUNEL staining confirmed the presence of apoptotic cells and CD11b+ microglia indicated initiation of an inflammatory reaction leading to secondary damage in these areas. Analysis of spleen mRNA by PCR microarray of an inflammation panel led to the identification of CCL20 as an important pro-inflammatory signal upregulated 24 h after TBI. Although, CCL20 expression was observed in spleen and thymus after 24h of TBI, it was not expressed in degenerating cortex or hippocampal neurons until 48 h after insult. Splenectomy partially but significantly decreased the CCL20 expression in brain tissues. Conclusion These results demonstrate that the systemic inflammatory reaction to TBI starts earlier than the local brain response and suggest that spleen- and/ or thymus-derived CCL20 might play a role in

  9. Traumatic brain injury Nature and genetic influences

    Institute of Scientific and Technical Information of China (English)

    Yong Jiang; Xiaochuan Sun

    2008-01-01

    At present,much evidence indicates that TBI is similar in pathology and severity during the acute stage,yet may result in varied outcomes.Known prognostic factors,such as age and severity of injury and treatments,only partially explain this variability.In addition,it has been demonstrated that genetic polymorphisms may play an important role in TBI susceptibility,as well as outcome following TBI.

  10. Extracorporeal shock wave therapy for painful chronic neurogenic heterotopic ossification after traumatic brain injury: a case report.

    Science.gov (United States)

    Choi, Yong Min; Hong, Seok Hyun; Lee, Chang Hyun; Kang, Jin Ho; Oh, Ju Sun

    2015-04-01

    Neurogenic heterotopic ossification (NHO) is a process of benign bone formation and growth in soft tissues surrounding major synovial joints and is associated with central nervous system (CNS) injuries. It is a common complication in major CNS injuries, such as traumatic brain injury, spinal cord injury, and stroke. Here, we report the case of a 72-year-old male, who experienced a traumatic brain injury and painful chronic NHO around the left hip joint. Three applications of extracorporeal shock wave therapy (ESWT) were administered to the area of NHO, which resulted in pain relief and an improvement in the loss of motion in the left hip joint. Improvements were also noted in walking performance and activities of daily living, although the size of NHO remained unchanged. Therapeutic effects of ESWT lasted for 12 weeks.

  11. S-Nitrosoglutathione reduces oxidative injury and promotes mechanisms of neurorepair following traumatic brain injury in rats

    Directory of Open Access Journals (Sweden)

    Gilg Anne G

    2011-07-01

    Full Text Available Abstract Background Traumatic brain injury (TBI induces primary and secondary damage in both the endothelium and the brain parenchyma, collectively termed the neurovascular unit. While neurons die quickly by necrosis, a vicious cycle of secondary injury in endothelial cells exacerbates the initial injury in the neurovascular unit following TBI. In activated endothelial cells, excessive superoxide reacts with nitric oxide (NO to form peroxynitrite. Peroxynitrite has been implicated in blood brain barrier (BBB leakage, altered metabolic function, and neurobehavioral impairment. S-nitrosoglutathione (GSNO, a nitrosylation-based signaling molecule, was reported not only to reduce brain levels of peroxynitrite and oxidative metabolites but also to improve neurological function in TBI, stroke, and spinal cord injury. Therefore, we investigated whether GSNO promotes the neurorepair process by reducing the levels of peroxynitrite and the degree of oxidative injury. Methods TBI was induced by controlled cortical impact (CCI in adult male rats. GSNO or 3-Morpholino-sydnonimine (SIN-1 (50 μg/kg body weight was administered orally two hours following CCI. The same dose was repeated daily until endpoints. GSNO-treated (GSNO group or SIN-1-treated (SIN-1 group injured animals were compared with vehicle-treated injured animals (TBI group and vehicle-treated sham-operated animals (Sham group in terms of peroxynitrite, NO, glutathione (GSH, lipid peroxidation, blood brain barrier (BBB leakage, edema, inflammation, tissue structure, axon/myelin integrity, and neurotrophic factors. Results SIN-1 treatment of TBI increased whereas GSNO treatment decreased peroxynitrite, lipid peroxides/aldehydes, BBB leakage, inflammation and edema in a short-term treatment (4-48 hours. GSNO also reduced brain infarctions and enhanced the levels of NO and GSH. In a long-term treatment (14 days, GSNO protected axonal integrity, maintained myelin levels, promoted synaptic plasticity

  12. Frequency-dependent viscoelastic parameters of mouse brain tissue estimated by MR elastography

    Energy Technology Data Exchange (ETDEWEB)

    Clayton, E H; Bayly, P V [Department of Mechanical Engineering and Materials Science, Washington University in St Louis, 1 Brookings Drive, Campus Box 1185, Saint Louis, MO 63130 (United States); Garbow, J R, E-mail: clayton@wustl.edu, E-mail: garbow@wustl.edu, E-mail: pvb@wustl.edu [Biomedical Magnetic Resonance Laboratory, Department of Radiology, Washington University in St Louis, 4525 Scott Avenue, Campus Box 8227, Saint Louis, MO 63110 (United States)

    2011-04-21

    Viscoelastic properties of mouse brain tissue were estimated non-invasively, in vivo, using magnetic resonance elastography (MRE) at 4.7 T to measure the dispersive properties of induced shear waves. Key features of this study include (i) the development and application of a novel MR-compatible actuation system which transmits vibratory motion into the brain through an incisor bar, and (ii) the investigation of the mechanical properties of brain tissue over a 1200 Hz bandwidth from 600-1800 Hz. Displacement fields due to propagating shear waves were measured during continuous, harmonic excitation of the skull. This protocol enabled characterization of the true steady-state patterns of shear wave propagation. Analysis of displacement fields obtained at different frequencies indicates that the viscoelastic properties of mouse brain tissue depend strongly on frequency. The average storage modulus (G') increased from approximately 1.6 to 8 kPa over this range; average loss modulus (G'') increased from approximately 1 to 3 kPa. Both moduli were well approximated by a power-law relationship over this frequency range. MRE may be a valuable addition to studies of disease in murine models, and to pre-clinical evaluations of therapies. Quantitative measurements of the viscoelastic parameters of brain tissue at high frequencies are also valuable for modeling and simulation of traumatic brain injury.

  13. Coronaviruses in brain tissue from patients with multiple sclerosis

    DEFF Research Database (Denmark)

    Dessau, R B; Lisby, G; Frederiksen, J L

    2001-01-01

    Brain tissue from 25 patients with clinically definite multiple sclerosis (MS) and as controls brain tissue from 36 patients without neurological disease was tested for the presence of human coronaviral RNA. Four PCR assays with primers specific for N-protein of human coronavirus strain 229E...... in the proportion of positive signals from the MS patients compared to controls. Evidence for a chronic infection with the human coronaviruses strain 229E or OC43 in brain tissue from patients with MS or controls has not been found in this study....

  14. Emergent Endotracheal Intubation and Mortality in Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Fine, Philip R

    2008-11-01

    Full Text Available Objective: To determine the relationship between emergent intubation (emergency department and field intubation cases combined and mortality in patients with traumatic brain injury (TBI while controlling for injury severity.Methods: Retrospective observational study of 981 (35.2% intubated, 64.8% not intubated patients with TBI evaluating the association between intubation status and mortality. Logistic regression was used to analyze the data. Injury severity measures included Head/Neck Abbreviated Injury Scale (H-AIS, systolic blood pressure, type of head injury (blunt vs. penetrating, and a propensity score combining the effects of several other potential confounding variables. Age was also included in the model.Results: The simple association of emergent endotracheal intubation with death had an odds ratio (OR of 14.3 (95% CI = 9.4 – 21.9. The logistic regression model including relevant covariates and a propensity score that adjusted for injury severity and age yielded an OR of 5.9 (95% CI = 3.2 – 10.9.Conclusions: This study indicates that emergent intubation is associated with increased risk of death after controlling for a number of injury severity indicators. We discuss the need for optimal paramedic training, and an understanding of the factors that guide patient selection and the decision to intubate in the field. [WestJEM.2008;9:184-189

  15. Effect of thyrotropin-releasing hormone on cerebral free radical reactions following acute brain injury in rabbits

    Institute of Scientific and Technical Information of China (English)

    牛光明; 顾秀娟; 苏玉林; 万锋; 苏芳忠; 薛德麟

    2003-01-01

    Objective: To investigate the early effect of thyrotropin-releasing hormone (TRH) on cerebral free radical reactions after acute brain injury in rabbits.Methods: 30 healthy white rabbits were randomly divided into three groups: Group A (n=10), Group B (n=12) and Group C (n=8). The rabbits in Group A and Group B were injured by direct hit. At 0.5-4 hours after injury, the rabbits in Group A were injected with TRH (8 mg/kg body weight) through a vein and the rabbits in Group B were injected with normal saline of equal volume. The rabbits in Group C served as the normal control. Then all the rabbits were killed and brain tissues were obtained. The content of lipoperoxide (LPO), the activity of superoxide dismutase (SOD) and the water content of the brain tissues were measured.Results: The contents of LPO and water in brain tissues in Group A were lower and the activity of SOD was higher than those of Group B (P<0.05). After injury, intracranial pressure (ICP) rose rapidly and continuously with time passing by. When TRH was given to the animals in Group A, the rising speed of ICP slowed down significantly.Conclusions: TRH can decrease the cerebral free radical reactions and cerebral edema after acute brain injury in rats.

  16. Reorganization of Functional Connectivity as a Correlate of Cognitive Recovery in Acquired Brain Injury

    Science.gov (United States)

    Castellanos, Nazareth P.; Paul, Nuria; Ordonez, Victoria E.; Demuynck, Olivier; Bajo, Ricardo; Campo, Pablo; Bilbao, Alvaro; Ortiz, Tomas; del-Pozo, Francisco; Maestu, Fernando

    2010-01-01

    Cognitive processes require a functional interaction between specialized multiple, local and remote brain regions. Although these interactions can be strongly altered by an acquired brain injury, brain plasticity allows network reorganization to be principally responsible for recovery. The present work evaluates the impact of brain injury on…

  17. Mild Traumatic Brain Injury Pocket Guide (CONUS)

    Science.gov (United States)

    2010-01-01

    without direct external trauma to the head `` Foreign body penetrating the brain `` Forces generated from events such as blast or explosion, or... Methylphenidate 5mg Q 0800 and Q 1300. Increase total daily dose by 5mg Q 2 weeks to maximum dose of 20mg BID `– Modafanil 100mg QAM. Increase by...prerequisite for basic and complex behaviors involving memory, judgment, social perception and executive skills `` Interventions should be based on a

  18. Traumatic Brain Injury Severity Affects Neurogenesis in Adult Mouse Hippocampus.

    Science.gov (United States)

    Wang, Xiaoting; Gao, Xiang; Michalski, Stephanie; Zhao, Shu; Chen, Jinhui

    2016-04-15

    Traumatic brain injury (TBI) has been proven to enhance neural stem cell (NSC) proliferation in the hippocampal dentate gyrus. However, various groups have reported contradictory results on whether TBI increases neurogenesis, partially due to a wide range in the severities of injuries seen with different TBI models. To address whether the severity of TBI affects neurogenesis in the injured brain, we assessed neurogenesis in mouse brains receiving different severities of controlled cortical impact (CCI) with the same injury device. The mice were subjected to mild, moderate, or severe TBI by a CCI device. The effects of TBI severity on neurogenesis were evaluated at three stages: NSC proliferation, immature neurons, and newly-generated mature neurons. The results showed that mild TBI did not affect neurogenesis at any of the three stages. Moderate TBI promoted NSC proliferation without increasing neurogenesis. Severe TBI increased neurogenesis at all three stages. Our data suggest that the severity of injury affects adult neurogenesis in the hippocampus, and thus it may partially explain the inconsistent results of different groups regarding neurogenesis following TBI. Further understanding the mechanism of TBI-induced neurogenesis may provide a potential approach for using endogenous NSCs to protect against neuronal loss after trauma.

  19. Impaired Cerebral Autoregulation during Head Up Tilt in Patients with Severe Brain Injury

    DEFF Research Database (Denmark)

    Riberholt, Christian Gunge; Olesen, Niels Damkjær; Thing, Mira;

    2016-01-01

    acquired brain injury and a low level of consciousness. Fourteen patients with severe acquired brain injury and orthostatic intolerance and fifteen healthy volunteers were enrolled. Blood pressure was evaluated by pulse contour analysis, heart rate and RR-intervals were determined by electrocardiography...... mean velocity and estimated cerebral perfusion pressure. Patients with acquired brain injury presented an increase in mean flow index during head-up tilt indicating impaired autoregulation (P ....1 Hz spectral power in patients compared to healthy controls suggesting baroreflex dysfunction. In conclusion, patients with severe acquired brain injury and orthostatic intolerance during head-up tilt have impaired cerebral autoregulation more than one month after brain injury....

  20. Integrated undergraduate research experience for the study of brain injury.

    Science.gov (United States)

    Barnes, Clifford L; Sierra, Michelle; Delay, Eugene R

    2003-01-01

    We developed a series of hands-on laboratory exercises on "Brain Injury" designed around several pedagogical goals that included the development of: 1) knowledge of the scientific method, 2) student problem solving skills by testing cause and effect relationships, 3) student analytical and critical thinking skills by evaluating and interpreting data, identifying alternative explanations for data, and identifying confounding variables, and 4) student writing skills by reporting their findings in manuscript form. Students, facilitated by the instructor, developed a testable hypothesis on short-term effects of brain injury by analyzing lesion size and astrocytic activity. Four sequential laboratory exercises were used to present and practice ablation techniques, histological processing, microscopic visualization and image-capture, and computer aided image analysis. This exercise culminated in a laboratory report that mimicked a research article. The effectiveness of the laboratory sequence was assessed by measuring the acquisition of 1) content on anatomical, physiological, and cellular responses of the brain to traumatic brain injury, and 2) laboratory skills and methods of data-collection and analysis using surgical procedures, histology, microscopy, and image analysis. Post-course test scores, significantly greater than pre-course test scores and greater than scores from a similar but unstructured laboratory class, indicated that this hands-on approach to teaching an undergraduate research laboratory was successful. Potential variations in the integrated laboratory exercise, including multidisciplinary collaborations, are also noted.

  1. Perinatal Hypoxic-Ischemic brain injury; MR findings

    Energy Technology Data Exchange (ETDEWEB)

    Park, Dong Woo; Seo, Chang Hye [Inje University Pusan Paik Hospital, Pusan (Korea, Republic of)

    1994-09-15

    To characterize the MR findings of hypoxic-ischemic brain injury and to assess the value of the MR imaging. SE T1-, T2-weighted, and IR brain MR images of 44 infants and children with the past history of perinatal hypoxic insults were reviewed. Abnormal brain MR findings of 8 patients with birth history of prematurity and 36 patients with birth history of full-term/posterm including 7 with severe anoxic insult history, were compared in regard to the location and the character of the lesions. MRI demonstrated the followings; (1)abnormal signal intensity lesions of subcortical and/or deep cerebral white matter, cortex, and deep gray matter, (2)atrophy of the cerebral white matter, cortex and corpus callosum, with/without ventriculomegaly, and (3)delay in myelination. Periventricular and deep white matter lesions were demonstrated in the prematurity, the deep white matter lesions and/ or subcortical white matter lesions in the term/post-term, and deep gray matter lesions in the 7 patients with severe anoxic insults history. MR imaging was useful in the diagnosis of the hypoxic-ischemic brain injury, and the white and gray matter lesions were correlated with the time of the injury and the severity of hypoxic insult.

  2. The Field of Tissue Injury in the Lung and Airway

    Science.gov (United States)

    Steiling, Katrina; Ryan, John; Brody, Jerome S.; Spira, Avrum

    2009-01-01

    The concept of field cancerization was first introduced over six decades ago in the setting of oral cancer. Later, field cancerization involving histologic and molecular changes of neoplasms and adjacent tissue began to be characterized in smokers with or without lung cancer. Investigators also described a diffuse, non-neoplastic field of molecular injury throughout the respiratory tract that is attributable to cigarette smoking and susceptibility to smoking-induced lung disease. The potential molecular origins of field cancerization and the field of injury following cigarette smoke exposure in lung and airway epithelia are critical to understanding the impact of the field of injury on clinical diagnostics and therapeutics for smoking-induced lung disease. PMID:19138985

  3. National Training Course. Emergency Medical Technician. Paramedic. Instructor's Lesson Plans. Module VIII. Soft Tissue Injuries.

    Science.gov (United States)

    National Highway Traffic Safety Administration (DOT), Washington, DC.

    This instructor's lesson plan guide on soft tissue injuries is one of fifteen modules designed for use in the training of emergency medical technicians (paramedics). Six units of study are presented: (1) anatomy and physiology of the skin; (2) patient assessment for soft-tissue injuries; (3) pathophysiology and management of soft tissue injuries;…

  4. Neurobehavioral Effects of Levetiracetam in Patients with Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Jared F Benge

    2013-12-01

    Full Text Available Moderate to severe traumatic brain injury (TBI is one of the leading causes of acquired epilepsy. Prophylaxis for seizures is the standard of care for individuals with moderate to severe injuries at risk for developing seizures, though relatively limited comparative data is available to guide clinicians in their choice of agents. There have however been experimental studies which demonstrate potential neuroprotective qualities of levetiracetam after TBI, and in turn there is hope that eventually such agents may improve neurobehavioral outcomes post-TBI. This mini-review summarizes the available studies and suggests areas for future studies.

  5. Metallothionein (MT -I and MT-II expression are induced and cause zinc sequestration in the liver after brain injury.

    Directory of Open Access Journals (Sweden)

    Michael W Pankhurst

    Full Text Available UNLABELLED: Experiments with transgenic over-expressing, and null mutant mice have determined that metallothionein-I and -II (MT-I/II are protective after brain injury. MT-I/II is primarily a zinc-binding protein and it is not known how it provides neuroprotection to the injured brain or where MT-I/II acts to have its effects. MT-I/II is often expressed in the liver under stressful conditions but to date, measurement of MT-I/II expression after brain injury has focused primarily on the injured brain itself. In the present study we measured MT-I/II expression in the liver of mice after cryolesion brain injury by quantitative reverse-transcriptase PCR (RT-PCR and enzyme-linked immunosorbent assay (ELISA with the UC1MT antibody. Displacement curves constructed using MT-I/II knockout (MT-I/II(-/- mouse tissues were used to validate the ELISA. Hepatic MT-I and MT-II mRNA levels were significantly increased within 24 hours of brain injury but hepatic MT-I/II protein levels were not significantly increased until 3 days post injury (DPI and were maximal at the end of the experimental period, 7 DPI. Hepatic zinc content was measured by atomic absorption spectroscopy and was found to decrease at 1 and 3 DPI but returned to normal by 7DPI. Zinc in the livers of MT-I/II(-/- mice did not show a return to normal at 7 DPI which suggests that after brain injury, MT-I/II is responsible for sequestering elevated levels of zinc to the liver. CONCLUSION: MT-I/II is up-regulated in the liver after brain injury and modulates the amount of zinc that is sequestered to the liver.

  6. Computational Assessment of Neural Probe and Brain Tissue Interface under Transient Motion

    Directory of Open Access Journals (Sweden)

    Michael Polanco

    2016-06-01

    Full Text Available The functional longevity of a neural probe is dependent upon its ability to minimize injury risk during the insertion and recording period in vivo, which could be related to motion-related strain between the probe and surrounding tissue. A series of finite element analyses was conducted to study the extent of the strain induced within the brain in an area around a neural probe. This study focuses on the transient behavior of neural probe and brain tissue interface with a viscoelastic model. Different stages of the interface from initial insertion of neural probe to full bonding of the probe by astro-glial sheath formation are simulated utilizing analytical tools to investigate the effects of relative motion between the neural probe and the brain while friction coefficients and kinematic frequencies are varied. The analyses can provide an in-depth look at the quantitative benefits behind using soft materials for neural probes.

  7. Computational Assessment of Neural Probe and Brain Tissue Interface under Transient Motion.

    Science.gov (United States)

    Polanco, Michael; Bawab, Sebastian; Yoon, Hargsoon

    2016-06-16

    The functional longevity of a neural probe is dependent upon its ability to minimize injury risk during the insertion and recording period in vivo, which could be related to motion-related strain between the probe and surrounding tissue. A series of finite element analyses was conducted to study the extent of the strain induced within the brain in an area around a neural probe. This study focuses on the transient behavior of neural probe and brain tissue interface with a viscoelastic model. Different stages of the interface from initial insertion of neural probe to full bonding of the probe by astro-glial sheath formation are simulated utilizing analytical tools to investigate the effects of relative motion between the neural probe and the brain while friction coefficients and kinematic frequencies are varied. The analyses can provide an in-depth look at the quantitative benefits behind using soft materials for neural probes.

  8. Multicenter trial of early hypothermia in severe brain injury.

    Science.gov (United States)

    Clifton, Guy L; Drever, Pamala; Valadka, Alex; Zygun, David; Okonkwo, David

    2009-03-01

    The North American Brain Injury Study: Hypothermia IIR (NABIS:H IIR) is a randomized clinical trial designed to enroll 240 patients with severe brain injury between the ages of 16 and 45 years. The primary outcome measure is the dichotomized Glasgow Outcome Scale (GOS) at 6 months after injury. The study has the power to detect a 17.5% absolute difference in the percentage of patients with a good outcome with a power of 80%. All patients are randomized by waiver of consent unless family is immediately available. Enrollment is within 2.5 h of injury. Patients may be enrolled in the field by emergency medical services personnel affiliated with the study or by study personnel when the patient arrives at the emergency department. Patients who do not follow commands and have no exclusion criteria and who are enrolled in the hypothermia arm of the study are cooled to 35 degrees C as rapidly as possible by intravenous administration of up to 2 liters of chilled crystalloid. Those patients who meet the criteria for the second phase of the protocol (primarily a post-resuscitation GCS 3-8 without hypotension and without severe associated injuries) are cooled to 33 degrees C. Patients enrolled in the normothermia arm receive standard management at normothermia. As of December 2007, 74 patients had been randomized into phase II of the protocol. Patients in the hypothermia arm reached 35 degrees C in 2.7 +/- 1.1 (SD) h after injury and reached 33 degrees C at 4.4 +/- 1.5 h after injury.

  9. Role of pyruvate dehydrogenase complex in traumatic brain injury and Measurement of pyruvate dehydrogenase enzyme by dipstick test

    Directory of Open Access Journals (Sweden)

    Sharma Pushpa

    2009-01-01

    Full Text Available Objectives: The present study was designed to investigate the role of a mitochondrial enzyme pyruvate dehydrogenase (PDH on the severity of brain injury, and the effects of pyruvate treatment in rats with traumatic brain injury (TBI. Materials and Methods: We examined rats subjected to closed head injury using a fluid percussion device, and treated with sodium pyruvate (antioxidant and substrate for PDH enzyme. At 72 h post injury, blood was analyzed for blood gases, acid-base status, total PDH enzyme using a dipstick test and malondialdehyde (MDA levels as a marker of oxidative stress. Brain homogenates from right hippocampus (injured area were analyzed for PDH content, and immunostained hippocampus sections were used to determine the severity of gliosis and PDH E1-∞ subunit. Results: Our data demonstrate that TBI causes a significant reduction in PDH enzyme, disrupt-acid-base balance and increase oxidative stress in blood. Also, lower PDH enzyme in blood is related to the increased gliosis and loss of its PDH E1-∞ subunit PDH in brain tissue, and these effects of TBI were prevented by pyruvate treatment. Conclusion: Lower PDH enzyme levels in blood are related to the global oxidative stress, increased gliosis in brain, and severity of brain injury following TBI. These effects can be prevented by pyruvate through the protection of PDH enzyme and its subunit E-1.

  10. [The effects of dancing on the brain and possibilities as a form of rehabilitation in severe brain injuries].

    Science.gov (United States)

    Kullberg-Turtiainen, Marjo

    2013-01-01

    Very little research has been done on the effect of dancing on the rehabilitation of patients having a severe brain injury. In addition to motor problems, the symptom picture of the sequelae of severe brain injuries often involves strong fatigability, reduced physiological arousal, disturbances of coordination of attention, difficulties of emotional control and impairment of memory. This review deals with the neural foundation of dancing and the possibilities of dancing in the rehabilitation of severe brain injuries.

  11. The acute phase of mild traumatic brain injury is characterized by a distance-dependent neuronal hypoactivity.

    Science.gov (United States)

    Johnstone, Victoria P A; Shultz, Sandy R; Yan, Edwin B; O'Brien, Terence J; Rajan, Ramesh

    2014-11-15

    The consequences of mild traumatic brain injury (TBI) on neuronal functionality are only now being elucidated. We have now examined the changes in sensory encoding in the whisker-recipient barrel cortex and the brain tissue damage in the acute phase (24 h) after induction of TBI (n=9), with sham controls receiving surgery only (n=5). Injury was induced using the lateral fluid percussion injury method, which causes a mixture of focal and diffuse brain injury. Both population and single cell neuronal responses evoked by both simple and complex whisker stimuli revealed a suppression of activity that decreased with distance from the locus of injury both within a hemisphere and across hemispheres, with a greater extent of hypoactivity in ipsilateral barrel cortex compared with contralateral cortex. This was coupled with an increase in spontaneous output in Layer 5a, but only ipsilateral to the injury site. There was also disruption of axonal integrity in various regions in the ipsilateral but not contralateral hemisphere. These results complement our previous findings after mild diffuse-only TBI induced by the weight-drop impact acceleration method where, in the same acute post-injury phase, we found a similar depth-dependent hypoactivity in sensory cortex. This suggests a common sequelae of events in both diffuse TBI and mixed focal/diffuse TBI in the immediate post-injury period that then evolve over time to produce different long-term functional outcomes.

  12. The Field of Tissue Injury in the Lung and Airway

    OpenAIRE

    Steiling, Katrina; Ryan, John; Brody, Jerome S.; Spira, Avrum

    2008-01-01

    The concept of field cancerization was first introduced over six decades ago in the setting of oral cancer. Later, field cancerization involving histologic and molecular changes of neoplasms and adjacent tissue began to be characterized in smokers with or without lung cancer. Investigators also described a diffuse, non-neoplastic field of molecular injury throughout the respiratory tract that is attributable to cigarette smoking and susceptibility to smoking-induced lung disease. The potentia...

  13. Modulation of the cAMP signaling pathway after traumatic brain injury

    OpenAIRE

    Atkins, Coleen M.; Oliva, Anthony A.; Alonso, Ofelia F.; Pearse, Damien D.; Bramlett, Helen M; Dietrich, W. Dalton

    2007-01-01

    Traumatic brain injury (TBI) results in both focal and diffuse brain pathologies that are exacerbated by the inflammatory response and progress from hours to days after the initial injury. Using a clinically relevant model of TBI, the parasagittal fluid-percussion brain injury (FPI) model, we found injury-induced impairments in the cyclic AMP (cAMP) signaling pathway. Levels of cAMP were depressed in the ipsilateral parietal cortex and hippocampus, as well as activation of its downstream targ...

  14. Development of Experimental Tissue Models for Blast Injury

    Science.gov (United States)

    Butler, Benjamin; Bo, Chiara; Williams, Alun; Jardine, Andy; Brown, Katherine

    2013-06-01

    There is a pressing need to better understand the relationship between the intensity of a blast wave and the clinical consequences for victims of an explosion. In order to quantitatively study how these factors correlate with one another, blast injury tissue models are being developed. Sections of larynx, trachea and pulmonary tissue were excised from a recently sacrificed pig and maintained on ice prior to testing. The samples were subjected to strain rates of between 0.001 s-1 and 1000 s-1 in the laboratory by using a Split Hopkinson Pressure Bar and quasi-static testing apparatus. During high strain rate testing, samples were housed in a polycarbonate chamber which permitted experimentation on tissue held in fluid. Data were analysed using 1, 2 and 3 wave analysis software in Matlab to yield information about the material properties of both undamaged and damaged tissues. In addition, macroscopic changes in tissue organization were also visualized using histopathological techniques. This work is being extended to cellular and animal models to derive more detailed information about the underlying molecular changes relating to blast-induced damage and repair. The Royal British Legion Centre for Blast Injury Studies.

  15. Carcinoma cells misuse the host tissue damage response to invade the brain

    Science.gov (United States)

    Chuang, Han-Ning; van Rossum, Denise; Sieger, Dirk; Siam, Laila; Klemm, Florian; Bleckmann, Annalen; Bayerlová, Michaela; Farhat, Katja; Scheffel, Jörg; Schulz, Matthias; Dehghani, Faramarz; Stadelmann, Christine; Hanisch, Uwe-Karsten; Binder, Claudia; Pukrop, Tobias

    2013-01-01

    The metastatic colonization of the brain by carcinoma cells is still barely understood, in particular when considering interactions with the host tissue. The colonization comes with a substantial destruction of the surrounding host tissue. This leads to activation of damage responses by resident innate immune cells to protect, repair, and organize the wound healing, but may distract from tumoricidal actions. We recently demonstrated that microglia, innate immune cells of the CNS, assist carcinoma cell invasion. Here we report that this is a fatal side effect of a physiological damage response of the brain tissue. In a brain slice coculture model, contact with both benign and malignant epithelial cells induced a response by microglia and astrocytes comparable to that seen at the interface of human cerebral metastases. While the glial damage response intended to protect the brain from intrusion of benign epithelial cells by inducing apoptosis, it proved ineffective against various malignant cell types. They did not undergo apoptosis and actually exploited the local tissue reaction to invade instead. Gene expression and functional analyses revealed that the C-X-C chemokine receptor type 4 (CXCR4) and WNT signaling were involved in this process. Furthermore, CXCR4-regulated microglia were recruited to sites of brain injury in a zebrafish model and CXCR4 was expressed in human stroke patients, suggesting a conserved role in damage responses to various types of brain injuries. Together, our findings point to a detrimental misuse of the glial damage response program by carcinoma cells resistant to glia-induced apoptosis. PMID:23832647

  16. Undifferentiated connective tissue diseases-related hepatic injury

    Institute of Scientific and Technical Information of China (English)

    Ying Zhang; Fu-Kui Zhang; Xiao-Ning Wu; Tai-Ling Wang; Ji-Dong Jia; Bao-En Wang

    2008-01-01

    Hepatic injury is rarely associated with undifferentiated connective tissue diseases (UCTD).We report,here,a case of a middle-aged woman with UCTD-related hepatic injury,including its case history,clinical manifestations,laboratory findings,treatment and its short-term effect.The patient was admitted to the hospital with symptoms of fatigue,anorexia,low-grade fever and skin rashes.She had a past history of left knee joint replacement.Laboratory tests showed elevated levels of serum transaminase,IgG and globulin,accelerated erythrocyte sedimentation rate,eosinophilia and a high titer of antinuclear antibodies (1:320).Imaging studies showed interstitial pneumonitis and hydropericardium.Liver biopsy showed the features which were consistent with those of connective tissue diseases-related polyangitis.After treatment with a low-dose of oral prednisone,both symptoms and laboratory findings were significantly improved.UCTD-related hepatic injury should be considered in the differential diagnosis of connective tissue diseases with abnormal liver function tests.Lowdose prednisone may effectively improve both symptoms and laboratory tests.

  17. Relationship between changes of N-methyl-D-aspartate receptor activity and brain edema after brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To investigate the relationship between the changes of N-methyl-D-aspartate (NMDA) receptor activity and brain edema after injury in rats.   Methods: The brain injury models were made by using a free-falling body. The treatment model was induced by means of injecting AP5 into lateral ventricle before brain injury; water contents in brain cortex were measured with dry-wet method; and NMDA receptor activity was detected with a radio ligand binding assay.   Results: The water contents began to increase at 30 minutes and reached the peak at 6 hours after brain injury. The maximal binding (Bmax) of NMDA receptor increased significantly at 15 minutes and reached the peak at 30 minutes, then decreased gradually and had the lowest value 6 hours after brain injury. Followed the treatment with AP5, NMDA receptor activity in the injured brain showed a normal value; and the water contents were lower than that of AP5-free injury group 24 hours after brain injury.   Conclusions: It suggests that excessive activation of NMDA receptor may be one of the most important factors to induce the secondary cerebral impairments, and AP5 may protect the brain from edema after brain injury.

  18. Aberrant innate immune activation following tissue injury impairs pancreatic regeneration.

    Directory of Open Access Journals (Sweden)

    Alexandra E Folias

    Full Text Available Normal tissue architecture is disrupted following injury, as resident tissue cells become damaged and immune cells are recruited to the site of injury. While injury and inflammation are critical to tissue remodeling, the inability to resolve this response can lead to the destructive complications of chronic inflammation. In the pancreas, acinar cells of the exocrine compartment respond to injury by transiently adopting characteristics of progenitor cells present during embryonic development. This process of de-differentiation creates a window where a mature and stable cell gains flexibility and is potentially permissive to changes in cellular fate. How de-differentiation can turn an acinar cell into another cell type (such as a pancreatic β-cell, or a cell with cancerous potential (as in cases of deregulated Kras activity is of interest to both the regenerative medicine and cancer communities. While it is known that inflammation and acinar de-differentiation increase following pancreatic injury, it remains unclear which immune cells are involved in this process. We used a combination of genetically modified mice, immunological blockade and cellular characterization to identify the immune cells that impact pancreatic regeneration in an in vivo model of pancreatitis. We identified the innate inflammatory response of macrophages and neutrophils as regulators of pancreatic regeneration. Under normal conditions, mild innate inflammation prompts a transient de-differentiation of acinar cells that readily dissipates to allow normal regeneration. However, non-resolving inflammation developed when elevated pancreatic levels of neutrophils producing interferon-γ increased iNOS levels and the pro-inflammatory response of macrophages. Pancreatic injury improved following in vivo macrophage depletion, iNOS inhibition as well as suppression of iNOS levels in macrophages via interferon-γ blockade, supporting the impairment in regeneration and the

  19. Neuroimaging biomarkers in mild traumatic brain injury (mTBI).

    Science.gov (United States)

    Bigler, Erin D

    2013-09-01

    Reviewed herein are contemporary neuroimaging methods that detect abnormalities associated with mild traumatic brain injury (mTBI). Despite advances in demonstrating underlying neuropathology in a subset of individuals who sustain mTBI, considerable disagreement persists in neuropsychology about mTBI outcome and metrics for evaluation. This review outlines a thesis for the select use of sensitive neuroimaging methods as potential biomarkers of brain injury recognizing that the majority of individuals who sustain an mTBI recover without neuroimaging signs or neuropsychological sequelae detected with methods currently applied. Magnetic resonance imaging (MRI) provides several measures that could serve as mTBI biomarkers including the detection of hemosiderin and white matter abnormalities, assessment of white matter integrity derived from diffusion tensor imaging (DTI), and quantitative measures that directly assess neuroanatomy. Improved prediction of neuropsychological outcomes in mTBI may be achieved with the use of targeted neuroimaging markers.

  20. Traumatic Brain Injury and NADPH Oxidase: A Deep Relationship

    Directory of Open Access Journals (Sweden)

    Cristina Angeloni

    2015-01-01

    Full Text Available Traumatic brain injury (TBI represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox, ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS, have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after TBI, suggesting Nox critical role in the onset and development of this pathology. In this review, we summarize the current evidence about the role of Nox enzymes in the pathophysiology of TBI.

  1. Sigma-1 Receptor Modulates Neuroinflammation After Traumatic Brain Injury.

    Science.gov (United States)

    Dong, Hui; Ma, Yunfu; Ren, Zengxi; Xu, Bin; Zhang, Yunhe; Chen, Jing; Yang, Bo

    2016-07-01

    Traumatic brain injury (TBI) remains a significant clinical problem and contributes to one-third of all injury-related deaths. Activated microglia-mediated inflammatory response is a distinct characteristic underlying pathophysiology of TBI. Here, we evaluated the effect and possible mechanisms of the selective Sigma-1 receptor agonist 2-(4-morpholinethyl)-1-phenylcyclohexanecarboxylate (PRE-084) in mice TBI model. A single intraperitoneal injection 10 μg/g PRE-084, given 15 min after TBI significantly reduced lesion volume, lessened brain edema, attenuated modified neurological severity score, increased the latency time in wire hang test, and accelerated body weight recovery. Moreover, immunohistochemical analysis with Iba1 staining showed that PRE-084 lessened microglia activation. Meanwhile, PRE-084 reduced nitrosative and oxidative stress to proteins. Thus, Sigma-1 receptors play a major role in inflammatory response after TBI and may serve as useful target for TBI treatment in the future.

  2. Minding and Caring about Ethics in Brain Injury.

    Science.gov (United States)

    Gillett, Grant

    2016-05-01

    Joseph Fins's book Rights Come to Mind: Brain Injury, Ethics, and the Struggle for Consciousness (Cambridge UP, 2015) is a considerable addition to the literature on disorders of consciousness and the murky area of minimally conscious states. Fins brings to this fraught area of clinical practice and neuroethical analysis a series of stories and reflections resulting in a pressing and sustained ethical challenge both to clinicians and to health care systems. The challenge is multifaceted, with diagnostic and therapeutic demands to be met by clinicians and a mix of moral, scientific-economic, and political resonances for health care analysts. Everything in the book resonates with my own clinical experience and the often messy and emotionally wrenching business of providing ongoing care for patients with severe brain injuries and disorders, people who frequently resist the categorizations that well-organized health care systems prefer and that can dictate terms of patient management.

  3. Stress and Traumatic Brain Injury: A Behavioral, Proteomics, and Histological Study

    Science.gov (United States)

    2011-03-07

    traumatic brain injury ( TBI ) can both result in lasting neurobehavioral abnormalities. Post- traumatic stress disorder and blast...factor on the battlefield INTRODUCTION Traumatic brain injury ( TBI ) is one of the leading causes of death and chronic disability worldwide (Bruns and...ulcer devel- opment. Brain Res. Bull. 25, 691–695. Jaffee, M. S., and Meyer, K. S. (2009). A brief overview of traumatic brain injury ( TBI ) and

  4. Acute respiratory distress syndrome assessment after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Shahrooz Kazemi

    2016-01-01

    Full Text Available Background: Acute respiratory distress syndrome (ARDS is one of the most important complications associated with traumatic brain injury (TBI. ARDS is caused by inflammation of the lungs and hypoxic damage with lung physiology abnormalities associated with acute respiratory distress syndrome. Aim of this study is to determine the epidemiology of ARDS and the prevalence of risk factors. Methods: This prospective study performed on patients with acute traumatic head injury hospitalization in the intensive care unit of the Shohaday-e Haftom-e-Tir Hospital (September 2012 to September 2013 done. About 12 months, the data were evaluated. Information including age, sex, education, employment, drug and alcohol addiction, were collected and analyzed. The inclusion criteria were head traumatic patients and exclusion was the patients with chest trauma. Questionnaire was designed with doctors supervision of neurosurgery. Then the collected data were analysis. Results: In this study, the incidence of ARDS was 23.8% and prevalence of metabolic acidosis was 31.4%. Most injury with metabolic acidosis was Subarachnoid hemorrhage (SAH 48 (60% and Subdural hemorrhage (SDH was Next Level with 39 (48% Correlation between Glasgow Coma Scale (GCS and Respiratory Distress Syndrome (ARDS were significantly decreased (P< 0.0001. The level of consciousness in patients with skull fractures significantly lower than those without fractures (P= 0.009 [(2.3±4.6 vs (4.02±7.07]. Prevalence of metabolic acidosis during hospitalization was 80 patients (31.4%. Conclusion: Acute respiratory distress syndrome is a common complication of traumatic brain injury. Management and treatment is essential to reduce the mortality. In this study it was found the age of patients with ARDS was higher than patients without complications. ARDS risk factor for high blood pressure was higher in men. Most victims were pedestrians. The most common injury associated with ARDS was SDH. Our analysis

  5. Traumatic brain injury neuropsychology in Cali, Colombia

    Directory of Open Access Journals (Sweden)

    Quijano María Cristina

    2012-04-01

    Full Text Available Objetive: comparative analysis between control group and patients with TBI to determine whetherthere neuropsychological differences at 6 months of evolution, to guide timely interventioncommensurate with the needs of this population. Materials and methods: a total of 79 patientswith a history of TBI with a minimum of 6 months of evolution and 79 control subjects were evaluated.Both groups with a mean age of 34 and without previous neurological or psychiatric disorders and an average schooling of 11 years for the control group and 9 years for the TBI group.The Glasgow Coma Scale in the TBI group was classified as moderate with 11 points. The BriefNeuropsychological Evaluation in Spanish Neuropsi was applied to both groups. Results: significantdifferences (p≤0.05 in the tasks of orientation, attention, memory, language, reading andwriting were found. Conclusions: TBI generates significant neuropsychological changes, even sixmonths after discharge from the health service. It suggests that patients with head injury requiretreatment after overcoming the initial stage.

  6. A social identity approach to acquired brain injury (ABI)

    OpenAIRE

    Walsh, Stephen R.

    2014-01-01

    peer-reviewed The central argument put forward in this thesis is that, in the context of acquired brain injury (ABI) social identity matters. The first article is a theoretical paper which reviews an emerging literature that is trying to draw together social psychology and neuropsychology in the study of ABI. This article argues that the social identity approach is an appropriate vehicle for such integration and introduces the concept of identity sub-types based on belonging and based on p...

  7. Comment: importance of cognitive reserve in traumatic brain injury.

    Science.gov (United States)

    Bigler, Erin D

    2014-05-01

    The expectation for moderate to severe traumatic brain injury (TBI) is permanent damage and lasting deficits. However, in a multicenter investigation, Schneider et al.(1) show that by 1 year postinjury, one-fourth of patients with TBI achieve disability-free recovery (DFR), defined as a score of zero on the Disability Rating Scale. Of importance, cognitive reserve (CR) in the form of educational attainment was related to DFR.

  8. Adolescents’ experience of a parental traumatic brain injury

    Directory of Open Access Journals (Sweden)

    D Harris

    2006-04-01

    Full Text Available This study explores the experiences of four adolescents, each living with a parent who has sustained a traumatic brain injury, against the theoretical backdrop of existential-phenomenological psychology. Opsomming Hierdie navorsing verken die belewenisse van vier adolessente wat saam met ‘n ouer wat ‘n traumatiese breinbesering opgedoen het, leef. *Please note: This is a reduced version of the abstract. Please refer to PDF for full text.

  9. Brain Injury Following Repetitive Apnea in Newborn Piglets

    Science.gov (United States)

    Schears, Gregory; Creed, Jennifer; Antoni, Diego; Zaitseva, Tatiana; Greeley, William; Wilson, David F.; Pastuszko, Anna

    Repetitive apnea is associated with a significant increase in extracellular dopamine, generation of free radicals as determined by o-tyrosine formation and increase in Fluoro-Jade staining of degenerating neurons. This increase in extracellular dopamine and of hydroxyl radicals in striatum of newborn brain is likely to be at least partly responsible for the neuronal injury and neurological side effects of repetitive apnea.

  10. Cognitive rehabilitation in children with acquired brain injuries

    OpenAIRE

    Hagberg-van't Hooft, Ingrid

    2005-01-01

    Deficits in attention, memory and executive functions are the most common cognitive dysfunctions after acquired brain injuries (ABI) and may have a major negative influence on academic and social adjustment. Neuropsychological measures can assess these dysfunctions and shortcomings in academic and social life, but there is a great need for new efficacious cognitive treatment programmes. The main aims of this thesis were to evaluate the direct and maintained effects of a ...

  11. Novel Treatment for Patients with Traumatic Brain Injury (TBI)

    Science.gov (United States)

    2016-06-01

    craniectomy for urgent evacuation of intracranial hemorrhage improves intracranial and cerebral perfusion pressures and overrides benefits of vasopressors in...for the management of CPP (cerebral perfusion pressure ) after TBI (traumatic brain injury) and support the continued investigation and use of AVP...and 12 patients received vasopressin (AVP). Those in the "no vasopressor" group were the least severely injured and had the best outcomes. Those in the

  12. Personalized Medicine in Veterans with Traumatic Brain Injuries

    Science.gov (United States)

    2012-05-01

    prepared a manuscript entitled “Select non-coding RNA in blood components provide novel clinically accessible biological surrogates for improved...Dooley C, Abbi B, Lange G. (2012). Select non-coding RNA in blood components provide novel clinically accessible biological surrogates for improved...in blood components provide novel clinically accessible biological surrogates for improved identification of traumatic brain injury in OEF/OIF

  13. The Diagnosis of Traumatic Brain Injury on the Battlefield

    OpenAIRE

    Schmid, Kara E.; Frank C Tortella

    2012-01-01

    The conflicts in Iraq and Afghanistan have placed an increased awareness on traumatic brain injury (TBI). Various publications have estimated the incidence of TBI for our deployed servicemen, however all have been based on extrapolations of data sets or subjective evaluations due to our current method of diagnosing a TBI. Therefore it has been difficult to get an accurate rate and severity of deployment related TBIs, or the incidence of multiple TBIs our service members are experiencing. As s...

  14. Is management of acute traumatic brain injury effective?

    OpenAIRE

    Lei, Jin; Gao, Guo-Yi; Jiang, Ji-Yao

    2012-01-01

    【Abstract】 Objective: To evaluate all the possible therapeutic measures concerning the acute management of traumatic brain injury (TBI) mentioned in Cochrane System-atic Reviews published in the Cochrane Database of Sys-tematic Reviews (CDSR). Methods: An exhausted literature search for all pub-lished Cochrane Systematic Reviews discussing therapeu-tic rather than prevention or rehabilitative interventions of TBI was conducted. We retrieved such databases as CDSR and Coch...

  15. PTSD and traumatic brain injury: folklore and fact?

    Science.gov (United States)

    King, Nigel S

    2008-01-01

    A number of controversies and debates have arisen over the years surrounding the dual diagnosis of post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI). Many of these have centred around the around the degree of protection provided by TBI against developing the disorder. The following is brief review of the literature in this area to help resolve some of these issues and to address a number of specific challenges which arise when working with this patient group.

  16. Expression of Hsp70 and Caspase-3 in rabbits after severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    ZHANG Jing; TAO Dai-qin; ZHAO Hui; YIN Zhi-yong

    2012-01-01

    Objective:To investigate the expression of Caspase-3 and Hsp70 in rabbits after severe traumatic brain injury (TBI) and to explore the feasibility of its application in estimation of injury time in forensic medicine.Methods:A rabbit model of heavy TBI was developed by high velocity impact on the parietal bone with an iron stick.Totally 8 healthy adult New Zealand white rabbits were randomly divided into control group (n=2) and injury group (n=6).Four hours after injury,tissue specimens from the parietal lobe,temporal lobe,occipital lobe,cerebellum and brainstem were harvested to detect the expression of Hsp70 and Caspase-3 by immunohistochemistry.Besides,the gray values of cells positive for Hsp70 and Caspase-3 were analyzed with an image analyzer.Results:Immunohistochemistry staining demonstrated a low level of Caspase-3 and Hsp70 expression in normal control group.While in injury group,both the Caspase-3and Hsp70 expression was significantly elevated (P<0.05).Positive cells gathered around the lesion focus.Occipital lobe and cerebellum had fewer positive cells while temporal and brainstem had the fewest.Conclusion:The expression of Caspase-3 and Hsp70 at an early stage following severe TBI is characteristic and can be applied to estimate the time of injury.

  17. Study the efficacy of neuroprotective drugs on brain physiological properties during focal head injury using optical spectroscopy data analysis

    Science.gov (United States)

    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.

  18. Effect observation of hyperbaric oxygen on repairing of injured brain tissue after child encephalitis%高压氧促进儿童脑炎受损脑组织修复的疗效观察

    Institute of Scientific and Technical Information of China (English)

    王湘渝; 王强; 晏莉娜; 谭聪; 张香菊; 郑世钢

    2003-01-01

    @@ BACKGROUND: There are no effective methods to treatmentof epidemic encephalitis B and sporadic encephalitis at present. Inearly stage of disease course, most patients present with coma thatis the inflammatory reaction of brain parenchyma, leads to ischemiaand hypoxia of brain tissue and encephaloedema and was the ex-pression of serious injury of brain tissue.

  19. Effects of magnesium sulfate on brain mitochondrial respiratory function in rats after experimental traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    许民辉; 代文光; 邓洵鼎

    2002-01-01

    Objective: To study the effects of magnesium sulfate on brain mitochondrial respiratory function in rats after experimental traumatic brain injury and the possible mechanism.Methods: The middle degree brain injury in rats was made by BIM-III multi-function impacting machine. The brain mitochondrial respiratory function was measured with oxygen electrode and the ultra-structural changes were observed with transmission electron microscope (TEM).Results: 1. The brain mitochondrial respiratory stage III and respiration control rate reduced significantly in the untreated groups within 24 and 72 hours. But treated Group A showed certain degree of recovery of respiratory function; treated Group B showed further improvement. 2. Untreated Group, treated Groups A and B had different degrees of mitochondrial ultra-structural damage respectively, which could be attenuated after the treatment with magnesium sulfate.Conclusions: The mitochondrial respiratory function decreases significantly after traumatic brain injury. But it can be apparently improved after magnesium sulfate management along with the attenuated damage of mitochondria discovered by TEM. The longer course of treatment can obtain a better improvement of mitochondrial respiratory function.

  20. Magnetic micelles for DNA delivery to rat brains after mild traumatic brain injury.

    Science.gov (United States)

    Das, Mahasweta; Wang, Chunyan; Bedi, Raminder; Mohapatra, Shyam S; Mohapatra, Subhra

    2014-10-01

    Traumatic brain injury (TBI) causes significant mortality, long term disability and psychological symptoms. Gene therapy is a promising approach for treatment of different pathological conditions. Here we tested chitosan and polyethyleneimine (PEI)-coated magnetic micelles (CP-mag micelles or CPMMs), a potential MRI contrast agent, to deliver a reporter DNA to the brain after mild TBI (mTBI). CPMM-tomato plasmid (ptd) conjugate expressing a red-fluorescent protein (RFP) was administered intranasally immediately after mTBI or sham surgery in male SD rats. Evans blue extravasation following mTBI suggested CPMM-ptd entry into the brain via the compromised blood-brain barrier. Magnetofection increased the concentration of CPMMs in the brain. RFP expression was observed in the brain (cortex and hippocampus), lung and liver 48 h after mTBI. CPMM did not evoke any inflammatory response by themselves and were excreted from the body. These results indicate the possibility of using intranasally administered CPMM as a theranostic vehicle for mTBI. From the clinical editor: In this study, chitosan and PEI-coated magnetic micelles (CPMM) were demonstrated as potentially useful vehicles in traumatic brain injury in a rodent model. Magnetofection increased the concentration of CPMMs in the brain and, after intranasal delivery, CPMM did not evoke any inflammatory response and were excreted from the body.

  1. Exosome platform for diagnosis and monitoring of traumatic brain injury.

    Science.gov (United States)

    Taylor, Douglas D; Gercel-Taylor, Cicek

    2014-09-26

    We have previously demonstrated the release of membranous structures by cells into their extracellular environment, which are termed exosomes, microvesicles or extracellular vesicles depending on specific characteristics, including size, composition and biogenesis pathway. With activation, injury, stress, transformation or infection, cells express proteins and RNAs associated with the cellular responses to these events. The exosomes released by these cells can exhibit an array of proteins, lipids and nucleic acids linked to these physiologic events. This review focuses on exosomes associated with traumatic brain injury, which may be both diagnostic and a causative factor in the progression of the injury. Based on current data, exosomes play essential roles as conveyers of intercellular communication and mediators of many of the pathological conditions associated with development, progression and therapeutic failures and cellular stress in a variety of pathologic conditions. These extracellular vesicles express components responsible for angiogenesis promotion, stromal remodelling, signal pathway activation through growth factor/receptor transfer, chemoresistance, immunologic activation and genetic exchange. These circulating exosomes not only represent a central mediator of the pro-inflammatory microenvironment linked with secondary brain injury, but their presence in the peripheral circulation may serve as a surrogate for biopsies, enabling real-time diagnosis and monitoring of neurodegenerative progression.

  2. Percutaneous dilatational tracheostomy for ICU patients with severe brain injury

    Directory of Open Access Journals (Sweden)

    Guo Dongyuan

    2014-12-01

    Full Text Available 【Abstract】Objective: To sum up our experience in percutaneous dilatational tracheostomy (PDT in ICU patient with severe brain injury. Methods: Between November 2011 and April 2014, PDTs were performed on 32 severe brain injury patients in ICU by a team of physicians and intensivists. The success rate, effi cacy, safety, and complications including stomal infection and bleeding, paratracheal insertion, pneumothorax, pneumomediastinum, tracheal laceration, as well as clinically significant tracheal stenosis were carefully monitored and recorded respectively. Results: The operations took 4-15 minutes (mean 9.1 minutes±4.2 minutes. Totally 4 cases suffered from complications in the operations: 3 cases of stomal bleeding, and 1 case of intratracheal bloody secretion, but none required intervention. Paratracheal insertion, pneumothorax, pneumomediastinum, tracheal laceration, or clinically signifi cant tracheal stenosis were not found in PDT patients. There was no procedure-related death occurring during or after PDT. Conclusion: Our study demonstrats that PDT is a safe, highly effective, and minimally invasive procedure. The appropriate sedation and airway management perioperatively help to reduce complication rates. PDT should be performed or supervised by a team of physicians with extensive experience in this procedure, and also an intensivist with experience in diffi cult airway management. Key words: Brain injuries; Percutaneous dilatational tracheostomy; ICU

  3. Brain injury impairs working memory and prefrontal circuit function

    Directory of Open Access Journals (Sweden)

    Colin James Smith

    2015-11-01

    Full Text Available More than 2.5 million Americans suffer a traumatic brain injury (TBI each year. Even mild to moderate traumatic brain injury causes long-lasting neurological effects. Despite its prevalence, no therapy currently exists to treat the underlying cause of cognitive impairment suffered by TBI patients. Following lateral fluid percussion injury (LFPI, the most widely used experimental model of TBI, we investigated alterations in working memory and excitatory/inhibitory synaptic balance in the prefrontal cortex. LFPI impaired working memory as assessed with a T-maze behavioral task. Field excitatory postsynaptic potentials recorded in the prefrontal cortex were reduced in slices derived from brain-injured mice. Spontaneous and miniature excitatory postsynaptic currents onto layer 2/3 neurons were more frequent in slices derived from LFPI mice while inhibitory currents onto layer 2/3 neurons were smaller after LFPI. Additionally, an increase in action potential threshold and concomitant decrease in firing rate was observed in layer 2/3 neurons in slices from injured animals. Conversely, no differences in excitatory or inhibitory synaptic transmission onto layer 5 neurons were observed; however, layer 5 neurons demonstrated a decrease in input resistance and action potential duration after LFPI. These results demonstrate synaptic and intrinsic alterations in prefrontal circuitry that may underlie working memory impairment caused by TBI.

  4. The clinical spectrum of sport-related traumatic brain injury.

    Science.gov (United States)

    Jordan, Barry D

    2013-04-01

    Acute and chronic sports-related traumatic brain injuries (TBIs) are a substantial public health concern. Various types of acute TBI can occur in sport, but detection and management of cerebral concussion is of greatest importance as mismanagement of this syndrome can lead to persistent or chronic postconcussion syndrome (CPCS) or diffuse cerebral swelling. Chronic TBI encompasses a spectrum of disorders that are associated with long-term consequences of brain injury, including chronic traumatic encephalopathy (CTE), dementia pugilistica, post-traumatic parkinsonism, post-traumatic dementia and CPCS. CTE is the prototype of chronic TBI, but can only be definitively diagnosed at autopsy as no reliable biomarkers of this disorder are available. Whether CTE shares neuropathological features with CPCS is unknown. Evidence suggests that participation in contact-collision sports may increase the risk of neurodegenerative disorders such as Alzheimer disease, but the data are conflicting. In this Review, the spectrum of acute and chronic sport-related TBI is discussed, highlighting how examination of athletes involved in high-impact sports has advanced our understanding of pathology of brain injury and enabled improvements in detection and diagnosis of sport-related TBI.

  5. Emerging potential of exosomes for treatment of traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Ye Xiong

    2017-01-01

    Full Text Available Traumatic brain injury (TBI is one of the major causes of death and disability worldwide. No effective treatment has been identified from clinical trials. Compelling evidence exists that treatment with mesenchymal stem cells (MSCs exerts a substantial therapeutic effect after experimental brain injury. In addition to their soluble factors, therapeutic effects of MSCs may be attributed to their generation and release of exosomes. Exosomes are endosomal origin small-membrane nano-sized vesicles generated by almost all cell types. Exosomes play a pivotal role in intercellular communication. Intravenous delivery of MSC-derived exosomes improves functional recovery and promotes neuroplasticity in rats after TBI. Therapeutic effects of exosomes derive from the exosome content, especially microRNAs (miRNAs. miRNAs are small non-coding regulatory RNAs and play an important role in posttranscriptional regulation of genes. Compared with their parent cells, exosomes are more stable and can cross the blood-brain barrier. They have reduced the safety risks inherent in administering viable cells such as the risk of occlusion in microvasculature or unregulated growth of transplanted cells. Developing a cell-free exosome-based therapy may open up a novel approach to enhancing multifaceted aspects of neuroplasticity and to amplifying neurological recovery, potentially for a variety of neural injuries and neurodegenerative diseases. This review discusses the most recent knowledge of exosome therapies for TBI, their associated challenges and opportunities.

  6. Emerging potential of exosomes for treatment of traumatic brain injury

    Science.gov (United States)

    Xiong, Ye; Mahmood, Asim; Chopp, Michael

    2017-01-01

    Traumatic brain injury (TBI) is one of the major causes of death and disability worldwide. No effective treatment has been identified from clinical trials. Compelling evidence exists that treatment with mesenchymal stem cells (MSCs) exerts a substantial therapeutic effect after experimental brain injury. In addition to their soluble factors, therapeutic effects of MSCs may be attributed to their generation and release of exosomes. Exosomes are endosomal origin small-membrane nano-sized vesicles generated by almost all cell types. Exosomes play a pivotal role in intercellular communication. Intravenous delivery of MSC-derived exosomes improves functional recovery and promotes neuroplasticity in rats after TBI. Therapeutic effects of exosomes derive from the exosome content, especially microRNAs (miRNAs). miRNAs are small non-coding regulatory RNAs and play an important role in posttranscriptional regulation of genes. Compared with their parent cells, exosomes are more stable and can cross the blood-brain barrier. They have reduced the safety risks inherent in administering viable cells such as the risk of occlusion in microvasculature or unregulated growth of transplanted cells. Developing a cell-free exosome-based therapy may open up a novel approach to enhancing multifaceted aspects of neuroplasticity and to amplifying neurological recovery, potentially for a variety of neural injuries and neurodegenerative diseases. This review discusses the most recent knowledge of exosome therapies for TBI, their associated challenges and opportunities.

  7. Thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    QIU Wu-si; WANG Wei-min; DU Hong-ying; LIU Wei-guo; SHEN Hong; SHEN Lei-fen; ZHU Ming-lan

    2006-01-01

    Objective: To investigate the clinical characteristics and significance of thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury (TBI).Methods: Ninety-six inpatients with severe brain injury were randomized into three groups: SBC (selective brain cooling ) group (n =24), MSH ( mild systemic hypothermia ) group ( n = 30), and control (normothermia) group ( n = 42). The platelet counts and prognosis were retrospectively analyzed.Results: Thrombocytopenia was present in 18 (75 % ), 23 (77 % ) and 15 (36 % ) patients in SBC group,MSH group and control group, respectively (P <0.01 ).Thrombocytopenia, in which the minimum platelet count was seen 3 days after hypothermia, showed no significant difference between SBC and MSH group (P > 0.05). Most platelet counts (37 cases, 90% ) in hypothermia group were returned to normal level after 1 to 2 days of natural rewarming. The platelet count in SBC group reduced by 16%, 27% and 29% at day 1, 3 and 5 respectively compared with the baseline value. Good recovery (GOS score 4-5) rate of thrombocytopenia 1 year after injury for hypothermia group ( 17 cases, 37 % ) was significantly lower than that of control group (P <0.01).Conclusions: Therapeutic hypothermia increases the incidence of thrombocytopenia in severe TBI, and patients with thrombocytopenia after therapeutic hypothermia are associated with unfavorable neurological prognosis.

  8. When Physics Meets Biology: Low and High-Velocity Penetration, Blunt Impact, and Blast Injuries to the Brain

    Science.gov (United States)

    Young, Leanne; Rule, Gregory T.; Bocchieri, Robert T.; Walilko, Timothy J.; Burns, Jennie M.; Ling, Geoffrey

    2015-01-01

    The incidence of traumatic brain injuries (TBI) in the US has reached epidemic proportions with well over 2 million new cases reported each year. TBI can occur in both civilians and warfighters, with head injuries occurring in both combat and non-combat situations from a variety of threats, including ballistic penetration, acceleration, blunt impact, and blast. Most generally, TBI is a condition in which physical loads exceed the capacity of brain tissues to absorb without injury. More specifically, TBI results when sufficient external force is applied to the head and is subsequently converted into stresses that must be absorbed or redirected by protective equipment. If the stresses are not sufficiently absorbed or redirected, they will lead to damage of extracranial soft tissue and the skull. Complex interactions and kinematics of the head, neck and jaw cause strains within the brain tissue, resulting in structural, anatomical damage that is characteristic of the inciting insult. This mechanical trauma then initiates a neuro-chemical cascade that leads to the functional consequences of TBI, such as cognitive impairment. To fully understand the mechanisms by which TBI occurs, it is critically important to understand the effects of the loading environments created by these threats. In the following, a review is made of the pertinent complex loading conditions and how these loads cause injury. Also discussed are injury thresholds and gaps in knowledge, both of which are needed to design improved protective systems. PMID:25999910

  9. Bcl-2 gene therapy for apoptosis following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    YANG Xiao-feng; ZHENG Xue-sheng; LIU Wei-guo; FENG Jun-feng

    2006-01-01

    Objective: To investigate the therapeutic effect of Bcl- 2 fusion protein on apoptosis in brain following traumatic brain injury.Methods: Bcl-2 gene was cloned by RT-PCR. Bcl-2 and EGFP genes were linked together and inserted into pAdeno-X vector. This recombinant vector was packaged into infectious adenovirus in HEK293 cells. Ninety Wistar rats were assigned randomly into experimental group(n=45) and control group (n=45). All rats were subjected to traumatic brain injury. Then recombinant adenovirus (for experimental group) or saline (for control group) was injected into the traumatic brain. The expression of Bcl-2 fusion protein was investigated by Western blotting, immunohistochemistry and fluorescence microscopy. Apoptosis in the injured brain was studied by TUNEL. Animals' behavior capacity was evaluated by tiltboard test.Results: In the experimental group, many fluorescent cells were found around the traumatic locus,which were also proven to be Bcl-2-positive by immunohistochemistry. On the contrary, few Bcl-2-positive cells and no fluorescent cell were detected in the control group. Bcl-2 expression of experimental group was much higher than that of control group, which was illustrated by Western blotting. The apoptosis index of experimental group was 0.027 ± 0.005, and that of control group was 0.141±0.025 (P<0.01). Two weeks after injury, animals of the experimental group behaved better than those of the control group.Conclusions: A recombinant adenovirus vector expressing Bcl-2 fusion protein has been constructed. Bcl-2 fusion protein can suppress apoptosis and promote cell survival. Moreover, the behavior recovery of the injured animal is promoted. Bcl-2 fusion protein provides a way to track the target cells in vivo.

  10. The thresholds and mechanisms of tissue injury by focused ultrasound

    Science.gov (United States)

    Simon, Julianna

    Therapeutic ultrasound is used in clinics around the world to treat ailments such as uterine fibroids, kidney stones, and plantar fasciitis. While many of the therapeutic effects of ultrasound are elicited by hyperthermia, bubbles can also interact with tissue to produce beneficial effects. For example, bubbles are used in boiling histotripsy to de-bulk tissue and are used in shock wave lithotripsy to break kidney stones. However, the same bubbles that break the kidney stones also damage the kidney, which is why bubble damage is a concern in every ultrasound application including fetal imaging. Whether the aim is to emulsify a tumor or image a fetus, understanding the thresholds and mechanisms of tissue injury by bubbles in an ultrasound field is important for all ultrasound applications and was the goal of this dissertation. One specific application of therapeutic ultrasound, known as boiling histotripsy, uses shock wave heating to explosively expand a millimeter-size boiling bubble at the transducer focus and fractionate bulk tissue. Yet it was unclear how the millimeter-size boiling or vapor bubble broke down the tissue into its submicron components. In this dissertation, we experimentally tested the hypothesis that ultrasonic atomization, or the emission of fine droplets from an acoustically excited liquid film, is the mechanism by which the millimeter-size boiling bubble in boiling histotripsy fractionates tissue into its submicron components. Using high speed photography, we showed that tissue can behave as a liquid such that a miniature acoustic fountain forms and atomization occurs within a millimeter-size cavity that approximates the boiling or vapor bubble produced by boiling histotripsy. The end result of tissue atomization was a hole in the tissue surface. After showing that tissue can be eroded by atomization, a series of experiments were conducted to determine the tissue properties that influence atomization. The results indicated that highly

  11. Effects of α-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats

    Directory of Open Access Journals (Sweden)

    Gaafar M Ishaq

    2013-01-01

    Full Text Available Background: Traumatic brain injury (TBI is accompanied by substantial accumulation of biomarkers of oxidative stress and depletion of antioxidants reserve which initiate chain reactions that damage brain cells. The present study investigated the role of ascorbic acid and α-tocopherol on the severity and management of TBI in rats. Materials and Methods: Wistar rats were subjected to closed head injury using an accelerated impact device. Rats were administered 45 mg/kg and 60 mg/kg body weight of ascorbic acid, α-tocopherol or a combination of the two vitamins for 2 weeks pre- and post injury. Blood and brain tissue homogenates were analyzed for vitamin C, vitamin E, malondialdehyde, superoxide dismutase, and creatine kinase activities. Results: The results indicated that TBI caused significant (P < 0.05 decreased in vitamins C and E levels in the blood and brain tissue of TBI-untreated rats. The activities of superoxide dismutase in TBI rats were markedly reduced when compared with non traumatized control and showed a tendency to increased following supplementation with vitamins C and E. Supplementation of the vitamins significantly (P < 0.05 reduced malondialdehyde in the treatment groups compared with the TBI-untreated group. Conclusion: The study indicated that pre and post treatment with ascorbic acid and α-tocopherol reduced oxidative stress induced by brain injury and effectively reduced mortality rate in rats.

  12. Atypical moral judgment following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Angelica Muresan

    2012-07-01

    Full Text Available Previous research has shown an association between emotions, particularly social emotions, and moral judgments. Some studies suggested an association between blunted emotion and the utilitarian moral judgments observed in patients with prefrontal lesions. In order to investigate how prefrontal brain damage affects moral judgment, we asked a sample of 29 TBI patients (12 females and 17 males and 41 healthy participants (16 females and 25 males to judge 22 hypothetical dilemmas split into three different categories (non-moral, impersonal and personal moral. The TBI group presented a higher proportion of affirmative (utilitarian responses for personal moral dilemmas when compared to controls, suggesting an atypical pattern of utilitarian judgements. We also found a negative association between the performance on recognition of social emotions and the proportion of affirmative responses on personal moral dilemmas. These results suggested that the preference for utilitarian responses in this type of dilemmas is accompanied by difficulties in social emotion recognition. Overall, our findings suggest that deontological moral judgments are associated with normal social emotion processing and that frontal lobe plays an important role in both emotion and moral judgment.

  13. Brain tumor imaging of rat fresh tissue using terahertz spectroscopy

    Science.gov (United States)

    Yamaguchi, Sayuri; Fukushi, Yasuko; Kubota, Oichi; Itsuji, Takeaki; Ouchi, Toshihiko; Yamamoto, Seiji

    2016-07-01

    Tumor imaging by terahertz spectroscopy of fresh tissue without dye is demonstrated using samples from a rat glioma model. The complex refractive index spectrum obtained by a reflection terahertz time-domain spectroscopy system can discriminate between normal and tumor tissues. Both the refractive index and absorption coefficient of tumor tissues are higher than those of normal tissues and can be attributed to the higher cell density and water content of the tumor region. The results of this study indicate that terahertz technology is useful for detecting brain tumor tissue.

  14. Accumulation of 23 kDa lipocalin during brain development and injury in Hyphantria cunea.

    Science.gov (United States)

    Kim, Hong Ja; Je, Hyun Jeong; Cheon, Hyang Mi; Kong, Sun Young; Han, JikHyun; Yun, Chi Young; Han, Yeon Su; Lee, In Hee; Kang, Young Jin; Seo, Sook Jae

    2005-10-01

    The cDNA corresponding to a novel lipocalin was identified from the fall webworm, Hyphantria cunea. This lipocalin cDNA encodes a 194 residue protein with a calculated molecular mass of 23 kDa. Sequence analyses revealed that the 23 kDa lipocalin cDNA is most similar to Drosophila lazarillo, human apolipoprotein D, and Bombyrin. Northern blot analyses showed that 23 kDa lipocalin transcript is expressed in the whole body only in 4- and 6-day-old pupae. By Western blot analysis it was confirmed that 23 kDa lipocalin is mainly accumulated in brain and subesophageal ganglion, though it is detected in a small amount in fat body and epidermis of Hyphantria cunea. The accumulation of 23 kDa lipocalin in brain tissue was upregulated in response to injury. The putative function of 23 kDa lipocalin in brain is discussed.

  15. The Protective Effect of Rosuvastatin on Ischemic Brain Injury and Its Mechanism

    Institute of Scientific and Technical Information of China (English)

    2006-01-01

    To study the protective effect of rosuvastatin on ischemic brain injury and its mechanism,in on ischemic brain injury and its mechanism,focal cerebral ischemia/reperfusion was induced by occlusion of the middle cerebral artery (MCA)-luminal filament technique. The cerebral blood flow was monitored with laser-Doppler flowmetry (LDF). The slices of brain tissue were stained with cresyl-violet. The cerebral e quantified with ImageJ software. The expressions of endothelial NO synthase (eNOS) and activated caspase-3 were detected with Western blot. The inducible NO were immunohistochemically observed. The results demonstrated that rosuvastatin (20 mg/kg) could remarkably decrease infarct volume and cerebral edema after MCAO ots showed that the expression of eNOS in cerebral cortex before and after ischemia was (100±43.3) %, (1668.9±112.2) % respectively (P<0.001), rosuvastatin gulated the expression of eNOS in non-ischemic cortex (P<0.001), whereas in ischemic cortex of rosuvastatin group the expression of eNOS was (1678.8±121.3) %. There was no hemic cortex, nonetheless the expression of activated caspase-3 increased after ischemia, and rosuvastatin significantly diminished it (P<0.01). Immunoaled no iNOS-positive cells in non-ischemic brain area, while in ischemic brain area the number of iNOS positive cells went up, and rosuvastatin could significantly reduced them.'s neural protection on ischemic brain injury are to enhance expression of eNOS, to inhibit expression of iNOS and activated caspase-3.mia/reperfusion; NOS; caspase-3

  16. A peptide for targeted, systemic delivery of imaging and therapeutic compounds into acute brain injuries

    Science.gov (United States)

    Mann, Aman P.; Scodeller, Pablo; Hussain, Sazid; Joo, Jinmyoung; Kwon, Ester; Braun, Gary B.; Mölder, Tarmo; She, Zhi-Gang; Kotamraju, Venkata Ramana; Ranscht, Barbara; Krajewski, Stan; Teesalu, Tambet; Bhatia, Sangeeta; Sailor, Michael J.; Ruoslahti, Erkki

    2016-01-01

    Traumatic brain injury (TBI) is a major health and socio-economic problem, but no pharmacological agent is currently approved for the treatment of acute TBI. Thus, there is a great need for advances in this field. Here, we describe a short peptide (sequence CAQK) identified by in vivo phage display screening in mice with acute brain injury. The CAQK peptide selectively binds to injured mouse and human brain, and systemically injected CAQK specifically homes to sites of brain injury in mouse models. The CAQK target is a proteoglycan complex upregulated in brain injuries. Coupling to CAQK increased injury site accumulation of systemically administered molecules ranging from a drug-sized molecule to nanoparticles. CAQK-coated nanoparticles containing silencing oligonucleotides provided the first evidence of gene silencing in injured brain parenchyma by systemically administered siRNA. These findings present an effective targeting strategy for the delivery of therapeutics in clinical management of acute brain injuries. PMID:27351915

  17. A peptide for targeted, systemic delivery of imaging and therapeutic compounds into acute brain injuries

    Science.gov (United States)

    Mann, Aman P.; Scodeller, Pablo; Hussain, Sazid; Joo, Jinmyoung; Kwon, Ester; Braun, Gary B.; Mölder, Tarmo; She, Zhi-Gang; Kotamraju, Venkata Ramana; Ranscht, Barbara; Krajewski, Stan; Teesalu, Tambet; Bhatia, Sangeeta; Sailor, Michael J.; Ruoslahti, Erkki

    2016-06-01

    Traumatic brain injury (TBI) is a major health and socio-economic problem, but no pharmacological agent is currently approved for the treatment of acute TBI. Thus, there is a great need for advances in this field. Here, we describe a short peptide (sequence CAQK) identified by in vivo phage display screening in mice with acute brain injury. The CAQK peptide selectively binds to injured mouse and human brain, and systemically injected CAQK specifically homes to sites of brain injury in mouse models. The CAQK target is a proteoglycan complex upregulated in brain injuries. Coupling to CAQK increased injury site accumulation of systemically administered molecules ranging from a drug-sized molecule to nanoparticles. CAQK-coated nanoparticles containing silencing oligonucleotides provided the first evidence of gene silencing in injured brain parenchyma by systemically administered siRNA. These findings present an effective targeting strategy for the delivery of therapeutics in clinical management of acute brain injuries.

  18. Effect of PLGA NP size on efficiency to target traumatic brain injury.

    Science.gov (United States)

    Cruz, Luis J; Stammes, Marieke A; Que, Ivo; van Beek, Ermond R; Knol-Blankevoort, Vicky T; Snoeks, Thomas J A; Chan, Alan; Kaijzel, Eric L; Löwik, Clemens W G M

    2016-02-10

    Necrotic cell death occurs exclusively under pathological conditions, such as ischemic diseases. Necrosis imaging is of diagnostic value and enables early measurement of treatment efficiency in ischemic patients. Here we explored the targeted delivery of particles, with diameters of approximately 100nm, 200nm and 800nm, consisting of a poly(lactic-co-glycolic acid) (PLGA) nanoparticle (NP) core coated with a polyethylene glycol-lipid (PEG) layer. Targeted delivery was facilitated by coupling the amino end group of the polyethylene glycol-layer to 800CW imaging agent, which specifically binds to intracellular proteins of cells that have lost membrane integrity, thus revealing the extent of the damaged area. We found that smaller NPs (100nm), with an appropriate coating, diffuse throughout the traumatic brain injury (TBI) in mice. Optical imaging revealed that smaller (100-nm) PEG-coated NPs carrying 800CW penetrated deeper into the mouse brain than large 800CW containing NPs (800nm). The importance of the 800CW as a ligand to target the necrotic tissue was further confirmed in living mice. The ability to achieve brain penetration with smaller NPs is expected to allow more uniform, longer-lasting, and effective delivery of drugs within the brain, and may find application in the treatment of stroke, brain tumors, neuroinflammation, and other brain diseases where the blood-brain barrier is compromised or where local delivery strategies are feasible.

  19. Local neutrophil influx following lateral fluid-percussion brain injury in rats is associated with accumulation of complement activation fragments of the third component (C3) of the complement system.

    Science.gov (United States)

    Keeling, K L; Hicks, R R; Mahesh, J; Billings, B B; Kotwal, G J

    2000-06-01

    Traumatic brain injury can lead to locally destructive secondary events mediated by several inflammatory components. Following lateral fluid-percussion (FP) brain injury in rats, we examined cortical and hippocampal sections for neutrophil infiltration and accumulation of complement component C3. Neutrophil influx into the brain after injury was detected by an improved myeloperoxidase (MPO) microassay and manual cell counting, while C3 accumulation was detected using immunocytochemistry. MPO levels were elevated in the injured cortical tissue, whereas C3 immunoreactivity was increased in both injured cortical and ipsilateral hippocampal sections. These results show that the FP model of head injury leads to an intense local inflammatory reaction and subsequent tissue destruction.

  20. Magnetic Resonance Imaging Profile of Blood–Brain Barrier Injury in Patients With Acute Intracerebral Hemorrhage

    Science.gov (United States)

    Aksoy, Didem; Bammer, Roland; Mlynash, Michael; Venkatasubramanian, Chitra; Eyngorn, Irina; Snider, Ryan W.; Gupta, Sandeep N.; Narayana, Rashmi; Fischbein, Nancy; Wijman, Christine A. C.

    2013-01-01

    Background Spontaneous intracerebral hemorrhage (ICH) is associated with blood–brain barrier (BBB) injury, which is a poorly understood factor in ICH pathogenesis, potentially contributing to edema formation and perihematomal tissue injury. We aimed to assess and quantify BBB permeability following human spontaneous ICH using dynamic contrast‐enhanced magnetic resonance imaging (DCE MRI). We also investigated whether hematoma size or location affected the amount of BBB leakage. Methods and Results Twenty‐five prospectively enrolled patients from the Diagnostic Accuracy of MRI in Spontaneous intracerebral Hemorrhage (DASH) study were examined using DCE MRI at 1 week after symptom onset. Contrast agent dynamics in the brain tissue and general tracer kinetic modeling were used to estimate the forward leakage rate (Ktrans) in regions of interest (ROI) in and surrounding the hematoma and in contralateral mirror–image locations (control ROI). In all patients BBB permeability was significantly increased in the brain tissue immediately adjacent to the hematoma, that is, the hematoma rim, compared to the contralateral mirror ROI (P30 mL) had higher Ktrans values than small hematomas (P<0.005). Ktrans values of lobar hemorrhages were significantly higher than the Ktrans values of deep hemorrhages (P<0.005), independent of hematoma volume. Higher Ktrans values were associated with larger edema volumes. Conclusions BBB leakage in the brain tissue immediately bordering the hematoma can be measured and quantified by DCE MRI in human ICH. BBB leakage at 1 week is greater in larger hematomas as well as in hematomas in lobar locations and is associated with larger edema volumes. PMID:23709564

  1. Pharmacologically induced hypothermia attenuates traumatic brain injury in neonatal rats.

    Science.gov (United States)

    Gu, Xiaohuan; Wei, Zheng Zachory; Espinera, Alyssa; Lee, Jin Hwan; Ji, Xiaoya; Wei, Ling; Dix, Thomas A; Yu, Shan Ping

    2015-05-01

    Neonatal brain trauma is linked to higher risks of mortality and neurological disability. The use of mild to moderate hypothermia has shown promising potential against brain injuries induced by stroke and traumatic brain injury (TBI) in various experimental models and in clinical trials. Conventional methods of physical cooling, however, are difficult to use in acute treatments and in induction of regulated hypothermia. In addition, general anesthesia is usually required to mitigate the negative effects of shivering during physical cooling. Our recent investigations demonstrate the potential therapeutic benefits of pharmacologically induced hypothermia (PIH) using the neurotensin receptor (NTR) agonist HPI201 (formerly known as ABS201) in stroke and TBI models of adult rodents. The present investigation explored the brain protective effects of HPI201 in a P14 rat pediatric model of TBI induced by controlled cortical impact. When administered via intraperitoneal (i.p.) injection, HPI201 induced dose-dependent reduction of body and brain temperature. A 6-h hypothermic treatment, providing an overall 2-3°C reduction of brain and body temperature, showed significant effect of attenuating the contusion volume versus TBI controls. Attenuation occurs whether hypothermia is initiated 15min or 2h after TBI. No shivering response was seen in HPI201-treated animals. HPI201 treatment also reduced TUNEL-positive and TUNEL/NeuN-colabeled cells in the contusion area and peri-injury regions. TBI-induced blood-brain barrier damage was attenuated by HPI201 treatment, evaluated using the Evans Blue assay. HPI201 significantly decreased MMP-9 levels and caspase-3 activation, both of which are pro-apototic, while it increased anti-apoptotic Bcl-2 gene expression in the peri-contusion region. In addition, HPI201 prevented the up-regulation of pro-inflammatory tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6. In sensorimotor activity assessments, rats in the HPI201

  2. FeTPPS Reduces Secondary Damage and Improves Neurobehavioral Functions after Traumatic Brain Injury

    Science.gov (United States)

    Bruschetta, Giuseppe; Impellizzeri, Daniela; Campolo, Michela; Casili, Giovanna; Di Paola, Rosanna; Paterniti, Irene; Esposito, Emanuela; Cuzzocrea, Salvatore

    2017-01-01

    Traumatic brain injury (TBI) determinate a cascade of events that rapidly lead to neuron's damage and death. We already reported that administration of FeTPPS, a 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrin iron III chloride peroxynitrite decomposition catalyst, possessed evident neuroprotective effects in a experimental model of spinal cord damage. The present study evaluated the neuroprotective property of FeTPPS in TBI, using a clinically validated model of TBI, the controlled cortical impact injury (CCI). We observe that treatment with FeTPPS (30 mg/kg, i.p.) reduced: the state of brain inflammation and the tissue hurt (histological score), myeloperoxidase activity, nitric oxide production, glial fibrillary acidic protein (GFAP) and pro-inflammatory cytokines expression and apoptosis process. Moreover, treatment with FeTPPS re-established motor-cognitive function after CCI and it resulted in a reduction of lesion volumes. Our results established that FeTPPS treatment decreases the growth of inflammatory process and the tissue injury associated with TBI. Thus our study confirmed the neuroprotective role of FeTPPS treatment on TBI.

  3. Adult axolotls can regenerate original neuronal diversity in response to brain injury

    Science.gov (United States)

    Amamoto, Ryoji; Huerta, Violeta Gisselle Lopez; Takahashi, Emi; Dai, Guangping; Grant, Aaron K; Fu, Zhanyan; Arlotta, Paola

    2016-01-01

    The axolotl can regenerate multiple organs, including the brain. It remains, however, unclear whether neuronal diversity, intricate tissue architecture, and axonal connectivity can be regenerated; yet, this is critical for recovery of function and a central aim of cell replacement strategies in the mammalian central nervous system. Here, we demonstrate that, upon mechanical injury to the adult pallium, axolotls can regenerate several of the populations of neurons present before injury. Notably, regenerated neurons acquire functional electrophysiological traits and respond appropriately to afferent inputs. Despite the ability to regenerate specific, molecularly-defined neuronal subtypes, we also uncovered previously unappreciated limitations by showing that newborn neurons organize within altered tissue architecture and fail to re-establish the long-distance axonal tracts and circuit physiology present before injury. The data provide a direct demonstration that diverse, electrophysiologically functional neurons can be regenerated in axolotls, but challenge prior assumptions of functional brain repair in regenerative species. DOI: http://dx.doi.org/10.7554/eLife.13998.001 PMID:27156560

  4. Application of Ultrasonic Techniques for Brain Injury Diagnosis

    Energy Technology Data Exchange (ETDEWEB)

    Kasili, P.M.; Mobley, J.; Norton, S.J.; Vo-Dinh, T.

    1999-09-19

    In this work, we evaluate methods for detecting brain injury using ultrasound. We have used simulations of ultrasonic fields in the head to model the phase distortion of the skull. In addition we present experimental data from the crania of large animals. The experimental data help us understand and evaluate the performance of different transducers in acquiring the backscatter data from the brain through the skull. Both the simulations and acquired data illustrate the superiority of lower-frequency (<= 1 MHz) ultrasonic fields for transcranial acquisition of signals from inside the brain. Additionally, the experimental work shows that the higher-frequency (5 MHz) ultrasound can also be useful in acquiring clean nearfield data to help detect the position of the inner boundary of the skull.

  5. Resuscitation speed affects brain injury in a large animal model of traumatic brain injury and shock

    DEFF Research Database (Denmark)

    Sillesen, Martin; Jin, Guang; Johansson, Pär I

    2014-01-01

    infusion speed increment NS (n¿=¿7). Hemodynamic variables over a 6-hour observation phase were recorded. Following euthanasia, brains were harvested and lesion size as well as brain swelling was measured.ResultsBolus FFP resuscitation resulted in greater brain swelling (22.36¿±¿1.03% vs. 15.58¿±¿2.52%, p...

  6. Caffeic acid ameliorates early and delayed brain injuries after focal cerebral ischemia in rats

    Institute of Scientific and Technical Information of China (English)

    Yu ZHOU; San-hua FANG; Yi-lu YE; Li-sheng CHU; Wei-ping ZHANG; Meng-ling WANG; Er-qing WEI

    2006-01-01

    Aim: To investigate the effects of caffeic acid on early and delayed injuries after focal cerebral ischemia in rats, and the possible relation to 5-lipoxygenase inhibition. Methods: Transient focal cerebral ischemia was induced by middle cerebral artery occlusion in Sprague-Dawley rats. Caffeic acid (10 and 50 mg/kg) was ip injected for 5 d after ischemia. The brain injuries were observed, and the levels of cysteinyl leukotrienes and leukotriene B4 in the brain tissue were measured. Results: Caffeic acid (50 mg/kg) ameliorated neurological dysfunction and neuron loss, and decreased infarct volume 24 h after ischemia; it attenuated brain atrophy, infarct volume, and particularly astrocyte proliferation 14 d after ischemia. In addition, it reduced the production of leukotrienes (5-lipoxygenase metabolites) in the ischemic hemispheres 3 h and 7 d after ischemia. Conclusion: Caffeic acid has protective effect on both early and delayed injuries after focal cerebral ischemia in rats; and this effect may partly relate to 5-lipoxygenase inhibition.

  7. Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury

    Directory of Open Access Journals (Sweden)

    Eridan Rocha-Ferreira

    2016-01-01

    Full Text Available Hypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability and the subsequent clinical manifestations. The increased susceptibility to hypoxia-ischaemia (HI of periventricular white matter in preterm infants predisposes the immature brain to motor, cognitive, and sensory deficits, with cognitive impairment associated with earlier gestational age. In term infants HI causes selective damage to sensorimotor cortex, basal ganglia, thalamus, and brain stem. Even though the immature brain is more malleable to external stimuli compared to the adult one, a hypoxic-ischaemic event to the neonate interrupts the shaping of central motor pathways and can affect normal developmental plasticity through altering neurotransmission, changes in cellular signalling, neural connectivity and function, wrong targeted innervation, and interruption of developmental apoptosis. Models of neonatal HI demonstrate three morphologically different types of cell death, that is, apoptosis, necrosis, and autophagy, which crosstalk and can exist as a continuum in the same cell. In the present review we discuss the mechanisms of HI injury to the immature brain and the way they affect plasticity.

  8. Protective effects and time course of Huangqion early-stage free radical injury following brain trauma in rats

    Institute of Scientific and Technical Information of China (English)

    Hongjie Wang; Xingbo Liu; Xun Wang

    2008-01-01

    BACKGROUND: Huangqi (Astragalus mongholicus), a Chinese herb, has already been included in the "Chinese Pharmacopoeia" for the treatment of ischemic cerebrovascular disease. Secondary injury following brain injury is associated with free radical production, and Huangqi possesses the ability to ameliorate free radical-mediated injury. OBJECTIVE: This study was designed to observe the correlation between anti-free-radical properties of Huangqi and early histological changes of brain tissues following traumatic brain injury. DESIGN, TIME AND SETTING: This study, a randomized, controlled, animal experiment, was performed from May 2006 to June 2007 at the Experimental Center of Science and Technology, School of Basic Science, Liaoning Medical University, Jinzhou City, Liaoning Province, China. MATERIALS: Healthy, adult, Sprague Dawley rats of either gender were included. Huangqi injection was purchased from Heilongjiang Provincial Zhenbaodao Pharmaceutical Co., Ltd., China (National License Medical Number: Z23020781). Na+-K+-adenosine triphosphatase (ATPase), Ca2+-ATPase, and Mg2+-ATPase, as well as kits to measure superoxide dismutase (SOD) activity and malondialdehyde (MDA) content, were purchased from Nanjing Jiancheng Biological Reagent Company, China. METHODS: Seventy-two rats were randomly divided into three groups, with 24 rats in each group: (1) sham-operated group: rats were only exposed, but not injured; (2) model group: brain focal laceration rat models were established by free-falling. These groups were intraperitoneally injected with saline, once every 10 hours; (3) Huangqi group: rats were intraperitoneally injected with 4 mL/kg Huangqi (2 g/mL), once every 10 hours, following brain focal laceration by free-falling. MAIN OUTCOME MEASURES: Ultrastructural changes in brain tissue were observed under an electron microscope 24 hours after injury. The water content of brain tissue was measured using the dry-wet weight method. In addition, the activity of ATPase

  9. Blocking lymphocyte trafficking with FTY720 prevents inflammation-sensitized hypoxic-ischemic brain injury in newborns.

    Science.gov (United States)

    Yang, Dianer; Sun, Yu-Yo; Bhaumik, Siddhartha Kumar; Li, Yikun; Baumann, Jessica M; Lin, Xiaoyi; Zhang, Yujin; Lin, Shang-Hsuan; Dunn, R Scott; Liu, Chia-Yang; Shie, Feng-Shiun; Lee, Yi-Hsuan; Wills-Karp, Marsha; Chougnet, Claire A; Kallapur, Suhas G; Lewkowich, Ian P; Lindquist, Diana M; Murali-Krishna, Kaja; Kuan, Chia-Yi

    2014-12-03

    Intrauterine infection (chorioamnionitis) aggravates neonatal hypoxic-ischemic (HI) brain injury, but the mechanisms linking systemic inflammation to the CNS damage remain uncertain. Here we report evidence for brain influx of T-helper 17 (TH17)-like lymphocytes to coordinate neuroinflammatory responses in lipopolysaccharide (LPS)-sensitized HI injury in neonates. We found that both infants with histological chorioamnionitis and rat pups challenged by LPS/HI have elevated expression of the interleukin-23 (IL-23) receptor, a marker of early TH17 lymphocytes, in the peripheral blood mononuclear cells. Post-LPS/HI administration of FTY720 (fingolimod), a sphingosine-1-phosphate receptor agonist that blocks lymphocyte trafficking, mitigated the influx of leukocytes through the choroid plexus and acute induction of nuclear factor-κB signaling in the brain. Subsequently, the FTY720 treatment led to attenuated blood-brain barrier damage, fewer cluster of differentiation 4-positive, IL-17A-positive T-cells in the brain, less proinflammatory cytokine, and better preservation of growth and white matter functions. The FTY720 treatment also provided dose-dependent reduction of brain atrophy, rescuing >90% of LPS/HI-induced brain tissue loss. Interestingly, FTY720 neither opposed pure-HI brain injury nor directly inhibited microglia in both in vivo and in vitro models, highlighting its unique mechanism against inflammation-sensitized HI injury. Together, these results suggest that the dual hit of systemic inflammation and neonatal HI injury triggers early onset of the TH17/IL-17-mediated immunity, which causes severe brain destruction but responds remarkably to the therapeutic blockade of lymphocyte trafficking.

  10. Olive leaf extract inhibits lead poisoning-induced brain injury**

    Institute of Scientific and Technical Information of China (English)

    Yu Wang; Shengqing Wang; Wenhui Cui; Jiujun He; Zhenfu Wang; Xiaolu Yang

    2013-01-01

    Olive leaves have an antioxidant capacity, and olive leaf extract can protect the blood, spleen and hippocampus in lead-poisoned mice. However, little is known about the effects of olive leaf extract on lead-induced brain injury. This study was designed to determine whether olive leaf extract can inhibit lead-induced brain injury, and whether this effect is associated with antioxidant capacity. First, we established a mouse model of lead poisoning by continuous intragastric administration of lead acetate for 30 days. Two hours after successful model establishment, lead-poisoned mice were given olive leaf extract at doses of 250, 500 or 1 000 mg/kg daily by intragastric administration for 50 days. Under the transmission electron microscope, olive leaf extract attenuated neuronal and capil ary injury and reduced damage to organel es and the matrix around the capil aries in the frontal lobe of the cerebral cortex in the lead-poisoned mice. Olive leaf extract at a dose of 1 000 mg/kg had the greatest protective effect. Spectrophotometry showed that olive leaf extract significantly in-creased the activities of superoxide dismutase, catalase, alkaline phosphatase and acid phospha-tase, while it reduced malondialdehyde content, in a dose-dependent manner. Furthermore, im-munohistochemical staining revealed that olive leaf extract dose-dependently decreased Bax pro-tein expression in the cerebral cortex of lead-poisoned mice. Our findings indicate that olive leaf extract can inhibit lead-induced brain injury by increasing antioxidant capacity and reducing apop-tosis.

  11. Injury severity measures for predicting return-to-work after a traumatic brain injury.

    Science.gov (United States)

    Chien, Ding-Kuo; Hwang, Hei-Fen; Lin, Mau-Roung

    2017-01-01

    This study compared the ability of five injury severity measures, namely the Abbreviated Injury Scale to the Head (AIS-H), Glasgow Coma Scale (GCS), Glasgow Outcome Scale (GOS), Extended Glasgow Outcome Scale (GOSE), and Injury Severity Score (ISS), to predict return-to-work after a traumatic brain injury (TBI). Furthermore, factors potentially associated with return-to-work were investigated. In total, 207 individuals aged ≤65 years newly diagnosed with a TBI and employed at the time of injury were recruited and followed-up for 1year by telephone every 3 months. A bivariate proportional hazards model analysis revealed that all five injury severity measures were significantly associated with return-to-work after a TBI. The AIS-H and non-head ISS explained 23.8% of the variation in the duration of returning to work from discharge after hospitalization for a TBI; similarly, the GCS, GOS, GOSE, and ISS respectively accounted for 4.7%, 21.4%, 12.9%, and 48.4% of the variation. A multivariable analysis revealed that individuals with higher injury severity as measured by the ISS (hazard ratio [HR], 0.94; 95% confidence interval [CI], 0.92-0.97), a lack of autonomy in transportation (HR, 2.55; 95% CI, 1.23-5.32), cognitive impairment (HR, 0.47; 95% CI, 0.28-0.79), and depression (HR, 0.97; 95% CI, 0.95-0.99) were significantly less likely to be employed after a TBI. In conclusion, of the five injury severity measures, the ISS may be the most capable measure of predicting return-to-work after a TBI. In addition to injury severity, autonomy in transportation, cognitive function, and the depressive status may also influence the employment status during the first year after a TBI.

  12. Signal Transduction Pathways Involved in Brain Death-Induced Renal Injury

    NARCIS (Netherlands)

    Bouma, H. R.; Ploeg, R. J.; Schuurs, T. A.

    2009-01-01

    Kidneys derived from brain death organ donors show an inferior survival when compared to kidneys derived from living donors. Brain death is known to induce organ injury by evoking an inflammatory response in the donor. Neuronal injury triggers an inflammatory response in the brain, leading to endoth

  13. Art Therapy for Individuals with Traumatic Brain Injury: A Comprehensive Neurorehabilitation-Informed Approach to Treatment

    Science.gov (United States)

    Kline, Tori

    2016-01-01

    I describe an approach to art therapy treatment for survivors of traumatic brain injury developed at a rehabilitation facility for adults that serves inpatient, outpatient, and long-term residential clients. This approach is based on a review of the literature on traumatic brain injury, comprehensive neurorehabilitation, brain plasticity, and art…

  14. Effects of NOS inhibitor on dentate gyrus neurogenesis after diffuse brain injury in the adult rats

    Institute of Scientific and Technical Information of China (English)

    SunLi-Sha; XuJiang-ping

    2004-01-01

    Objective To investigate the effects of selective nitric oxide synthase (NOS) inhibitors on dentate gyrus neurogenesis after diffuse brain injury (DBI) in the adult rat brain. Methods Adult male SD rats were subjected to diffuse brain injury (DBI) model. By using systemic bromodeoxyuridine (BrdU) to label dividing cells, we compared the proliferation rate of

  15. Therapeutic administration of plasminogen activator inhibitor-1 prevents hypoxic-ischemic brain injury in newborns.

    Science.gov (United States)

    Yang, Dianer; Nemkul, Niza; Shereen, Ahmed; Jone, Alice; Dunn, R Scott; Lawrence, Daniel A; Lindquist, Diana; Kuan, Chia-Yi

    2009-07-08

    Disruption of the integrity of the blood-brain barrier (BBB) is an important mechanism of cerebrovascular diseases, including neonatal cerebral hypoxia-ischemia (HI). Although both tissue-type plasminogen activator (tPA) and matrix metalloproteinase-9 (MMP-9) can produce BBB damage, their relationship in neonatal cerebral HI is unclear. Here we use a rodent model to test whether the plasminogen activator (PA) system is critical for MMP-9 activation and HI-induced brain injury in newborns. To test this hypothesis, we examined the therapeutic effect of intracerebroventricular injection of plasminogen activator inhibitor-1 (PAI-1) in rat pups subjected to unilateral carotid artery occlusion and systemic hypoxia. We found that the injection of PAI-1 greatly reduced the activity of both tPA and urokinase-type plasminogen activator after HI. It also blocked HI-induced MMP-9 activation and BBB permeability at 24 h of recovery. Furthermore, magnetic resonance imaging and histological analysis showed the PAI-1 treatment reduced brain edema, axonal degeneration, and cortical cell death at 24-48 h of recovery. Finally, the PAI-1 therapy provided a dose-dependent decrease of brain tissue loss at 7 d of recovery, with the therapeutic window at 4 h after the HI insult. Together, these results suggest that the brain PA system plays a pivotal role in neonatal cerebral HI and may be a promising therapeutic target in infants suffering hypoxic-ischemic encephalopathy.

  16. Mean cortical curvature reflects cytoarchitecture restructuring in mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Jace B. King

    2016-01-01

    Full Text Available In the United States alone, the number of persons living with the enduring consequences of traumatic brain injuries is estimated to be between 3.2 and 5 million. This number does not include individuals serving in the United States military or seeking care at Veterans Affairs hospitals. The importance of understanding the neurobiological consequences of mild traumatic brain injury (mTBI has increased with the return of veterans from conflicts overseas, many of who have suffered this type of brain injury. However, identifying the neuroanatomical regions most affected by mTBI continues to prove challenging. The aim of this study was to assess the use of mean cortical curvature as a potential indicator of progressive tissue loss in a cross-sectional sample of 54 veterans with mTBI compared to 31 controls evaluated with MRI. It was hypothesized that mean cortical curvature would be increased in veterans with mTBI, relative to controls, due in part to cortical restructuring related to tissue volume loss. Mean cortical curvature was assessed in 60 bilateral regions (31 sulcal, 29 gyral. Of the 120 regions investigated, nearly 50% demonstrated significantly increased mean cortical curvature in mTBI relative to controls with 25% remaining significant following multiple comparison correction (all, pFDR < .05. These differences were most prominent in deep gray matter regions of the cortex. Additionally, significant relationships were found between mean cortical curvature and gray and white matter volumes (all, p < .05. These findings suggest potentially unique patterns of atrophy by region and indicate that changes in brain microstructure due to mTBI are sensitive to measures of mean curvature.

  17. Military-related traumatic brain injury and neurodegeneration.

    Science.gov (United States)

    McKee, Ann C; Robinson, Meghan E

    2014-06-01

    Mild traumatic brain injury (mTBI) includes concussion, subconcussion, and most exposures to explosive blast from improvised explosive devices. mTBI is the most common traumatic brain injury affecting military personnel; however, it is the most difficult to diagnose and the least well understood. It is also recognized that some mTBIs have persistent, and sometimes progressive, long-term debilitating effects. Increasing evidence suggests that a single traumatic brain injury can produce long-term gray and white matter atrophy, precipitate or accelerate age-related neurodegeneration, and increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease. In addition, repetitive mTBIs can provoke the development of a tauopathy, chronic traumatic encephalopathy. We found early changes of chronic traumatic encephalopathy in four young veterans of the Iraq and Afghanistan conflict who were exposed to explosive blast and in another young veteran who was repetitively concussed. Four of the five veterans with early-stage chronic traumatic encephalopathy were also diagnosed with posttraumatic stress disorder. Advanced chronic traumatic encephalopathy has been found in veterans who experienced repetitive neurotrauma while in service and in others who were accomplished athletes. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus; septal abnormalities; and abnormal deposits of hyperphosphorylated tau as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy has clinical and

  18. Endoplasmic reticulum stress, diabetes mellitus, and tissue injury.

    Science.gov (United States)

    Huang, Liu; Xie, Hong; Liu, Hao

    2014-01-01

    Endoplasmic reticulum (ER) stress is characterized by the accumulation of unfolded and misfolded proteins in the ER lumen. Unfolded and misfolded protein accumulation interferes with the ER function and triggers ER stress response. Thus, ER stress response, also called unfolded protein response (UPR), is an adaptive process that controls the protein amount in the ER lumen and the downstream protein demand. In normal conditions, the role of ER stress is to maintain ER homeostasis, restore ER function, and protect stressed cells from apoptosis, by coordinating gene expression, protein synthesis, and accelerating protein degradation through several molecular pathways. However, prolonged ER stress response plays a paradoxical role, which leads to cell damage, apoptosis, and concomitant tissue injuries. A number of tissue alterations are involved with diabetes mellitus progress and its comorbidities via ER stress. However, certain pharmacological agents affecting ER stress have been identified. In this review, we summarized the relationship between ER stress and insulin resistance development. Moreover, we aim to explain how ER stress influences type 2 diabetes mellitus (T2DM) development. In addition, we reviewed the literature on ER stress and UPR in three kinds of tissue injuries induced by T2DM. Finally, a retrospective analysis of the effects of anti-diabetes medications on ER stress is presented.

  19. The Relation of Focal Lesions to Cortical Thickness in Pediatric Traumatic Brain Injury.

    Science.gov (United States)

    Bigler, Erin D; Zielinski, Brandon A; Goodrich-Hunsaker, Naomi; Black, Garrett M; Huff, B S Trevor; Christiansen, Zachary; Wood, Dawn-Marie; Abildskov, Tracy J; Dennis, Maureen; Taylor, H Gerry; Rubin, Kenneth; Vannatta, Kathryn; Gerhardt, Cynthia A; Stancin, Terry; Yeates, Keith Owen

    2016-10-01

    In a sample of children with traumatic brain injury, this magnetic resonance imaging (MRI)-based investigation examined whether presence of a focal lesion uniquely influenced cortical thickness in any brain region. Specifically, the study explored the relation of cortical thickness to injury severity as measured by Glasgow Coma Scale score and length of stay, along with presence of encephalomalacia, focal white matter lesions or presence of hemosiderin deposition as a marker of shear injury. For comparison, a group of children without head injury but with orthopedic injury of similar age and sex were also examined. Both traumatic brain injury and orthopedic injury children had normally reduced cortical thickness with age, assumed to reflect neuronal pruning. However, the reductions observed within the traumatic brain injury sample were similar to those in the orthopedic injury group, suggesting that in this sample traumatic brain injury, per se, did not uniquely alter cortical thickness in any brain region at the group level. Injury severity in terms of Glasgow Coma Scale or longer length of stay was associated with greater reductions in frontal and occipitoparietal cortical thickness. However, presence of focal lesions were not related to unique changes in cortical thickness despite having a prominent distribution of lesions within frontotemporal regions among children with traumatic brain injury. Because focal lesions were highly heterogeneous, their association with cortical thickness and development appeared to be idiosyncratic, and not associated with group level effects.

  20. Are boys and girls that different? An analysis of traumatic brain injury in children.

    LENUS (Irish Health Repository)

    Collins, Niamh C

    2013-08-01

    The Phillips Report on traumatic brain injury (TBI) in Ireland found that injury was more frequent in men and that gender differences were present in childhood. This study determined when gender differences emerge and examined the effect of gender on the mechanism of injury, injury type and severity and outcome.