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Sample records for brain injury protects

  1. 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

  2. Suppression of Etk/Bmx protects against ischemic brain injury.

    Science.gov (United States)

    Chen, Kai-Yun; Wu, Chung-Che; Chang, Cheng-Fu; Chen, Yuan-Hao; Chiu, Wen-Ta; Lou, Ya-Hsin; Chen, Yen-Hua; Shih, Hsiu-Ming; Chiang, Yung-Hsiao

    2012-01-01

    Etk/Bmx (epithelial and endothelial tyrosine kinase, also known as BMX), a member of the Tec (tyrosine kinase expressed in hepatocellular carcinoma) family of protein-tyrosine kinases, is an important regulator of signal transduction for the activation of cell growth, differentiation, and development. We have previously reported that activation of Etk leads to apoptosis in MDA-MB-468 cells. The purpose of this study was to examine the role of Etk in neuronal injury induced by H(2)O(2) or ischemia. Using Western blot analysis and immunohistochemistry, we found that treatment with H(2)O(2) significantly enhanced phosphorylation of Etk and its downstream signaling molecule Stat1 in primary cortical neurons. Inhibiting Etk activity by LFM-A13 or knocking down Etk expression by a specific shRNA increased the survival of primary cortical neurons. Similarly, at 1 day after a 60-min middle cerebral artery occlusion (MCAo) in adult rats, both phosphorylated Etk and Stat1 were coexpressed with apoptotic markers in neurons in the penumbra. Pretreatment with LFM-A13 or an adenoviral vector encoding the kinase deletion mutant Etkk attenuated caspase-3 activity and infarct volume in ischemic brain. All together, our data suggest that Etk is activated after neuronal injury. Suppressing Etk activity protects against neurodegeneration in ischemic brain.

  3. 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

  4. Inhibition of histone deacetylation protects wildtype but not gelsolin-deficient mice from ischemic brain injury.

    Science.gov (United States)

    Yildirim, Ferah; Gertz, Karen; Kronenberg, Golo; Harms, Christoph; Fink, Klaus B; Meisel, Andreas; Endres, Matthias

    2008-04-01

    Acetylation/deactylation of histones is an important mechanism to regulate gene expression and chromatin remodeling. We have previously demonstrated that the HDAC inhibitor trichostatin A (TSA) protects cortical neurons from oxygen/glucose deprivation in vitro which is mediated--at least in part--via the up regulation of gelsolin expression. Here, we demonstrate that TSA treatment dose-dependently enhances histone acetylation in brains of wildtype mice as evidenced by immunoblots of total brain lysates and immunocytochemical staining. Along with increased histone acetylation dose-dependent up regulation of gelsolin protein was observed. Levels of filamentous actin were largely decreased by TSA pre-treatment in brain of wildtype but not gelsolin-deficient mice. When exposed to 1 h filamentous occlusion of the middle cerebral artery followed by reperfusion TSA pre-treated wildtype mice developed significantly smaller cerebral lesion volumes and tended to have improved neurological deficit scores compared to vehicle-treated mice. These protective effects could not be explained by apparent changes in physiological parameters. In contrast to wildtype mice, TSA pre-treatment did not protect gelsolin-deficient mice against MCAo/reperfusion suggesting that enhanced gelsolin expression is an important mechanism by which TSA protects against ischemic brain injury. Our results suggest that HDAC inhibitors such as TSA are a promising therapeutic strategy for reducing brain injury following cerebral ischemia.

  5. Blockade of N-acetylaspartylglutamate peptidases: a novel protective strategy for brain injuries and neurological disorders.

    Science.gov (United States)

    Zhong, Chunlong; Luo, Qizhong; Jiang, Jiyao

    2014-12-01

    The peptide neurotransmitter N-acetylaspartylglutamate (NAAG) is reported to suppress glutamate release mainly through selective activation of presynaptic Group II metabotropic glutamate receptor subtype 3 (mGluR3). Therefore, strategies of inhibition of NAAG peptidases and subsequent NAAG hydrolysis to elevate levels of NAAG could reduce glutamate release under pathological conditions and be neuroprotective by attenuating excitotoxic cell injury. A series of potent inhibitors of NAAG peptidases has been synthesized and demonstrated efficacy in experimental models of ischemic-hypoxic brain injury, traumatic brain injury, inflammatory pain, diabetic neuropathy, amyotrophic lateral sclerosis and phencyclidine-induced schizophrenia-like behaviors. The excessive glutamatergic transmission has been implicated in all of these neurological disorders. Thus, blockade of NAAG peptidases may augment an endogenous protective mechanism and afford neuroprotection in the brain. This review aims to summarize and provide insight into the current understanding of the novel neuroprotective strategy based on limiting glutamate excitotoxicity for a wide variety of brain injuries and neurological disorders.

  6. 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

  7. Treatment with Isorhamnetin Protects the Brain Against Ischemic Injury in Mice.

    Science.gov (United States)

    Zhao, Jin-Jing; Song, Jin-Qing; Pan, Shu-Yi; Wang, Kai

    2016-08-01

    Ischemic stroke is a major cause of morbidity and mortality, yet lacks effective neuroprotective treatments. The aim of this work was to investigate whether treatment with isorhamnetin protected the brain against ischemic injury in mice. Experimental stroke mice underwent the filament model of middle cerebral artery occlusion with reperfusion. Treatment with isorhamnetin or vehicle was initiated immediately at the onset of reperfusion. It was found that treatment of experimental stroke mice with isorhamnetin reduced infarct volume and caspase-3 activity (a biomarker of apoptosis), and improved neurological function recovery. Treatment of experimental stroke mice with isorhamnetin attenuated cerebral edema, improved blood-brain barrier function, and upregulated gene expression of tight junction proteins including occludin, ZO-1, and claudin-5. Treatment of experimental stroke mice with isorhamnetin activated Nrf2/HO-1, suppressed iNOS/NO, and led to reduced formation of MDA and 3-NT in ipsilateral cortex. In addition, treatment of experimental stroke mice with isorhamnetin suppressed activity of MPO (a biomarker of neutrophil infiltration) and reduced protein levels of IL-1β, IL-6, and TNF-α in ipsilateral cortex. Furthermore, it was found that treatment of experimental stroke mice with isorhamnetin reduced mRNA and protein expression of NMDA receptor subunit NR1 in ipsilateral cortex. In conclusion, treatment with isorhamnetin protected the brain against ischemic injury in mice. Isorhamnetin could thus be envisaged as a countermeasure for ischemic stroke but remains to be tested in humans.

  8. 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 ...

  9. 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 ...

  10. Protective effects of taurine in traumatic brain injury via mitochondria and cerebral blood flow.

    Science.gov (United States)

    Wang, Qin; Fan, Weijia; Cai, Ying; Wu, Qiaoli; Mo, Lidong; Huang, Zhenwu; Huang, Huiling

    2016-09-01

    In mammalian tissues, taurine is an important natural component and the most abundant free amino acid in the heart, retina, skeletal muscle, brain, and leukocytes. This study is to examine the taurine's protective effects on neuronal ultrastructure, the function of the mitochondrial respiratory chain complex, and on cerebral blood flow (CBF). The model of traumatic brain injury (TBI) was made for SD rats by a fluid percussion device, with taurine (200 mg/kg) administered by tail intravenous injection once daily for 7 days after TBI. It was found that CBF was improved for both left and right brain at 30 min and 7 days post-injury by taurine. Reaction time was prolonged relative to the TBI-only group. Neuronal damage was prevented by 7 days taurine. Mitochondrial electron transport chain complexes I and II showed greater activity with the taurine group. The improvement by taurine of CBF may alleviate edema and elevation in intracranial pressure. Importantly taurine improved the hypercoagulable state.

  11. Protective effects of Guizhi-Fuling-Capsules on rat brain ischemia/reperfusion injury.

    Science.gov (United States)

    Li, Tie-Jun; Qiu, Yan; Mao, Jun-Qin; Yang, Peng-Yuan; Rui, Yao-Cheng; Chen, Wan-Sheng

    2007-09-01

    Previous studies revealed that Guizhi-Fuling-Capsules (GZFLC), a traditional Chinese medical (Kampo) formulation composed of five kinds of medicinal plants, Cinnamomum cassia BLUME (Cinnamomi Cortex), Paeonia lactiflora PALL. (Peonies Radix), Paeonia suffruticosa ANDREWS (Moutan Cortex), Prunus persica BATSCH (Persicae Semen), and Poria cocos WOLF (Hoelen), exerts a protective effect against vascular injury and has a protective effect against glutamate- or nitro oxide-mediated neuronal damage. In the present study, the effect of GZFLC in a rat in vivo model of focal cerebral ischemia and reperfusion was investigated. Administration of GZFLC (0.3 and 0.9 g/kg, p.o.) after focal cerebral ischemia significantly decreased brain infarction and water contents in rats subjected to 2-h ischemia followed by 24-h reperfusion from 31.72 +/- 2.49%, 84.76 +/- 1.63% in the model group to 17.31 +/- 3.66%, 82.51 +/- 1.36% and 8.30 +/- 3.73%, 81.35 +/- 1.73%, respectively. Furthermore, analysis of inflammatory cytokines in ischemic brain showed that GZFLC treatment significantly down-regulated expressions of pro-inflammatory cytokines including interleukin (IL)-1beta and tissue necrosis factor-alpha and markedly up-regulated expressions of anti-inflammatory cytokines IL-10 and IL-10R both in mRNA and protein levels. The serum levels of these inflammatory cytokines were also regulated the same way. These results suggested that GZFLC may be beneficial for the treatment of brain ischemia-reperfusion injury partly due to its anti-inflammatory properties.

  12. 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...

  13. Pretreatment with Danhong injection protects the brain against ischemia-reperfusion injury.

    Science.gov (United States)

    Wang, Shaoxia; Guo, Hong; Wang, Xumei; Chai, Lijuan; Hu, Limin; Zhao, Tao; Zhao, Buchang; Tan, Xiaoxu; Jia, Feifei

    2014-08-01

    Danhong injection (DHI), a Chinese Materia Medica standardized product extracted from Radix Salviae miltiorrhizae and Flos Carthami tinctorii, is widely used in China for treating acute ischemic stroke. In the present study, we explored the neuroprotective efficacy of DHI in a rat model of temporary middle cerebral artery occlusion, and evaluated the potential mechanisms underlying its effects. Pretreatment with DHI (0.9 and 1.8 mL/kg) resulted in a significantly smaller infarct volume and better neurological scores than pretreatment with saline. Furthermore, DHI significantly reduced the permeability of the blood-brain barrier, increased occludin protein expression and decreased neutrophil infiltration, as well as profoundly suppressing the upregulation of matrix metallopeptidase-9 expression seen in rats that had received vehicle. Matrix metallopeptidase-2 expression was not affected by ischemia or DHI. Moreover, DHI (1.8 mL/kg) administered 3 hours after the onset of ischemia also improved neurological scores and reduced infarct size. Our results indicate that the neuroprotective efficacy of DHI in a rat model of cerebral ischemia-reperfusion injury is mediated by a protective effect on the blood-brain barrier and the reversal of neutrophil infiltration.

  14. 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 ...

  15. 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.

  16. Protective effects of ω-3 PUFA on the second liver injury in rats with traumatic brain injury and hemorrhagic shock

    Institute of Scientific and Technical Information of China (English)

    许会彬

    2014-01-01

    Objective To investigate the effects of preconditioning withω-3 polyunsaturated fatty acid(ω-3 PUFA)on the second liver injury in rats with traumatic brain injury and hemorrhagic shock(TBIS)and explore the underlying mechanism.Methods Total of 36 male Wistar rats were assigned randomly(random number)into 3 groups(n=12 in each):sham

  17. Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury

    DEFF Research Database (Denmark)

    Penkowa, Milena; Giralt, Mercedes; Lago, Natalia

    2003-01-01

    The effect of CNS-targeted IL-6 gene expression has been thoroughly investigated in the otherwise nonperturbed brain but not following brain injury. Here we examined the impact of astrocyte-targeted IL-6 production in a traumatic brain injury (cryolesion) model using GFAP-IL6 transgenic mice...... significantly increased up to but not including 20 dpl in the GFAP-IL6 mice. Oxidative stress as well as apoptotic cell death was significantly decreased throughout the time period studied in the GFAP-IL6 mice compared to controls. This could be linked to the altered inflammatory response as well...... as to the transgenic IL-6-induced increase of the antioxidant, neuroprotective proteins metallothionein-I + II. These results indicate that although in the brain the chronic astrocyte-targeted expression of IL-6 spontaneously induces an inflammatory response causing significant damage, during an acute...

  18. 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

    and SOD, as well as MDA content, was analyzed using biochemical indicators at 4, 24, and 48 hours after injury. RESULTS: All 72 rats were included in the fmal analysis. At 4, 24, and 48 hours after injury, ATPase activity was significantly reduced in the model and Huangqi groups than in the sham-operated group (P 0.05). At 24 and 48 hours after injury, ATPase activity in the Huangqi group gradually decreased, but remained significantly greater than that in the model group (P<0.05). At four hours after injury, when compared with the sham-operated group, the MDA content in the model group significantly increased and remained at a high level, while SOD activity significantly decreased (P<0.05). In the Huangqi group, MDA content and SOD activity did not change at four hours after injury. However, MDA content significantly decreased, and SOD activity significantly increased, at 24 and 48 hours after injury, compared with the model group (P<0.05). Moreover, at 24 and 48 hours after injury, the water content of brain tissue was significantly lower in the Huangqi group than in the model group (P<0.05). Ultrastructural examination of cerebral cortical neurons revealed severe damage in the model group, compared to the sham-operated group, while only mild injury was observed in the Huangqi group. CONCLUSION: The protective effects of Huangqi against traumatic brain injury correlates with decreasing MDA content and increasing SOD activity.

  19. Citicoline protects brain against closed head injury in rats through suppressing oxidative stress and calpain over-activation.

    Science.gov (United States)

    Qian, Ke; Gu, Yi; Zhao, Yumei; Li, Zhenzong; Sun, Ming

    2014-07-01

    Citicoline, a natural compound that functions as an intermediate in the biosynthesis of cell membrane phospholipids, is essential for membrane integrity and repair. It has been reported to protect brain against trauma. This study was designed to investigate the protective effects of citicoline on closed head injury (CHI) in rats. Citicoline (250 mg/kg i.v. 30 min and 4 h after CHI) lessened body weight loss, and improved neurological functions significantly at 7 days after CHI. It markedly lowered brain edema and blood-brain barrier permeability, enhanced the activities of superoxide dismutase and the levels of glutathione, reduced the levels of malondialdehyde and lactic acid. Moreover, citicoline suppressed the activities of calpain, and enhanced the levels of calpastatin, myelin basic protein and αII-spectrin in traumatic tissue 24 h after CHI. Also, it attenuated the axonal and myelin sheath damage in corpus callosum and the neuronal cell death in hippocampal CA1 and CA3 subfields 7 days after CHI. These data demonstrate the protection of citicoline against white matter and grey matter damage due to CHI through suppressing oxidative stress and calpain over-activation, providing additional support to the application of citicoline for the treatment of traumatic brain injury.

  20. A Fluid Helmet Liner for Protection Against Blast Induced Traumatic Brain Injury

    Science.gov (United States)

    2010-05-01

    Induced Traumatic Brain Injury 5a. CONTRACT NUMBER 5b. GRANT NUMBER N00014-08-1-0261 5c. PROGRAM ELEMENT NUMBER 6. AUTHOR(S) Young, Laurence , R... Laurence R. Young Steven F. Son George A. Christou Matthew D. Alley Rahul Goel Andrew P. Vechart Benjamin R. Schimizze Table of Contents...Beach, South Carolina, Battelle Press, Columbus, pp. 29-38,1997. 10. Grover ,R., Ree , F. A., and Holmes, N., "Equation of state from Si02 Aerogel

  1. Protective effect of anisodamine on respiratory function after severe brain injury

    Institute of Scientific and Technical Information of China (English)

    黄强; 戴伟民; 揭园庆; 余国峰

    2002-01-01

    Objective: To study the clinical therapeutic effect of anisodamine on respiratory function after severe brain injury.Methods: Ninety patients with respiratory dysfunction following severe brain injury were divided into two groups: a treatment group (n=45, treated with routine therapy plus anisodamine) and a control group (n=45, treated with routine therapy only). The pulmonary ventilation function and oxygenation function were compared between the two groups.Results: In the treatment group, 12 hours after treatment the respiratory rate reduced, the partial pressure of carbon dioxide (PCO2), the partial pressure of oxygen in arterial blood (PaO2) and oxygenation exponent increased, the dead space ventilation dose and the pulmonary alveolus-partial pressure of arterial oxygen difference decreased, and the ventilation function of the respiratory tract and pulmonary oxygenation function improved. There was a significant difference between the two groups (P<0.01). No side-effect was found except a slight increase of intracranial pressure and heart rate.Conclusions: Anisodamine can improve pulmonary ventilation function and oxygenation function and decrease the incidence of hypoxemia markedly. It is effective in treating respiratory dysfunction after severe brain injury.

  2. Protective Effects of Salubrinal on Liver Injury in Rat Models of Brain Death

    Institute of Scientific and Technical Information of China (English)

    Tao Wang; Shui-Jun Zhang; Sheng-Li Cao; Wen-Zhi Guo; Bing Yan; Hong-Bo Fang

    2015-01-01

    Background:Previous studies have indicated that endoplasmic reticulum stress participates in and mediates liver injury and apoptosis in brain-dead (BD) rats.In this study,we observed the effect ofsalubrinal (Sal,Sigma,USA) on liver cells in BD rats and explored its relevant mechanisms.Methods:Thirty Sprague-Dawley rats were equally randomized into three groups:BD group,Sal group,and DMSO group.The BD models were established by increasing intracranial pressure in a modified,slow,and intermittent way.In the drug groups,Sal was administered l h before the induction of BD.After modeling was completed,the blood and liver samples were harvested.CHOP and Caspase-12 mRNA expression was detected using quantitative polymerase chain reaction.PKR-like ER kinase (PERK),P-eukaryotic translation initiation factor 2α (eIF2α),eIF2α,CHOP and caspase-12 expression was detected using western blotting (WB).CHOP and caspase-12 distribution and expression in liver tissues were determined using immunohistochemistry (IHC).Alanine aminotransferase and aspartate aminotransferase level were detected using an automatic biochemical analyzer.Hepatic cell apoptosis was detected using TUNEL.The results were analyzed using Quantity-one v4.62 software (Bio-Rad,USA).Results:CHOP and caspase-12 expression and PERK,eIF2α,and P-eIF2α protein expression showed no significant difference between BD group and DMSO group.Compared with BD group,Sal group had a significantly higher P-eIF2C level and a lower P-PERK level 2 h and 6 h after BD (P < 0.05).However,eIF2α expression showed no significant difference (P > 0.05).After the Sal treatment,CHOP and caspase-12 mRNA expression significantly decreased 4 h after BD (P < 0.05).WB and IHC indicated that CHOP and caspase-12 expression also significantly decreased after Sal treatment.Sal was associated with improved liver function and decreased hepatic cell apoptosis.Conclusions:Sal can significantly reduce apoptosis in hepatic cells of BD rats

  3. Methylophiopogonanone A Protects against Cerebral Ischemia/Reperfusion Injury and Attenuates Blood-Brain Barrier Disruption In Vitro.

    Directory of Open Access Journals (Sweden)

    Mingbao Lin

    Full Text Available Methylophiopogonanone A (MO-A, an active homoisoflavonoid of the Chinese herb Ophiopogon japonicus which has been shown to have protective effects on cerebral ischemia/reperfusion (I/R injury, has been demonstrated to have anti-inflammatory and anti-oxidative properties. However, little is known about its role in cerebral I/R injury. Therefore, in this study, by using a middle cerebral artery occlusion (MCAO and reperfusion rat model, the effect of MO-A on cerebral I/R injury was examined. The results showed that MO-A treatment reduced infarct volume and brain edema, improved neurological deficit scores, reversed animal body weight decreases, and increased animal survival time in the stroke groups. Western blotting showed that MO-A suppressed MMP-9, but restored the expression of claudin-3 and claudin-5. Furthermore, transmission electron microscopy were monitored to determine the blood-brain barrier (BBB alterations in vitro. The results showed that MO-A markedly attenuated BBB damage in vitro. Additionally, MO-A inhibited ROS production in ECs and MMP-9 release in differentiated THP-1 cells in vitro, and suppressed ICAM-1 and VCAM-1 expression in ECs and leukocyte/EC adhesion. In conclusion, our data indicate that MO-A has therapeutic potential against cerebral I/R injury through its ability to attenuate BBB disruption by regulating the expression of MMP-9 and tight junction proteins.

  4. Protective effects of carbenoxolone are associated with attenuation of oxidative stress in ischemic brain injury

    Institute of Scientific and Technical Information of China (English)

    Lang Zhang; Yu-Min Li; Yu-Hong Jing; Shao-Yu Wang; Yan-Feng Song; Jie Yin

    2013-01-01

    Accumulating evidence has suggested that the gap junction plays an important role in the determination of cerebral ischemia,but the underlying mechanisms remain to be elucidated.In this study,we assessed the effect of a gap-junction blocker,carbenoxolone (CBX),on ischemia/reperfusion-induced brain injury and the possible mechanisms.By using the transient cerebral ischemia model induced by occlusion of the middle cerebral artery for 30 min followed by reperfusion for 24 h,we found that pre-administration of CBX (25 mg/kg,intracerebroventricular injection,30 min before cerebral ischemic surgery) diminished the infarction size in rats.And this was associated with a decrease of reactive oxygen species generation and inhibition of the activation of astrocytes and microglia.In PC12 cells,H202 treatment induced more coupling and apoptosis,while CBX partly inhibited the opening of gap junctions and improved the cell viability.These results suggest that cerebral ischemia enhances the opening of gap junctions.Blocking the gap junction with CBX may attenuate the brain injury after cerebral ischemia/reperfusion by partially contributing to amelioration of the oxidative stress and apoptosis.

  5. Phenolic Alkaloids from Menispermum dauricum Rhizome Protect against Brain Ischemia Injury via Regulation of GLT-1, EAAC1 and ROS Generation

    OpenAIRE

    Lian-Jun Guo; Jie Ding; Jin-Jin Zhan; Mei Zhou; Xi Sun; Yang Chen; Bo Zhao

    2012-01-01

    Menispermum dauricum rhizome has been widely used in China to treat various cardiovascular and thrombosis disorders. Some studies have reported that the phenolic alkaloids of Menispermum dauricum rhizome (PAM) have protective effects against brain ischemia injury, but the mechanism of this action remains to be clarified. In the present study, we investigated the possible mechanisms of action of PAM on experimental brain ischemia injury. Oxygen and glucose deprivation (OGD) in rat primary cort...

  6. Pycnogenol protects CA3-CA1 synaptic function in a rat model of traumatic brain injury.

    Science.gov (United States)

    Norris, Christopher M; Sompol, Pradoldej; Roberts, Kelly N; Ansari, Mubeen; Scheff, Stephen W

    2016-02-01

    Pycnogenol (PYC) is a patented mix of bioflavonoids with potent anti-oxidant and anti-inflammatory properties. Previously, we showed that PYC administration to rats within hours after a controlled cortical impact (CCI) injury significantly protects against the loss of several synaptic proteins in the hippocampus. Here, we investigated the effects of PYC on CA3-CA1 synaptic function following CCI. Adult Sprague-Dawley rats received an ipsilateral CCI injury followed 15 min later by intravenous injection of saline vehicle or PYC (10 mg/kg). Hippocampal slices from the injured (ipsilateral) and uninjured (contralateral) hemispheres were prepared at seven and fourteen days post-CCI for electrophysiological analyses of CA3-CA1 synaptic function and induction of long-term depression (LTD). Basal synaptic strength was impaired in slices from the ipsilateral, relative to the contralateral, hemisphere at seven days post-CCI and susceptibility to LTD was enhanced in the ipsilateral hemisphere at both post-injury timepoints. No interhemispheric differences in basal synaptic strength or LTD induction were observed in rats treated with PYC. The results show that PYC preserves synaptic function after CCI and provides further rationale for investigating the use of PYC as a therapeutic in humans suffering from neurotrauma.

  7. Neuregulin 1 protects against ischemic brain injury via ErbB4 receptors by increasing GABAergic transmission.

    Science.gov (United States)

    Guan, Y-F; Wu, C-Y; Fang, Y-Y; Zeng, Y-N; Luo, Z-Y; Li, S-J; Li, X-W; Zhu, X-H; Mei, L; Gao, T-M

    2015-10-29

    Identifying novel neuroprotectants that can halt or even reverse the effects of stroke is of interest to both clinicians and scientists. Neuregulin 1 (NRG1) is an effective neuroprotectant, but its molecular mechanisms are largely unclear. In this study, NRG1 rescued cortical neurons from oxygen-glucose deprivation (OGD) model, but the effect was blocked by neutralizing NRG1 and ErbB4 inhibition. In addition, γ-Aminobutyric acid (GABA) receptor agonists had no synergistic effect with NRG1, and the neuroprotective effect of NRG1 against OGD was partly blocked by GABA receptor antagonists. Importantly, NRG1 neuroprotection against brain ischemia was abolished in the mice with specific deletion of ErbB4 in parvalbumin (PV)-positive interneurons. In summary, NRG1 protects against ischemic brain injury via ErbB4 receptors by enhancing GABAergic transmission.

  8. Nelfinavir inhibits intra-mitochondrial calcium influx and protects brain against hypoxic-ischemic injury in neonatal mice.

    Directory of Open Access Journals (Sweden)

    Irina V Utkina-Sosunova

    Full Text Available Nelfinavir (NLF, an antiretroviral agent, preserves mitochondrial membranes integrity and protects mature brain against ischemic injury in rodents. Our study demonstrates that in neonatal mice NLF significantly limits mitochondrial calcium influx, the event associated with protection of the brain against hypoxic-ischemic insult (HI. Compared to the vehicle-treated mice, cerebral mitochondria from NLF-treated mice exhibited a significantly greater tolerance to the Ca(2+-induced membrane permeabilization, greater ADP-phosphorylating activity and reduced cytochrome C release during reperfusion. Pre-treatment with NLF or Ruthenium red (RuR significantly improved viability of murine hippocampal HT-22 cells, reduced Ca(2+ content and preserved membrane potential (Ψm in mitochondria following oxygen-glucose deprivation (OGD. Following histamine-stimulated Ca(2+ release from endoplasmic reticulum, in contrast to the vehicle-treated cells, the cells treated with NLF or RuR also demonstrated reduced Ca(2+ content in their mitochondria, the event associated with preserved Ψm. Because RuR inhibits mitochondrial Ca(2+ uniporter, we tested whether the NLF acts via the mechanism similar to the RuR. However, in contrast to the RuR, in the experiment with direct interaction of these agents with mitochondria isolated from naïve mice, the NLF did not alter mitochondrial Ca(2+ influx, and did not prevent Ca(2+ induced collapse of the Ψm. These data strongly argues against interaction of NLF and mitochondrial Ca(2+ uniporter. Although the exact mechanism remains unclear, our study is the first to show that NLF inhibits intramitochondrial Ca(2+ flux and protects developing brain against HI-reperfusion injury. This novel action of NLF has important clinical implication, because it targets a fundamental mechanism of post-ischemic cell death: intramitochondrial Ca(2+ overload → mitochondrial membrane permeabilization → secondary energy failure.

  9. Overexpression of Extracellular Superoxide Dismutase Protects against Brain Injury Induced by Chronic Hypoxia

    Science.gov (United States)

    Zaghloul, Nahla; Patel, Hardik; Codipilly, Champa; Marambaud, Philippe; Dewey, Stephen; Frattini, Stephen; Huerta, Patricio T.; Nasim, Mansoor; Miller, Edmund J.; Ahmed, Mohamed

    2014-01-01

    Extracellular superoxide dismutase (EC-SOD) is an isoform of SOD normally found both intra- and extra-cellularly and accounting for most SOD activity in blood vessels. Here we explored the role of EC-SOD in protecting against brain damage induced by chronic hypoxia. EC-SOD Transgenic mice, were exposed to hypoxia (FiO2.1%) for 10 days (H-KI) and compared to transgenic animals housed in room air (RA-KI), wild type animals exposed to hypoxia (H-WT or wild type mice housed in room air (RA-WT). Overall brain metabolism evaluated by positron emission tomography (PET) showed that H-WT mice had significantly higher uptake of 18FDG in the brain particularly the hippocampus, hypothalamus, and cerebellum. H-KI mice had comparable uptake to the RA-KI and RA-WT groups. To investigate the functional state of the hippocampus, electrophysiological techniques in ex vivo hippocampal slices were performed and showed that H-KI had normal synaptic plasticity, whereas H-WT were severely affected. Markers of oxidative stress, GFAP, IBA1, MIF, and pAMPK showed similar values in the H-KI and RA-WT groups, but were significantly increased in the H-WT group. Caspase-3 assay and histopathological studies showed significant apoptosis/cell damage in the H-WT group, but no significant difference in the H-KI group compared to the RA groups. The data suggest that EC-SOD has potential prophylactic and therapeutic roles in diseases with compromised brain oxygenation. PMID:25268361

  10. Overexpression of extracellular superoxide dismutase protects against brain injury induced by chronic hypoxia.

    Directory of Open Access Journals (Sweden)

    Nahla Zaghloul

    Full Text Available Extracellular superoxide dismutase (EC-SOD is an isoform of SOD normally found both intra- and extra-cellularly and accounting for most SOD activity in blood vessels. Here we explored the role of EC-SOD in protecting against brain damage induced by chronic hypoxia. EC-SOD Transgenic mice, were exposed to hypoxia (FiO2.1% for 10 days (H-KI and compared to transgenic animals housed in room air (RA-KI, wild type animals exposed to hypoxia (H-WT or wild type mice housed in room air (RA-WT. Overall brain metabolism evaluated by positron emission tomography (PET showed that H-WT mice had significantly higher uptake of 18FDG in the brain particularly the hippocampus, hypothalamus, and cerebellum. H-KI mice had comparable uptake to the RA-KI and RA-WT groups. To investigate the functional state of the hippocampus, electrophysiological techniques in ex vivo hippocampal slices were performed and showed that H-KI had normal synaptic plasticity, whereas H-WT were severely affected. Markers of oxidative stress, GFAP, IBA1, MIF, and pAMPK showed similar values in the H-KI and RA-WT groups, but were significantly increased in the H-WT group. Caspase-3 assay and histopathological studies showed significant apoptosis/cell damage in the H-WT group, but no significant difference in the H-KI group compared to the RA groups. The data suggest that EC-SOD has potential prophylactic and therapeutic roles in diseases with compromised brain oxygenation.

  11. Lung-protective Ventilation in Patients with Brain Injury: A Multicenter Cross-sectional Study and Questionnaire Survey in China

    Institute of Scientific and Technical Information of China (English)

    Xu-Ying Luo; Ying-Hong Hu; Xiang-Yuan Cao; Yan Kang; Li-Ping Liu; Shou-Hong Wang; Rong-Guo Yu

    2016-01-01

    Background:Over the years,the mechanical ventilation (MV) strategy has changed worldwide.The aim of the present study was to describe the ventilation practices,particularly lung-protective ventilation (LPV),among brain-injured patients in China.Methods:This study was a multicenter,1-day,cross-sectional study in 47 Intensive Care Units (ICUs) across China.Mechanically ventilated patients (18 years and older) with brain injury in a participating ICU during the time of the study,including traumatic brain injury,stroke,postoperation with intracranial tumor,hypoxic-ischemic encephalopathy,intracranial infection,and idiopathic epilepsy,were enrolled.Demographic data,primary diagnoses,indications for MV,MV modes and settings,and prognoses on the 60th day were collected.Multivariable logistic analysis was used to assess factors that might affect the use of LPV.Results:A total of 104 patients were enrolled in the present study,87 (83.7%) of whom were identified with severe brain injury based on a Glasgow Coma Scale <8 points.Synchronized intermittent mandatory ventilation (SIMV) was the most frequent ventilator mode,accounting for 46.2% of the entire cohort.The median tidal volume was set to 8.0 ml/kg (interquartile range [IQR],7.0-8.9 ml/kg) of the predicted body weight;50 (48.1%) patients received LPV.The median positive end-expiratory pressure (PEEP) was set to 5 cmH2O (IQR,5-6 cmH2O).No PEEP values were higher than 10 cmH2O.Compared with partially mandatory ventilation,supportive and spontaneous ventilation practices were associated with LPV.There were no significant differences in mortality and MV duration between patients subjected to LPV and those were not.Conclusions:Among brain-injured patients in China,SIMV was the most frequent ventilation mode.Nearly one-half of the brain-injured patients received LPV.Patients under supportive and spontaneous ventilation were more likely to receive LPV.

  12. Protection of Effective Component Group from Xiaoshuan Tongluo on Brain Injury after Chronic Hypoperfusion in Rats

    Institute of Scientific and Technical Information of China (English)

    TAN Chu-bing; WANG Hong-qing; TIAN Shuo; GAO Mei; XU Wei-ren; CHEN Ruo-yun; DU Guan-hua

    2011-01-01

    Objective To investigate the protective effects of purified effective component group in extract from Xiaoshuan Tongluo(CGXT)formula on chronic brain ischemia in rats.Methods CGXT 75,150,and 300 mg/kg or vehicle were ig administered daily for four weeks to rats with bilateral common carotid arteries ligation(BCCAL).From the day 24 to 28 after BCCAL,Morris water maze was performed to assess the learning and memory impairment of rats.Four weeks after BCCAL,brain gray and white matter damage were assessed.Results In Morris test,the mean escape latency of rats in the CGXT(150 and 300 mg/kg)groups was significantly shorter than that in the vehicle group.CGXT also attenuated the neuronal damage in hippocampus and cortex and reduced the pathological damage in the optic tract and corpus callosum.Conclusion CGXT could improve learning and memory impairment resulted from BCCAL in rats.These results provide the experimental basis for the clinical use of CGXT in stroke treatment and may help in investigation of multimodal therapy strategies in ischemic cerebrovascular diseases including stroke.

  13. Prohibitin reduces mitochondrial free radical production and protects brain cells from different injury modalities

    Science.gov (United States)

    Zhou, Ping; Qian, Liping; D’Aurelio, Marilena; Cho, Sunghee; Wang, Gang; Manfredi, Giovanni; Pickel, Virginia; Iadecola, Costantino

    2012-01-01

    Prohibitin is an essential mitochondrial protein that has been implicated in a wide variety of functions in many cell types, but its role in neurons remains unclear. In a proteomic screen of rat brains in which ischemic tolerance was induced by electrical stimulation of the cerebellar fastigial nucleus, we found that prohibitin is upregulated in mitochondria. This observation prompted us to investigate the role of prohibitin in neuronal death and survival. We found that prohibitin is upregulated also in the ischemic tolerance induced by transient ischemia in vivo, or oxygen-glucose deprivation in neuronal cultures. Cell fractionation and electron microscopic immunolabeling studies demonstrated that prohibitin is localized to neuronal mitochondria. Upregulation of prohibitin in neuronal cultures or hippocampal slices was markedly neuroprotective, whereas prohibitin gene-silencing increased neuronal vulnerability, an effect associated with loss of mitochondrial membrane potential and increased mitochondrial production of reactive oxygen species. Prohibitin upregulation was associated with reduced production of reactive oxygen species in mitochondria exposed to the complex I inhibitor rotenone. In addition, prohibitin protected complex I activity from the inhibitory effects of rotenone. These observations, collectively, establish prohibitin as an endogenous neuroprotective protein involved in ischemic tolerance. Prohibitin exerts beneficial effects on neurons by reducing mitochondrial free radical production. The data with complex I activity suggest that prohibitin may stabilize the function of complex I. The protective effect of prohibitin has potential translational relevance in diseases of the nervous system associated with mitochondrial dysfunction and oxidative stress. PMID:22238093

  14. 外源性神经节苷脂对脑损伤的保护作用%Protection function of ectogenesis ganglioside to brain injury

    Institute of Scientific and Technical Information of China (English)

    张强; 韩冰; 董珠

    2003-01-01

    AIM: To investigate protection function of ectogenesis ganglioside (GM1)to brain injury of epilepsy rats. METHODS: Inducing rat epilepsy model with sulfo-semicarbazide(7.5mg/kg), dynamically observe nerve growth factor (NGF) expression of epilepsy group and GM1 intervention group in Hippocampus and cerebral cortex nerve cell 24 h, 48 h, 72 h and 7 d after epileptic attack and control group after 72 h with immunohistochemistry method. At same time we observed change of nerve cell shape and structure with electron microscope techniques. RESULTS: Electron microscope showed nerve cell injury of epilepsy rats but injury relieved after GM1 intervention. CONCLUSION: GM1 play some protective function to brain injury of epilepsy rats through induced NGF expression increase.

  15. Hypoxia inducible factor-1alpha mediates protection of DL-3-n-butylphthalide in brain microvascular endothelial cells against oxygen glucose deprivation-induced injury

    Institute of Scientific and Technical Information of China (English)

    Weihong Yang; Ling Li; Ruxun Huang; Zhong Pei; Songjie Liao; Jinsheng Zeng

    2012-01-01

    Studies have demonstrated that DL-3-n-butylphthalide can significantly alleviate oxygen glucose deprivation-induced injury of human umbilical vein endothelial cells at least partly associated with its enhancement on oxygen glucose deprivation -induced hypoxia inducible factor-1α expression. In this study, we hypothesized that DL-3-n-butylphthalide can protect against oxygen glucose deprivation-induced injury of newborn rat brain microvascular endothelial cells by means of upregulating hypoxia inducible factor-1α expression. MTT assay and Hoechst staining results showed that DL-3-n-butylphthalide protected brain microvascular endothelial cells against oxygen glucose deprivation-induced injury in a dose-dependent manner. Western blot and immunofluorescent staining results further confirmed that the protective effect was related to upregulation of hypoxia inducible factor-1α. Real-time RT-PCR reaction results showed that DL-3-n-butylphthalide reduced apoptosis by inhibiting downregulation of pro-apoptotic gene caspase-3 mRNA expression and upregulation of apoptosis-executive protease bcl-2 mRNA expression; however, DL-3-n-butylphthalide had no protective effects on brain microvascular endothelial cells after knockdown of hypoxia inducible factor-1α by small interfering RNA. These findings suggest that DL-3-n-butylphthalide can protect brain microvascular endothelial cells against oxygen glucose deprivation-induced injury by upregulating bcl-2 expression and downregulating caspase-3 expression though hypoxia inducible factor-1α pathway.

  16. Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death.

    Science.gov (United States)

    Tian, Yong; Guo, Song-Xue; Li, Jian-Ru; Du, Hang-Gen; Wang, Chao-Hui; Zhang, Jian-Min; Wu, Qun

    2015-10-05

    Early brain injury (EBI) following aneurysmal subarachnoid haemorrhage (SAH) insults contributes to the poor prognosis and high mortality observed in SAH patients. Topiramate (TPM) is a novel, broad-spectrum, antiepileptic drug with a reported protective effect against several brain injuries. The current study aimed to investigate the potential of TPM for neuroprotection against EBI after SAH and the possible dose-dependency of this effect. An endovascular perforation SAH model was established in rats, and TPM was administered by intraperitoneal injection after surgery at three different doses (20mg/kg, 40mg/kg, and 80mg/kg). The animals' neurological scores and brain water content were evaluated, and ELISA, Western blotting and immunostaining assays were conducted to assess the effect of TPM. The results revealed that TPM lowers the elevated levels of myeloperoxidase and proinflammatory mediators observed after SAH in a dose-related fashion, and the nuclear factor-kappa B (NF-κB) signalling pathway is the target of neuroinflammation regulation. In addition, TPM ameliorated SAH-induced cortical neuronal apoptosis by influencing Bax, Bcl-2 and cleaved caspase-3 protein expression, and the effect of TPM was enhanced in a dose-dependent manner. Various dosages of TPM also upregulated the protein expression of the γ-aminobutyric acid (GABA)-ergic signalling molecules, GABAA receptor (GABAAR) α1, GABAAR γ2, and K(+)-Cl(-) co-transporter 2 (KCC2) together and downregulated Na(+)-K(+)-Cl(-) co-transporter 1 (NKCC1) expression. Thus, TPM may be an effective neuroprotectant in EBI after SAH by regulating neuroinflammation and neuronal cell death.

  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. 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 ...

  19. Apigenin protects blood-brain barrier and ameliorates early brain injury by inhibiting TLR4-mediated inflammatory pathway in subarachnoid hemorrhage rats.

    Science.gov (United States)

    Zhang, Tingting; Su, Jingyuan; Guo, Bingyu; Wang, Kaiwen; Li, Xiaoming; Liang, Guobiao

    2015-09-01

    Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is associated with high morbidity and mortality. Inflammation has been considered as the major contributor to brain damage after SAH. SAH induces a systemic increase in pro-inflammatory cytokines and chemokines. Disruption of blood-brain barrier (BBB) facilitates the influx of inflammatory cells. It has been reported that the activation of toll-like receptor 4 (TLR4)/NF-κB signaling pathway plays a vital role in the central nervous system diseases. Apigenin, a common plant flavonoid, possesses anti-inflammation effect. In this study, we focused on the effects of apigenin on EBI following SAH and its anti-inflammation mechanism. Our results showed that apigenin (20mg/kg) administration significantly attenuated EBI (including brain edema, BBB disruption, neurological deficient, severity of SAH, and cell apoptosis) after SAH in rats by suppressing the expression of TLR4, NF-κB and their downstream pro-inflammatory cytokines in the cortex and by up-regulating the expression of tight junction proteins of BBB. Double immunofluorescence staining demonstrated that TLR4 was activated following SAH in neurons, microglia cells, and endothelial cells but not in astrocytes. Apigenin could suppress the activation of TLR4 induced by SAH and inhibit apoptosis of cells in the cortex. These results suggested that apigenin could attenuate EBI after SAH in rats by suppressing TLR4-mediated inflammation and protecting against BBB disruption.

  20. 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 ...

  1. Protective effect of polydatin on learning and memory impairments in neonatal rats with hypoxic‑ischemic brain injury by up‑regulating brain‑derived neurotrophic factor.

    Science.gov (United States)

    Sun, Jin; Qu, Yunxia; He, Huiming; Fan, Xiaolei; Qin, Yuanhua; Mao, Weifeng; Xu, Lixin

    2014-12-01

    Polydatin is a key component of Polygonum cuspidatum, a herb with medical and nutritional value. The present study investigated the protective effect of polydatin against learning and memory impairment in neonatal rats with hypoxic‑ischemic brain injury (HIBI). The unilateral common carotid artery ligation method was used to generate neonatal HIBI rats. Y‑maze testing revealed that rats with HIBI exhibited memory impairment, while rats with HIBI treated with polydatin displayed enhanced long‑term learning and memory. Of note, polydatin was found to upregulate the expression of hippocampal brain‑derived neurotrophic factor (BDNF) in rats with HIBI. BDNF has a role in protecting HIBI‑induced brain tissue injury and alleviating memory impairment. These findings showed that polydatin had a protective effect against learning and memory impairment in neonatal rats with HIBI and that the protective effect may be mediated through the upregulation of BDNF.

  2. 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 & ...

  3. Early treatment with lyophilized plasma protects the brain in a large animal model of combined traumatic brain injury and hemorrhagic shock

    DEFF Research Database (Denmark)

    Imam, Ayesha M; Jin, Guang; Sillesen, Martin

    2013-01-01

    Combination of traumatic brain injury (TBI) and hemorrhagic shock (HS) can result in significant morbidity and mortality. We have previously shown that early administration of fresh frozen plasma (FFP) in a large animal model of TBI and HS reduces the size of the brain lesion as well as the assoc......Combination of traumatic brain injury (TBI) and hemorrhagic shock (HS) can result in significant morbidity and mortality. We have previously shown that early administration of fresh frozen plasma (FFP) in a large animal model of TBI and HS reduces the size of the brain lesion as well...

  4. Phenolic alkaloids from Menispermum dauricum rhizome protect against brain ischemia injury via regulation of GLT-1, EAAC1 and ROS generation.

    Science.gov (United States)

    Zhao, Bo; Chen, Yang; Sun, Xi; Zhou, Mei; Ding, Jie; Zhan, Jin-Jin; Guo, Lian-Jun

    2012-03-06

    Menispermum dauricum rhizome has been widely used in China to treat various cardiovascular and thrombosis disorders. Some studies have reported that the phenolic alkaloids of Menispermum dauricum rhizome (PAM) have protective effects against brain ischemia injury, but the mechanism of this action remains to be clarified. In the present study, we investigated the possible mechanisms of action of PAM on experimental brain ischemia injury. Oxygen and glucose deprivation (OGD) in rat primary cortical cultures and middle cerebral artery occlusion in rats were used to mimic ischemia-reperfusion injury, respectively. The results suggested that PAM protected rat primary cortical cultures against OGD-reoxygenation induced cytotoxicity. PAM decreased extracellular glutamate content and markedly prevented the effects induced by OGD on protein level of GLT-1 and EAAC1 glutamate transporters. In addition, it reduced intracellular ROS generation. In vivo, PAM significantly reduced cerebral infarct area and ameliorated neurological functional deficits at different time points. Our findings revealed that the possible mechanism of action of PAM protected against brain ischemia injury involves regulation of GLT-1, EAAC1 and ROS generation.

  5. Phenolic Alkaloids from Menispermum dauricum Rhizome Protect against Brain Ischemia Injury via Regulation of GLT-1, EAAC1 and ROS Generation

    Directory of Open Access Journals (Sweden)

    Lian-Jun Guo

    2012-03-01

    Full Text Available Menispermum dauricum rhizome has been widely used in China to treat various cardiovascular and thrombosis disorders. Some studies have reported that the phenolic alkaloids of Menispermum dauricum rhizome (PAM have protective effects against brain ischemia injury, but the mechanism of this action remains to be clarified. In the present study, we investigated the possible mechanisms of action of PAM on experimental brain ischemia injury. Oxygen and glucose deprivation (OGD in rat primary cortical cultures and middle cerebral artery occlusion in rats were used to mimic ischemia-reperfusion injury, respectively. The results suggested that PAM protected rat primary cortical cultures against OGD-reoxygenation induced cytotoxicity. PAM decreased extracellular glutamate content and markedly prevented the effects induced by OGD on protein level of GLT-1 and EAAC1 glutamate transporters. In addition, it reduced intracellular ROS generation. In vivo, PAM significantly reduced cerebral infarct area and ameliorated neurological functional deficits at different time points. Our findings revealed that the possible mechanism of action of PAM protected against brain ischemia injury involves regulation of GLT-1, EAAC1 and ROS generation.

  6. 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.

  7. Phycocyanin for protecting brain ischemia-reperfusion injury and its effect on the expression of Caspase-3 mRNA

    Institute of Scientific and Technical Information of China (English)

    Xuewei Yang; Yunliang Guo; Hongbing Chen

    2006-01-01

    3.34), (23.11 ±± 1.89), (10.75±2.63)/visual field]than in the control group [(94.38 ±8.28), (108.81 ±16.11), (140.88 ±14.47), (98.13 ±11.31), (81.03 ±9.31),(31.22±8.86), (16.06±5.96)/visual field] ( P < 0.05); and those at central ischemic area were also significantly lower in the phycocyanin-treated group [(33.86±4.01), (39.51 ±3.46), (50.96±2.53), (43.07±4.09),(36.25±3.72), (9.03±3.87), (4.91 ±5.59)/visual field ]than in the control group [(51.35±2.13), (54.87±3.42),(61.77±4.94), (55.69±6.06), (49.01 ±5.73), (12.84±3.37), (7.32±2.39)/visual field](P < 0.05).CONCLUSION: Phycocyanin can obviously improve the neurologic function, reduce the size of brain infarction and down-regulate the expression of Caspase-3 mRNA of rats with ischemia and reperfusion injury,thus protect brain.

  8. Neuronal deletion of caspase 8 protects against brain injury in mouse models of controlled cortical impact and kainic acid-induced excitotoxicity.

    Directory of Open Access Journals (Sweden)

    Maryla Krajewska

    Full Text Available Acute brain injury is an important health problem. Given the critical position of caspase 8 at the crossroads of cell death pathways, we generated a new viable mouse line (Ncasp8(-/-, in which the gene encoding caspase 8 was selectively deleted in neurons by cre-lox system.Caspase 8 deletion reduced rates of neuronal cell death in primary neuronal cultures and in whole brain organotypic coronal slice cultures prepared from 4 and 8 month old mice and cultivated up to 14 days in vitro. Treatments of cultures with recombinant murine TNFα (100 ng/ml or TRAIL (250 ng/mL plus cyclohexamide significantly protected neurons against cell death induced by these apoptosis-inducing ligands. A protective role of caspase 8 deletion in vivo was also demonstrated using a controlled cortical impact (CCI model of traumatic brain injury (TBI and seizure-induced brain injury caused by kainic acid (KA. Morphometric analyses were performed using digital imaging in conjunction with image analysis algorithms. By employing virtual images of hundreds of brain sections, we were able to perform quantitative morphometry of histological and immunohistochemical staining data in an unbiased manner. In the TBI model, homozygous deletion of caspase 8 resulted in reduced lesion volumes, improved post-injury motor performance, superior learning and memory retention, decreased apoptosis, diminished proteolytic processing of caspases and caspase substrates, and less neuronal degeneration, compared to wild type, homozygous cre, and caspase 8-floxed control mice. In the KA model, Ncasp8(-/- mice demonstrated superior survival, reduced seizure severity, less apoptosis, and reduced caspase 3 processing. Uninjured aged knockout mice showed improved learning and memory, implicating a possible role for caspase 8 in cognitive decline with aging.Neuron-specific deletion of caspase 8 reduces brain damage and improves post-traumatic functional outcomes, suggesting an important role for this

  9. Shear Stress Induces Differentiation of Endothelial Lineage Cells to Protect Neonatal Brain from Hypoxic-Ischemic Injury through NRP1 and VEGFR2 Signaling

    Directory of Open Access Journals (Sweden)

    Chia-Wei Huang

    2015-01-01

    Full Text Available Neonatal hypoxic-ischemic (HI brain injuries disrupt the integrity of neurovascular structure and lead to lifelong neurological deficit. The devastating damage can be ameliorated by preserving the endothelial network, but the source for therapeutic cells is limited. We aim to evaluate the beneficial effect of mechanical shear stress in the differentiation of endothelial lineage cells (ELCs from adipose-derived stem cells (ASCs and the possible intracellular signals to protect HI injury using cell-based therapy in the neonatal rats. The ASCs expressed early endothelial markers after biochemical stimulation of endothelial growth medium. The ELCs with full endothelial characteristics were accomplished after a subsequential shear stress application for 24 hours. When comparing the therapeutic potential of ASCs and ELCs, the ELCs treatment significantly reduced the infarction area and preserved neurovascular architecture in HI injured brain. The transplanted ELCs can migrate and engraft into the brain tissue, especially in vessels, where they promoted the angiogenesis. The activation of Akt by neuropilin 1 (NRP1 and vascular endothelial growth factor receptor 2 (VEGFR2 was important for ELC migration and following in vivo therapeutic outcomes. Therefore, the current study demonstrated importance of mechanical factor in stem cell differentiation and showed promising protection of brain from HI injury using ELCs treatment.

  10. 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

  11. 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…

  12. 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…

  13. Prodigiosin inhibits gp91{sup phox} and iNOS expression to protect mice against the oxidative/nitrosative brain injury induced by hypoxia-ischemia

    Energy Technology Data Exchange (ETDEWEB)

    Chang, Chia-Che [Institute of Biomedical Sciences, National Chung-Hsing University, Taichung, Taiwan (China); Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan (China); Agricultural Biotechnology Center, National Chung-Hsing University, Taichung, Taiwan (China); Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan (China); Wang, Yea-Hwey [Department of Nursing, College of Medicine and Nursing, Hungkuang University, Taichung, Taiwan (China); Chern, Chang-Ming [Division of Neurovascular Disease, Neurological Institute, Taipei Veterans General Hospital and School of Medicine, National Yang-Ming University, Taipei, Taiwan (China); Liou, Kuo-Tong [Department of Chinese Martial Arts, Chinese Culture University, Taipei, Taiwan (China); Hou, Yu-Chang [Department of Chinese Medicine, Taoyuan General Hospital, Department of Health, Taiwan (China); Department of Nursing, Yuanpei University, Hsinchu, Taiwan (China); Department of Bioscience Technology, Chuan-Yuan Christian University, Taoyuan, Taiwan (China); Peng, Yu-Ta [Institute of Biomedical Sciences, National Chung-Hsing University, Taichung, Taiwan (China); Shen, Yuh-Chiang, E-mail: yuhcs@nricm.edu.tw [National Research Institute of Chinese Medicine, Taipei, Taiwan (China); Institute of Biomedical Sciences, National Chung-Hsing University, Taichung, Taiwan (China)

    2011-11-15

    This study aimed to explore the mechanisms by which prodigiosin protects against hypoxia-induced oxidative/nitrosative brain injury induced by middle cerebral artery occlusion/reperfusion (MCAo/r) injury in mice. Hypoxia in vitro was modeled using oxygen-glucose deprivation (OGD) followed by reoxygenation of BV-2 microglial cells. Our results showed that treatment of mice that have undergone MCAo/r injury with prodigiosin (10 and 100 {mu}g/kg, i.v.) at 1 h after hypoxia ameliorated MCAo/r-induced oxidative/nitrosative stress, brain infarction, and neurological deficits in the mice, and enhanced their survival rate. MCAo/r induced a remarkable production in the mouse brains of reactive oxygen species (ROS) and a significant increase in protein nitrosylation; this primarily resulted from enhanced expression of NADPH oxidase 2 (gp91{sup phox}), inducible nitric oxide synthase (iNOS), and the infiltration of CD11b leukocytes due to breakdown of blood-brain barrier (BBB) by activation of nuclear factor-kappa B (NF-{kappa}B). All these changes were significantly diminished by prodigiosin. In BV-2 cells, OGD induced ROS and nitric oxide production by up-regulating gp91{sup phox} and iNOS via activation of the NF-{kappa}B pathway, and these changes were suppressed by prodigiosin. In conclusion, our results indicate that prodigiosin reduces gp91{sup phox} and iNOS expression possibly by impairing NF-{kappa}B activation. This compromises the activation of microglial and/or inflammatory cells, which then, in turn, mediates prodigiosin's protective effect in the MCAo/r mice. -- Highlights: Black-Right-Pointing-Pointer Prodigiosin ameliorated brain infarction and deficits. Black-Right-Pointing-Pointer Prodigiosin protected against hypoxia/reperfusion-induced brain injury. Black-Right-Pointing-Pointer Prodigiosin diminished oxidative/nitrosativestress and leukocytes infiltration. Black-Right-Pointing-Pointer Prodigiosin reduced BBB breakdown. Black

  14. 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.

  15. Protective effect of ultrashortwave versus radix salviae miltiorrhizae on brains of rats with cerebral ischemia-reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Lixin Zhang; Zhiqiang Wang; Zhiqiang Zhang; Xiuhua Yuan; Xiaojie Tong

    2006-01-01

    BACKGROUND: How to control the effect of oxygen-derived free radicals on development of cerebral injury and cerebral edema is a key factor for treating cerebral ischemia-reperfusion injury.OBJECTIVE: To observe and compare the protective effects, synergistic action and mechanisms of ultrashortwave (USW) and radix salviae miltiorrhizae (RSM) on the focal cerebral ischemia-reperfusion injuries in rats.DESIGN: Randomized controlled animal study.SETTING: Department of Rehabilitation Medicine, First Hospital affiliated to China Medical University.MATERIALS: A total of 160 healthy Wistar rats of both genders and aged 18-20 weeks weighing 250-300 gof clean grade were selected in this study. 5 mL/ampoule RSM injection fluid was produced by the First Pharmaceutical Corporation of Shanghai (batch number: 011019, 0.01 mL/g). The USW therapeutic device was produced by Shanghai Electronic Device Factory with the frequency of 40.68 MHz and the maximal export power of 40 W. The first channel of power after modulation was 11 W.METHODS: The experiment was carried out in the Rehabilitation Medicine Department of the First Hospital affiliated to China Medical University from May 2002 to January 2003. Focal ischemia-reperfusion model was established in rats by reversible right middle cerebral artery occlusion with filament. Right cerebral ischemia was for 2 hours and then with 24 hours reperfusion. The scores of neurological deficits were evaluated by 0 to 4 scales. After surgery, 64 successful rats models were divided into four groups according to digital table: control group, USW group, RSM group and RSM + USW group with 16 cases in each group.Rats in control group were intraperitoneally injected with the same volume of saline (0.1 mL/g); rats in USW group were given small dosage of USW on head for 10 minutes at 6 hours after reperfusion; rats in RSM group were intraperitoneally injected with 0.01 mL/g RSM solution at 30 minutes before reperfusion; rats in RSM + USW group were

  16. 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.

  17. 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...

  18. 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…

  19. The protective effect of erdosteine on short-term global brain ischemia/reperfusion injury in rats.

    Science.gov (United States)

    Ozerol, Elif; Bilgic, Sedat; Iraz, Mustafa; Cigli, Ahmet; Ilhan, Atilla; Akyol, Omer

    2009-02-01

    Experimental studies have demonstrated that free radicals play a major role on neuronal injury during ischemia/reperfusion (I/R) in rats. Erdosteine is a thioderivative endowed with mucokinetic, mucolytic and free-radical-scavenging properties. The aim of the present study was to investigate the effect of erdosteine treatment against short-term global brain ischemia/reperfusion injury in rats. The study was carried out on Wistar rats divided into four groups. (i) Control group, (ii) ischemia/reperfusion group, (iii) ischemia/reperfusion+erdosteine group, and (iv) erdosteine group. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities as well as thiobarbituric acid reactive substances (TBARSs) and nitric oxide (NO) levels were analysed in erythrocyte and plasma of rats. Plasma NO levels were significantly higher in the ischemia/reperfusion group than the other groups. The activities of SOD and GSH-Px were decreased, while TBARS levels increased in the ischemia/reperfusion group compared to other groups in both plasma and erythrocyte. The erythrocyte CAT activity was higher in erdosteine group and there was a statistically significant increase, when compared with the erdosteine plus ischemia/reperfusion group. By treating the rats with erdosteine, the depletion of endogenous antioxidant enzymes (SOD, CAT, GSH-Px) and increase of TBARS and NO levels were prevented. This study, therefore, suggests that erdosteine reduces parameters of oxidative stress is well supported by the data.

  20. Protective effects of melatonin against 12C6+ beam irradiation-induced oxidative stress and DNA injury in the mouse brain

    Science.gov (United States)

    Wu, Z. H.; Zhang, H.; Wang, X. Y.; Yang, R.; Liu, B.; Liu, Y.; Zhao, W. P.; Feng, H. Y.; Xue, L. G.; Hao, J. F.; Niu, B. T.; Wang, Z. H.

    2012-01-01

    The purpose of this experiment was to estimate the protective effects of melatonin against radiation-induced brain damages in mice induced by heavy ion beams. Kun-Ming mice were randomly divided into five groups: normal control group, irradiation control group, and three different doses of melatonin (5, 10, and 20 mg/kg, i.p.) treated groups. Apart from the normal control group, the other four groups were exposed to whole-body 4.0 Gy carbon ion beam irradiation (approximately 0.5 Gy/min) after i.p. administration of normal saline or melatonin 1 h before irradiation. The oxidative redox status of brain tissue was assessed by measurement of malondiadehyde (MDA) levels, total superoxide dismutase (T-SOD), cytosolic superoxide dismutase (Cu/ZnSOD, SOD1) and mitochondrial superoxide dismutase (MnSOD, SOD2) activities at 8 h after irradiation. DNA damages were determined using the Comet assay and apoptosis and cell cycle distribution were detected by flow cytometric analyses. A dramatic dose-dependent decrease in MDA levels, tail moment, rates of tailing cells, and apoptosis, and a dose-dependent increase in T-SOD and SOD2 activities, in brain tissues in the melatonin-treated groups were detected compared with the irradiation only group. Furthermore, flow cytometric analysis demonstrated that the percentage of brain cells in the G0/G1 phase decreased significantly, while those in the S and G2/M stage increased dramatically, with mice pretreated with melatonin compared to the irradiation control group. These data indicate that melatonin has protective effects against irradiation-induced brain injury, and that its underlying protective mechanisms may relate to modulation of oxidative stress induced by heavy ionirradiation.

  1. 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.

  2. 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 ...

  3. 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 ...

  4. 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/ ...

  5. 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.

  6. Experimental study of the protective effect of Edaravone on brain after traumatic brain injury%脑创伤后Edaravone脑保护作用机制的实验研究

    Institute of Scientific and Technical Information of China (English)

    尹立国; 崔建忠; 高俊玲; 赵雅宁

    2015-01-01

    Objective To investigate the possible action mechanism of protective effect of Edaravone on brain after traumatic brain injury .Methods The middle degree closed diffused craniocerebral injury models in rats were established by improved Marmarou's method.After the models were successfully established ,the free radical in cortex of the rats ,Cyt-c and apoptosis cell numbers were detected and observed dynamically by TAB ,immunohistochemry,TUNEL,respectively.Results Edaravone could decrease obviously the levels of free radical ,the expression of Cyt-c and apoptosis nerve cells after traumatic brain injury Conclusion Edaravone is effective in treating traumatic brain injury ,and one of action mechanisms is to reduce generation of free radical,inhibit opening of mitochondrial permeability transition pore (MPTP),reduce releasing of Cytc,and then decrease nerve cell apoptosis .%目的:探讨Edaravone对脑创伤后保护作用的可能机制。方法采用改进的Marmarou’ s法建立大鼠中度闭合性弥漫性颅脑损伤模型,应用TAB法、免疫组化,TUNEL法对大鼠伤后皮质自由基、细胞色素C及凋亡细胞数进行动态观察。结果伤后给予Edaravone 能明显减少自由基水平,降低细胞色素 c表达和神经元细胞凋亡数。结论 Edaravone对颅脑创伤有治疗作用,其机制之一是通过减少自由基生成,抑制线粒体膜通透性转换孔( MPTP)开放,减少细胞色素c释放,进而减少神经细凋亡。

  7. Argon protects against hypoxic-ischemic brain injury in neonatal rats through activation of nuclear factor (erythroid-derived 2)-like 2

    Science.gov (United States)

    Zhao, Hailin; Mitchell, Sian; Ciechanowicz, Sarah; Savage, Sinead; Wang, Tianlong; Ji, Xunming; Ma, Daqing

    2016-01-01

    Perinatal hypoxic ischaemic encephalopathy (HIE) has a high mortality rate with neuropsychological impairment. This study investigated the neuroprotective effects of argon against neonatal hypoxic-ischaemic brain injury. In vitro cortical neuronal cell cultures derived from rat foetuses were subjected to an oxygen and glucose deprivation (OGD) challenge for 90 minutes and then exposed to 70% argon or nitrogen with 5% carbon dioxide and balanced with oxygen for 2 hours. In vivo, seven-day-old rats were subjected to unilateral common carotid artery ligation followed by hypoxic (8% oxygen balanced with nitrogen) insult for 90 minutes. They were exposed to 70% argon or nitrogen balanced with oxygen for 2 hours. In vitro, argon treatment of cortical neuronal cultures resulted in a significant increase of p-mTOR and Nuclear factor (erythroid-derived 2)-like 2(Nrf2) and protection against OGD challenge. Inhibition of m-TOR through Rapamycin or Nrf2 through siRNA abolished argon-mediated cyto-protection. In vivo, argon exposure significantly enhanced Nrf2 and its down-stream effector NAD(P)H Dehydrogenase, Quinone 1(NQO1) and superoxide dismutase 1(SOD1). Oxidative stress, neuroinflammation and neuronal cell death were significantly decreased and brain infarction was markedly reduced. Blocking PI-3K through wortmannin or ERK1/2 through U0126 attenuated argon-mediated neuroprotection. These data provide a new molecular mechanism for the potential application of argon as a neuroprotectant in HIE. PMID:27016422

  8. Ecdysterone protects gerbil brain from temporal global cerebral ischemia/reperfusion injury via preventing neuron apoptosis and deactivating astrocytes and microglia cells.

    Science.gov (United States)

    Wang, Wei; Wang, Tao; Feng, Wan-Yu; Wang, Zhan-You; Cheng, Mao-Sheng; Wang, Yun-Jie

    2014-01-01

    Ecdysterone (EDS), a common derivative of ecdysteroid, has shown its effects on alleviating cognitive impairment and improving the cognition and memory. However, the mechanisms remain unknown. Using temporal global forebrain ischemia and reperfusion-induced brain injury as a model system, we investigated the roles of EDS in improving cognitive impairment in gerbil. Our results demonstrated that intraperitoneal injection of EDS obviously increased the number of surviving neuron cells by Nissl and neuronal nuclei (NeuN) staining. Indeed, the protecting effects of EDS are because of its ability to prevent the apoptosis of neuron cells as evidenced by TUNEL staining and caspase-3 deactivation in the brain of temporal global forebrain ischemia/reperfusion-treated gerbil. Moreover, EDS administration suppressed the ischemia stimulated activity of astrocytes and microglia cells by inhibiting the production of tumor necrosis alpha (TNF-α) in the brain of gerbil. More importantly, these actions of neurons and astrocytes/microglia cells in response to EDS treatment played pivotal roles in ameliorating the cognitive impairment in the ischemia/reperfusion-injured gerbil. In view of these observations, we not only decipher the mechanisms of EDS in reducing the syndrome of ischemia, but also provide novel perspectives to combat ischemic stroke.

  9. 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.)

  10. 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

  11. 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.

  12. 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…

  13. 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…

  14. 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.

  15. 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.

  16. 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.

  17. 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

  18. Inhibition of nuclear factor-κB by 6-O-acetyl shanzhiside methyl ester protects brain against injury in a rat model of ischemia and reperfusion

    Directory of Open Access Journals (Sweden)

    Jiang Wanglin

    2010-09-01

    Full Text Available Abstract Background Recent studies have demonstrated an inflammatory response associated with the pathophysiology of cerebral ischemia. The beneficial effects of anti-inflammatory drugs in cerebral ischemia have been documented. When screening natural compounds for drug candidates in this category, we isolated 6-O-acetyl shanzhiside methyl ester (ND02, an iridoid glucoside compound, from the leaves of Lamiophlomis rotata (Benth. Kudo. The objectives of this study were to determine the effects of ND02 on a cultured neuronal cell line, SH-SY5Y, in vitro, and on experimental ischemic stroke in vivo. Methods For TNF-α-stimulated SH-SY5Y cell line experiments in vitro, SH-SY5Y cells were pre-incubated with ND02 (20 μM or 40 μM for 30 min and then incubated with TNF-α (20 ng/ml for 15 min. For in vivo experiments, rats were subjected to middle cerebral artery occlusion (MCAO for 1 h followed by reperfusion for 23 h. Results ND02 treatment of SH-SY5Y cell lines blocked TNF-α-induced nuclear factor-κB (NF-κB and IκB-α phosphorylation and increased Akt phosphorylation. LY294002 blocked TNF-α-induced phosphorylation of Akt and reduced the phosphorylation of both IκB-α and NF-κB. At doses higher than 10 mg/kg, ND02 had a significant neuroprotective effect in rats with cerebral ischemia and reperfusion (I/R. ND02 (25 mg/kg demonstrated significant neuroprotective activity even after delayed administration 1 h, 3 h and 5 h after I/R. ND02, 25 mg/kg, attenuated histopathological damage, decreased cerebral Evans blue extravasation, inhibited NF-κB activation, and enhanced Akt phosphorylation. Conclusion These data show that ND02 protects brain against I/R injury with a favorable therapeutic time-window by alleviating cerebral I/R injury and attenuating blood-brain barrier (BBB breakdown, and that these protective effects may be due to blocking of neuronal inflammatory cascades through an Akt-dependent NF-κB signaling pathway.

  19. 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

  20. 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.

  1. 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

  2. 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

  3. [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.

  4. 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.

  5. 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 ...

  6. 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:…

  7. 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

  8. miR-203 protects microglia mediated brain injury by regulating inflammatory responses via feedback to MyD88 in ischemia.

    Science.gov (United States)

    Yang, Zhao; Zhong, Lina; Zhong, Shanchuan; Xian, Ronghua; Yuan, Bangqing

    2015-06-01

    Much evidence demonstrates that microglia mediated inflammatory responses play an important role in brain injury in ischemia. miRNA is the important factor in regulation of inflammation. However, the effect of miRNA in microglia mediated inflammatory responses has not been well studied. In the study, we demonstrate that miR-203 negatively regulates ischemia induced microglia activation by targeting MyD88, an important adapter protein involved in most Toll-like receptors (TLRs) and interleukin-1 receptor (IL-1R) pathways. Through negative feedback, enforced expression of miR-203 or MyD88 siRNA silencing inhibits downstream NF-κβ signaling and microglia activation, thereby alleviating neuronal injury. These findings reveal that miR-203 represents a novel target regulating neuroinflammation and brain injury, thus offering a new therapeutical strategy for cerebral hypoxic diseases.

  9. 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.

  10. Protection by Neuroglobin Expression in Brain Pathologies

    Science.gov (United States)

    Baez, Eliana; Echeverria, Valentina; Cabezas, Ricardo; Ávila-Rodriguez, Marco; Garcia-Segura, Luis Miguel; Barreto, George E.

    2016-01-01

    Astrocytes play an important role in physiological, metabolic, and structural functions, and when impaired, they can be involved in various pathologies including Alzheimer, focal ischemic stroke, and traumatic brain injury. These disorders involve an imbalance in the blood flow and nutrients such as glucose and lactate, leading to biochemical and molecular changes that cause neuronal damage, which is followed by loss of cognitive and motor functions. Previous studies have shown that astrocytes are more resilient than neurons during brain insults as a consequence of their more effective antioxidant systems, transporters, and enzymes, which made them less susceptible to excitotoxicity. In addition, astrocytes synthesize and release different protective molecules for neurons, including neuroglobin, a member of the globin family of proteins. After brain injury, neuroglobin expression is induced in astrocytes. Since neuroglobin promotes neuronal survival, its increased expression in astrocytes after brain injury may represent an endogenous neuroprotective mechanism. Here, we review the role of neuroglobin in the central nervous system, its relationship with different pathologies, and the role of different factors that regulate its expression in astrocytes. PMID:27672379

  11. Protection by neuroglobin expression in brain pathologies

    Directory of Open Access Journals (Sweden)

    Eliana Baez

    2016-09-01

    Full Text Available Astrocytes play an important role in physiological, metabolic and structural functions and, when impaired, they can be involved in various pathologies including Alzheimer, focal ischemic stroke and traumatic brain injury. These disorders involve an imbalance in the blood flow and nutrients such as glucose and lactacte, leading to biochemical and molecular changes that cause neuronal damage, which is followed by loss of cognitive and motor functions. Previous studies have shown that astrocytes are more resilient than neurons during brain insults as a consequence of their more effective antioxidant systems, transporters and enzymes, which made them less susceptible to excitotoxicity. In addition, astrocytes synthesize and release different protective molecules for neurons, including neuroglobin, a member of the globin family of proteins. After brain injury neuroglobin expression is induced in astrocytes. Since neuroglobin promotes neuronal survival, its increased expression in astrocytes after brain injury may represent an endogenous neuroprotective mechanism. Here, we review the role of neuroglobin in the CNS, its relationship with different pathologies, and the role of different factors that regulate its expression in astrocytes.

  12. Protection by Neuroglobin Expression in Brain Pathologies.

    Science.gov (United States)

    Baez, Eliana; Echeverria, Valentina; Cabezas, Ricardo; Ávila-Rodriguez, Marco; Garcia-Segura, Luis Miguel; Barreto, George E

    2016-01-01

    Astrocytes play an important role in physiological, metabolic, and structural functions, and when impaired, they can be involved in various pathologies including Alzheimer, focal ischemic stroke, and traumatic brain injury. These disorders involve an imbalance in the blood flow and nutrients such as glucose and lactate, leading to biochemical and molecular changes that cause neuronal damage, which is followed by loss of cognitive and motor functions. Previous studies have shown that astrocytes are more resilient than neurons during brain insults as a consequence of their more effective antioxidant systems, transporters, and enzymes, which made them less susceptible to excitotoxicity. In addition, astrocytes synthesize and release different protective molecules for neurons, including neuroglobin, a member of the globin family of proteins. After brain injury, neuroglobin expression is induced in astrocytes. Since neuroglobin promotes neuronal survival, its increased expression in astrocytes after brain injury may represent an endogenous neuroprotective mechanism. Here, we review the role of neuroglobin in the central nervous system, its relationship with different pathologies, and the role of different factors that regulate its expression in astrocytes.

  13. 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

  14. 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.

  15. 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.

  16. 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.

  17. 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...

  18. 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.

  19. 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...

  20. 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.

  1. 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

  2. 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.

  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. 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...

  5. 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.

  6. 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...

  7. [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.

  8. 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

  9. 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

  10. 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 ...

  11. 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...

  12. Voltage-dependent anion channels (VDACs) promote mitophagy to protect neuron from death in an early brain injury following a subarachnoid hemorrhage in rats.

    Science.gov (United States)

    Li, Jian; Lu, Jianfei; Mi, Yongjie; Shi, Zhao; Chen, Chunhua; Riley, John; Zhou, Changman

    2014-07-21

    The term mitophagy is coined to describe the selective removal of mitochondria by autophagy but the process itself is still contentious, especially in the early period following subarachnoid hemorrhage (SAH). In the present study, we investigated the role of mitophagy following 48h after SAH injury in rats. Specifically evaluating whether mitophagy, through voltage dependant anion channels (VDACs) interacting with microtubule-associated protein 1 light chain 3, could orchestrate the induction of apoptotic and necrotic cell death in neurons, a VDAC1siRNA and an activitor Rapamycian (RAPA), were engaged. One hundred and twelve male Sprague-Dawley rats were randomly divided into 4 groups: Sham, SAH, SAH+VDAC1siRNA, and SAH+RAPA. Outcomes measured included mortality rate, brain edema, BBB disruption, and neurobehavioral testing. We also used western blotting techniques to analyze the expressions of key mitophagic/autophagic proteins and pro-apoptotic protein such as ROS, VDAC1, LC-3II and Caspase-3. Rapamycin treatment significantly improved the mortality rate, cerebral edema, and neurobehavioral deficits; apoptotic and necrotic cell death in neurons were reduced by Rapamycin following SAH injury. However, VDAC1siRNA worsened the brain injury following SAH. Immunohistochemical staining and western blot analysis demonstrated a decreased expression of VDAC1, LC3II, and an increase of ROS and Caspase-3 followed by VDAC1siRNA administration. In conclusion, mitophagy induced by VDAC1 following SAH injury may in fact play a significant role in neuroprotection, the mechanism which may be through the attenuation of the apoptosic and necrosic molecular pathways. This translates a preservation of functional integrity and an improvement in mortality.

  13. 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,…

  14. 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...

  15. 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 ...

  16. 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.

  17. 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

  18. 78 FR 12334 - Proposed Collection; Comment Request: Federal Interagency Traumatic Brain Injury Research (FITBIR...

    Science.gov (United States)

    2013-02-22

    ... Traumatic Brain Injury Research (FITBIR) Informatics System Data Access Request SUMMARY: In compliance with.... Proposed Collection: Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System Data... with approved assurance from the DHHS Office of Human Research Protections to access data or...

  19. [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.

  20. 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.

  1. The common antitussive agent dextromethorphan protects against hyperoxia-induced cell death in established in vivo and in vitro models of neonatal brain injury.

    Science.gov (United States)

    Posod, A; Pinzer, K; Urbanek, M; Wegleiter, K; Keller, M; Kiechl-Kohlendorfer, U; Griesmaier, E

    2014-08-22

    Preterm infants are prematurely subjected to relatively high oxygen concentrations, even when supplemental oxygen is not administered. There is increasing evidence to show that an excess of oxygen is toxic to the developing brain. Dextromethorphan (DM), a frequently used antitussive agent with pleiotropic mechanisms of action, has been shown to be neuroprotective in various models of central nervous system pathology. Due to its numerous beneficial properties, it might also be able to counteract detrimental effects of a neonatal oxygen insult. The aim of the current study was to evaluate its therapeutic potential in established cell culture and rodent models of hyperoxia-induced neonatal brain injury. For in vitro studies pre- and immature oligodendroglial (OLN-93) cells were subjected to hyperoxic conditions for 48 h after pre-treatment with increasing doses of DM. For in vivo studies 6-day-old Wistar rat pups received a single intraperitoneal injection of DM in two different dosages prior to being exposed to hyperoxia for 24h. Cell viability and caspase-3 activation were assessed as outcome parameters at the end of exposure. DM significantly increased cell viability in immature oligodendroglial cells subjected to hyperoxia. In pre-oligodendroglial cells cell viability was not significantly affected by DM treatment. In vivo caspase-3 activation induced by hyperoxic exposure was significantly lower after administration of DM in gray and white matter areas. In control animals kept under normoxic conditions DM did not significantly influence caspase-3-dependent apoptosis. The present results indicate that DM is a promising and safe treatment strategy for neonatal hyperoxia-induced brain injury that merits further investigation.

  2. 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.

  3. 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.

  4. 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.

  5. 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.

  6. 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.

  7. 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.

  8. 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.

  9. 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.

  10. 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.

  11. 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...

  12. 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.

  13. 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...

  14. 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.

  15. 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.

  16. 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.

  17. 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...

  18. 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 ...

  19. 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.

  20. 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.

  1. 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.

  2. 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.

  3. 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.

  4. 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.

  5. 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.

  6. 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...

  7. 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…

  8. 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…

  9. 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.

  10. 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.

  11. 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

  12. 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…

  13. 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.

  14. 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...

  15. 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...

  16. 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...

  17. 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'.

  18. 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...

  19. 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…

  20. 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

  1. 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.

  2. 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.

  3. Triptolide protects astrocytes from hypoxia/ reoxygenation injury

    Institute of Scientific and Technical Information of China (English)

    Minfang Guo; Hongcui Fan; Jiezhong Yu; Ning Ji; Yongsheng Sun; Liyun Liang; Baoguo Xiao; Cungen Ma

    2011-01-01

    Astrocytes in an in vitro murine astrocyte model of oxygen and glucose deprivation/hypoxia and reoxygenation were treated with different concentrations of triptolide (250, 500, 1 000 ng/mL) in a broader attempt to elucidate the protection and mechanism underlying triptolide treatment on astrocytes exposed to hypoxia/reoxygenation injury. The results showed that the matrix metalloproteinase-9, interleukin-1β, tumor necrosis factor α and interleukin-6 expressions were significantly decreased after triptolide treatment in the astrocytes exposed to hypoxia/ reoxygenation injury, while interleukin-10 expression was upregulated. In addition, the vitality of the injured astrocytes was enhanced, the triptolide's effect was apparent at 500 ng/mL. These experimental findings indicate that triptolide treatment could protect astrocytes against hypoxia/ reoxygenation injury through the inhibition of inflammatory response and the reduction of matrix metalloproteinase-9 expression.

  4. 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...

  5. 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

  6. 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

  7. 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. ...

  8. Astrocytes mediate the neuroprotective effects of Tibolone following brain injury

    Directory of Open Access Journals (Sweden)

    Luis Miguel Garcia-Segura

    2015-04-01

    Full Text Available Recently, astrocytes have become a key central player in mediating important functions in the brain. These physiological processes include neurotransmitter recycling, energy management, metabolic shuttle, immune sensing, K+ buffer, antioxidant supply and release of neurotrophic factors and gliotransmitters. These astrocytic roles are somehow altered upon brain injury, therefore strategies aimed at better protecting astrocytes are an essential asset to maintain brain homeostasis. In this context, estrogenic compounds, such as Tibolone, have attracted attention for their beneficial effects in acute and chronic degenerative diseases. Tibolone may act through binding to estrogen, androgen or progesterone receptors and exert protective effects by reducing astrocytes cell death and oxidative stress signaling mechanisms. Although Tibolone has a multifactorial effect in the brain, its mechanisms of action are not completely understood. In this work, we highlight the role of Tibolone in brain protection upon damage, how astrocytes might mediate part of its neuroprotective actions and discuss the effects of Tibolone in diminishing the harmful consequences of a metabolic insult and energy failure in the setting of a pathological event.

  9. Correlation between heat shock protein 70 expression in the brain stem and sudden death after experimental traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    ZHAO Lian-xu; XU Xiao-hu; LIU Chao; PAN Su-yue; ZHU Jia-zhen; ZHANG Cheng

    2001-01-01

    Objective: The aim of this study was to determine the patterns of heat-shock protein 70 (HSP70) biosynthesis following traumatic brain injury, and observe the effect of HSP70 induction on the function of the vital center in the brain stem. Methods: Rat models of sudden death resulted form traumatic brain injury were produced, and HSP70 expression in the rat brain stem was determined by immunohistochemistry, the induction of HSP70 mRNA detected by RT-PCR. Results: The level of HSP70 mRNA was prominently elevated in the brain stem as early as 1 5 min following the impact injury, while HSP70 expression was only observed 3 to 6 h after the injury. It was also observed that the levels of HSP70 mRNA but not the protein were elevated in the brain stem of sudden death rats. Conclusion: The synthesis of HSP70 was significantly enhanced in the brain stem following traumatic injury, and the expression of HSP70 is beneficial to eliminate the stress agents, and to sustain the cellular protein homeostasis. When the injury disturbs the synthesis of HSP70 to disarm the protective mechanism of heat-shock proteins, dysfunction of the vital center in the brain stem, and consequently death may occur. Breach in the synchronization of HSP70 mRNA-protein can be indicative of fatal damage to the nerve cells.

  10. 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.

  11. 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 ...

  12. 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...

  13. 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

  14. 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.

  15. 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...

  16. 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.

  17. 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

  18. G-CSF Protects Human Brain Vascular Endothelial Cells Injury Induced by High Glucose, Free Fatty Acids and Hypoxia through MAPK and Akt Signaling

    Science.gov (United States)

    Tao, Yinghong; Guo, Jingchun; Guo, Zhuangli; Zhang, Shuo; Zhang, Yu; Huang, Yanyan; Tang, Yuping; Dong, Qiang; Hu, Renming

    2015-01-01

    Granulocyte-colony stimulating factor (G-CSF) has been shown to play a neuroprotective role in ischemic stroke by mobilizing bone marrow (BM)-derived endothelial progenitor cells (EPCs), promoting angiogenesis, and inhibiting apoptosis. Impairments in mobilization and function of the BM-derived EPCs have previously been reported in animal and human studies of diabetes where there is both reduction in the levels of the BM-derived EPCs and its ability to promote angiogenesis. This is hypothesized to account for the pathogenesis of diabetic vascular complications such as stroke. Here, we sought to investigate the effects of G-CSF on diabetes-associated cerebral vascular defect. We observed that pretreatment of the cultured human brain vascular endothelial cells (HBVECs) with G-CSF largely prevented cell death induced by the combination stimulus with high glucose, free fatty acids (FFA) and hypoxia by increasing cell viability, decreasing apoptosis and caspase-3 activity. Cell ultrastructure measured by transmission electron microscope (TEM) revealed that G-CSF treatment nicely reduced combination stimulus-induced cell apoptosis. The results from fluorescent probe Fluo-3/AM showed that G-CSF greatly suppressed the levels of intracellular calcium ions under combination stimulus. We also found that G-CSF enhanced the expression of cell cycle proteins such as human cell division cycle protein 14A (hCdc14A), cyclinB and cyclinE, inhibited p53 activity, and facilitated cell cycle progression following combination stimulus. In addition, activation of extracellular signal-regulated kinase1/2 (ERK1/2) and Akt, and deactivation of c-Jun N terminal kinase (JNK) and p38 were proved to be required for the pro-survival effects of G-CSF on HBVECs exposed to combination stimulus. Overall, G-CSF is capable of alleviating HBVECs injury triggered by the combination administration with high glucose, FFA and hypoxia involving the mitogen-activated protein kinases (MAPK) and Akt signaling

  19. 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

  20. 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.

  1. 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

  2. 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.

  3. Investigation of the relationship between facial injuries and traumatic brain injuries using a realistic subject-specific finite element head model.

    Science.gov (United States)

    Tse, Kwong Ming; Tan, Long Bin; Lee, Shu Jin; Lim, Siak Piang; Lee, Heow Pueh

    2015-06-01

    In spite of anatomic proximity of the facial skeleton and cranium, there is lack of information in the literature regarding the relationship between facial and brain injuries. This study aims to correlate brain injuries with facial injuries using finite element method (FEM). Nine common impact scenarios of facial injuries are simulated with their individual stress wave propagation paths in the facial skeleton and the intracranial brain. Fractures of cranio-facial bones and intracranial injuries are evaluated based on the tolerance limits of the biomechanical parameters. General trend of maximum intracranial biomechanical parameters found in nasal bone and zygomaticomaxillary impacts indicates that severity of brain injury is highly associated with the proximity of location of impact to the brain. It is hypothesized that the midface is capable of absorbing considerable energy and protecting the brain from impact. The nasal cartilages dissipate the impact energy in the form of large scale deformation and fracture, with the vomer-ethmoid diverging stress to the "crumpling zone" of air-filled sphenoid and ethmoidal sinuses; in its most natural manner, the face protects the brain. This numerical study hopes to provide surgeons some insight in what possible brain injuries to be expected in various scenarios of facial trauma and to help in better diagnosis of unsuspected brain injury, thereby resulting in decreasing the morbidity and mortality associated with facial trauma.

  4. 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.)

  5. Poly-IC preconditioning protects against cerebral and renal ischemia-reperfusion injury.

    Science.gov (United States)

    Packard, Amy E B; Hedges, Jason C; Bahjat, Frances R; Stevens, Susan L; Conlin, Michael J; Salazar, Andres M; Stenzel-Poore, Mary P

    2012-02-01

    Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which generally induce significant inflammatory responses, poly-IC elicits only modest systemic inflammation. Results show that poly-IC is a new powerful prophylactic treatment that offers promise as a clinical therapeutic strategy to minimize damage in patient populations at risk of ischemic injury.

  6. 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.

  7. What Protects Certain Nerves from Stretch Injury?

    Science.gov (United States)

    Schraut, Nicholas B; Walton, Sharon; Bou Monsef, Jad; Shott, Susan; Serici, Anthony; Soulii, Lioubov; Amirouche, Farid; Gonzalez, Mark H; Kerns, James M

    2016-01-01

    The human tibial nerves is less prone to injury following joint arthroplasty compared with the peroneal nerves. Besides the anatomical distribution, other features may confer protection from stretch injury. We therefore examined the size, shape and connective tissue distribution for the two nerves. The tibial and peroneal nerves from each side of nine fresh human cadavers we reharvested mid-thigh. Proximal segments manually stretched 20%-25% were fixed in aldehyde, while the adjacent distal segments were fixed in their natural length. Paraffin sections stained by Masson's trichrome method for connective tissue were examined by light microscopy. Tibial nerves had 2X more fascicles compared with the peroneal, but the axonal content appeared similar. Analysis showed that neither nerve had a significant reduction in cross sectional area of the fascicles following stretch. However, fascicles from stretched tibial nerves become significantly more oval compared with those from unstretched controls and peroneal nerves. Tibial nerves had a greater proportion that was extrafascicular tissue (50-55%) compared with peroneal nerves (38%-42%). This epineurium was typically adipose tissue. Perineurial thickness in both nerves was directly related to fascicular size. Tibial nerves have several unique histological features associated with size, shape and tissue composition compared with the peroneal nerve. We suggest that more fascicles with their tightly bound perineurium and more robust epineurium afford protection against stretch injury. Mechanical studies should clarify how size and shape contribute to nerve protection and/or neurapraxia.

  8. 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.

  9. 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.

  10. 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.

  11. 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...

  12. Inflicted traumatic brain injury: advances in evaluation and collaborative diagnosis.

    Science.gov (United States)

    Glick, Jill C; Staley, Kelley

    2007-01-01

    The determination that a traumatic brain injury is not accidental requires data collection from multiple domains: historical, clinical, laboratory, radiographic, environmental and psychosocial. These essential, yet disparate, types of information must be synthesized in a collaborative and interdisciplinary process to formulate a medical opinion with regard to the cause of an injury, and the final opinion has tremendous consequences for children and families. Medically directed child protection teams have emerged as the standard of care in many children's hospitals and child abuse pediatrics is now a recognized medical subspecialty with board certification available in the next several years. Not only do the child and family benefit from this coordinated effort, but there are also great benefits for the members of the child protection team: more clearly defined responsibilities, redirected focus on treatment for the surgeon, and increased confidence that the opinion is based upon consensus and current scientific knowledge. By this process and its division of labor, the child abuse pediatrician assumes responsibility for ensuring that a final medical opinion is arrived at, and then advocates for appropriate disposition for the child. The child abuse pediatrician is responsible for establishing institutional standards for family evaluation, collecting all necessary medical data and directing a consensus-based decision making process that is based upon current medical knowledge, medical literature and experience. The child abuse pediatrician also assumes the role of primary communication conduit for investigational agencies and the courts. The neurosurgeon is a key member of the child protection team and relies on the team to obtain necessary historical information to address consistency of the mechanism with the sustained injuries and has an integral role in determining the team's final opinion. An interdisciplinary response to inflicted traumatic brain injury is the

  13. 电磁辐射致脑损伤与防护若干问题的思考%Potential solutions to brain injury induced by electromagnetic radiation and its protection

    Institute of Scientific and Technical Information of China (English)

    彭瑞云

    2011-01-01

    随着电磁波在通讯、医疗、工业、军事和家庭等各个领域的应用,电磁辐射已广泛存在于人们的日常生活和工作环境之中,其对健康造成的危害越来越引起人们的高度重视.研究发现,一定强度的电磁辐射可引起脑、生殖、心血管、免疫和眼等的损伤,其中对脑的危害备受关注.本文就电磁辐射致脑损伤效应、机制和防护研究现状进行综述,在此基础上,提出电磁辐射生物效应和防护研究的意见和建议.%Electromagnetic radiation has come to be widespread in daily lives and work environment following the wide use of electromagnetic wave in telecommunications, medicine , industry, the military and households. The harm of electromagnetic radiation to health has become a concern. It was found that elec:tromagnetic radiation of a particular magnitude may cause damage to such organs as the testicles, heart, spleen, and eyes, especially to the brain. The present review summarizes the effects, and mechanisms of and protection against the injury to the brain induced by electromagnetic radiation. Furthermore, the author advises on the bio-effect of and protection against electromagnetic radiation.

  14. Wearable nanosensor system for monitoring mild traumatic brain injuries in football players

    Science.gov (United States)

    Ramasamy, Mouli; Varadan, Vijay K.

    2016-04-01

    Football players are more to violent impacts and injuries more than any athlete in any other sport. Concussion or mild traumatic brain injuries were one of the lesser known sports injuries until the last decade. With the advent of modern technologies in medical and engineering disciplines, people are now more aware of concussion detection and prevention. These concussions are often overlooked by football players themselves. The cumulative effect of these mild traumatic brain injuries can cause long-term residual brain dysfunctions. The principle of concussion is based the movement of the brain in the neurocranium and viscerocranium. The brain is encapsulated by the cerebrospinal fluid which acts as a protective layer for the brain. This fluid can protect the brain against minor movements, however, any rapid movements of the brain may mitigate the protective capability of the cerebrospinal fluid. In this paper, we propose a wireless health monitoring helmet that addresses the concerns of the current monitoring methods - it is non-invasive for a football player as helmet is not an additional gear, it is efficient in performance as it is equipped with EEG nanosensors and 3D accelerometer, it does not restrict the movement of the user as it wirelessly communicates to the remote monitoring station, requirement of individual monitoring stations are not required for each player as the ZigBee protocol can couple multiple transmitters with one receiver. A helmet was developed and validated according to the above mentioned parameters.

  15. 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.

  16. [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.

  17. 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.

  18. Occupant injury protection in automobile collisions.

    Science.gov (United States)

    Peters, G A; Peters, B J

    1999-12-01

    Modern technology has produced automotive vehicles that have become both a luxury and a necessity in modern civilization. They have become highly useful, even more varied in form and function, and capable of high speeds on crowded roadways. One unfortunate consequence is the high frequency of accidents and the greater severity of injuries when collisions do occur. In response, modern technology has produced a variety of safety and health features, devices and designs intended for better occupant protection on in high speed vehicles. Injury reduction has become a prime design objective, but there are residual risks, which, as technology evolves, require effective communication to those risk. There can be little risk avoidance behavior without awareness of the hazards and effective communication to the vehicle occupant, as to what could and should be done for self-protection. For example, one out of three drivers apparently fails to understand the function of head restraints, few understand the 'safe zone' posture required for air bags and many believe safety features should be adjusted only for comfort. Some of the current residual injury producing problems in occupant systems are specifically described here in order to illustrate what is needed in terms of both design remedies and health promotion activities.

  19. 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...

  20. 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

  1. 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.

  2. 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

  3. 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.

  4. 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

  5. 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.

  6. 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.

  7. Motorcycle-Related Traumatic Brain Injuries: Helmet Use and Treatment Outcome

    Directory of Open Access Journals (Sweden)

    Mathias Ogbonna Nnanna Nnadi

    2015-01-01

    Full Text Available Summary. With increasing use of motorcycle as means of transport in developing countries, traumatic brain injuries from motorcycle crashes have been increasing. The only single gadget that protects riders from traumatic brain injury is crash helmet. Objective. The objectives were to determine the treatment outcome among traumatic brain injury patients from motorcycle crashes and the rate of helmet use among them. Methods. It was a prospective, cross-sectional study of motorcycle-related traumatic brain injury patients managed in our center from 2010 to 2014. Patients were managed using our unit protocol for traumatic brain injuries. Data for the study were collected in accident and emergency, intensive care unit, wards, and outpatient clinic. The data were analyzed using Environmental Performance Index (EPI info 7 software. Results. Ninety-six patients were studied. There were 87 males. Drivers were 65. Only one patient wore helmet. Majority of them were between 20 and 40 years. Fifty-three patients had mild head injuries. Favorable outcome among them was 84.35% while mortality was 12.5%. Severity of the injury affected the outcome significantly. Conclusion. Our study showed that the helmet use by motorcycle riders was close to zero despite the existing laws making its use compulsory in Nigeria. The outcome was related to severity of injuries.

  8. Post-traumatic stress disorder and traumatic brain injury.

    Science.gov (United States)

    Motzkin, Julian C; Koenigs, Michael R

    2015-01-01

    Disentangling the effects of "organic" neurologic damage and psychological distress after a traumatic brain injury poses a significant challenge to researchers and clinicians. Establishing a link between traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) has been particularly contentious, reflecting difficulties in establishing a unique diagnosis for conditions with overlapping and sometimes contradictory symptom profiles. However, each disorder is linked to a variety of adverse health outcomes, underscoring the need to better understand how neurologic and psychiatric risk factors interact following trauma. Here, we present data showing that individuals with a TBI are more likely to develop PTSD, and that individuals with PTSD are more likely to develop persistent cognitive sequelae related to TBI. Further, we describe neurobiological models of PTSD, highlighting how patterns of neurologic damage typical in TBI may promote or protect against the development of PTSD in brain-injured populations. These data highlight the unique course of PTSD following a TBI and have important diagnostic, prognostic, and treatment implications for individuals with a dual diagnosis.

  9. 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.

  10. 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

  11. 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.

  12. 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…

  13. 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

  14. 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

  15. [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.

  16. 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

  17. 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

  18. 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.

  19. Protect Your Brain (A Minute of Health with CDC)

    Centers for Disease Control (CDC) Podcasts

    2013-03-21

    At least three and a half million people in the U.S. sustained a traumatic brain injury (TBI), either with or without other injuries. This podcast discusses the importance of early diagnosis and treatment of brain injuries.  Created: 3/21/2013 by MMWR.   Date Released: 3/21/2013.

  20. 重型颅脑创伤大鼠后期脑水肿研究及牛磺酸转运体的作用%Protection role of taurine transporter in rats brain edema followed severe traumatic head injury

    Institute of Scientific and Technical Information of China (English)

    蔡英; 黄慧玲; 范维佳; 武俏丽; 李晓茜; 苏彦华; 温晓昶

    2015-01-01

    Objective To investigate the effect of taurine transporter in the process of protection of brain edema in rats with severe traumatic head injury. Methods A total of 24 Male Sprague-Dawley rats were randomly divided into 4 groups. Except the control rats (Group Sham), all other three groups were subjected to lateral fluid percussion head injury. The TBI (Traumatic brain injury) models (Group TBI) and surgical control rats (Group Sham) were injected with saline through caudal vein after surgery, while the Taurine prevention and Taurine treatment models (Group Pre Tau and Group Tau) were injected with 120 g/L taurine solution before or after surgeries respectively. Water content in each brain, mRNA and protein expres⁃sion of aquaporin 4 and taurine transporter in the injured rat brain hemispheres were all evaluated over the time course of the study (7 d) in each group. Results Compared with rats in Group Sham, water content in each brain increase, mRNA tran⁃scription and protein expression of AQP4 were both up regulated but the mRNA transcription and protein expression of TauT were both down-regulated in rats in TBI group. Compared with rats in TBI group, brain water content, mRNA transcription and protein expression of AQP4 all decrease while mRNA transcription and protein expression of TauT all increase in rats in Pre tau and Tau groups. There is no statistical difference of TauT expression between rats in pre-tau group and Tau group. Conclusion Taurine exert its neuron protection role through draining water content from brain and down regulating expres⁃sion of AQP4 but rising expression of TauT after TBI.%目的:研究牛磺酸转运体(TauT)在牛磺酸调节重型颅脑创伤大鼠后期脑水肿中的作用。方法将40只大鼠按随机数字表法分为4组:假手术组(Sham组)、脑外伤组(TBI组)、牛磺酸预防组(Pre-Tau组)和牛磺酸治疗组(Tau组)。液压冲击法制作重型颅脑创伤大鼠模型。Pre-Tau组和Tau

  1. 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.

  2. 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.)

  3. 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.

  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. Working toward exposure thresholds for blast-induced traumatic brain injury: thoracic and acceleration mechanisms

    CERN Document Server

    Courtney, Michael; 10.1016/j.neuroimage.2010.05.025

    2011-01-01

    Research in blast-induced lung injury resulted in exposure thresholds that are useful in understanding and protecting humans from such injury. Because traumatic brain injury (TBI) due to blast exposure has become a prominent medical and military problem, similar thresholds should be identified that can put available research results in context and guide future research toward protecting warfighters as well as diagnosis and treatment. At least three mechanical mechanisms by which the blast wave may result in brain injury have been proposed - a thoracic mechanism, head acceleration and direct cranial transmission. These mechanisms need not be mutually exclusive. In this study, likely regions of interest for the first two mechanisms based on blast characteristics (positive pulse duration and peak effective overpressure) are developed using available data from blast experiments and related studies, including behind-armor blunt trauma and ballistic pressure wave studies. These related studies are appropriate to in...

  8. Synthetic neurosteroids on brain protection

    Institute of Scientific and Technical Information of China (English)

    Mariana Rey; Hctor Coirini

    2015-01-01

    Neurosteroids, like allopregnanolone and pregnanolone, are endogenous regulators of neuronal excitability. Inside the brain, they are highly selective and potent modulators of GABAA receptor activity. Their anticonvulsant, anesthetics and anxiolytic properties are useful for the treatments of several neurological and psychiatric disordersvia reducing the risks of side effects obtained with the commercial drugs. The principal disadvantages of endogenous neurosteroids adminis-tration are their rapid metabolism and their low oral bioavailability. Synthetic steroids analogues with major stability or endogenous neurosteroids stimulation synthesis might constitute prom-ising novel strategies for the treatment of several disorders. Numerous studies indicate that the 3α-hydroxyl conifguration is the key for binding and activity, but modiifcations in the steroid nucleus may emphasize different pharmacophores. So far, several synthetic steroids have been developed with successful neurosteroid-like effects. In this work, we summarize the properties of various synthetic steroids probed in trials throughout the analysis of several neurosteroids-like actions.

  9. 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.

  10. 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.

  11. Alcohol Withdrawal and Brain Injuries: Beyond Classical Mechanisms

    Directory of Open Access Journals (Sweden)

    Marianna E. Jung

    2010-07-01

    Full Text Available Unmanaged sudden withdrawal from the excessive consumption of alcohol (ethanol adversely alters neuronal integrity in vulnerable brain regions such as the cerebellum, hippocampus, or cortex. In addition to well known hyperexcitatory neurotransmissions, ethanol withdrawal (EW provokes the intense generation of reactive oxygen species (ROS and the activation of stress-responding protein kinases, which are the focus of this review article. EW also inflicts mitochondrial membranes/membrane potential, perturbs redox balance, and suppresses mitochondrial enzymes, all of which impair a fundamental function of mitochondria. Moreover, EW acts as an age-provoking stressor. The vulnerable age to EW stress is not necessarily the oldest age and varies depending upon the target molecule of EW. A major female sex steroid, 17β-estradiol (E2, interferes with the EW-induced alteration of oxidative signaling pathways and thereby protects neurons, mitochondria, and behaviors. The current review attempts to provide integrated information at the levels of oxidative signaling mechanisms by which EW provokes brain injuries and E2 protects against it. Unmanaged sudden withdrawal from the excessive consumption of alcohol (ethanol adversely alters neuronal integrity in vulnerable brain regions such as the cerebellum, hippocampus, or cortex. In addition to well known hyperexcitatory neurotransmissions, ethanol withdrawal (EW provokes the intense generation of reactive oxygen species (ROS and the activation of stress-responding protein kinases, which are the focus of this review article. EW also inflicts mitochondrial membranes/membrane potential, perturbs redox balance, and suppresses mitochondrial enzymes, all of which impair a fundamental function of mitochondria. Moreover, EW acts as an age-provoking stressor. The vulnerable age to EW stress is not necessarily the oldest age and varies depending upon the target molecule of EW. A major female sex steroid, 17

  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. 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

  14. 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…

  15. 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.

  16. 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.

  17. 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.

  18. 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.

  19. 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.

  20. 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

  1. 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.

  2. 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.

  3. 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

  4. Lateral fluid percussion injury of the brain induces CCL20 inflammatory chemokine expression in rats

    OpenAIRE

    2011-01-01

    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 thi...

  5. 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.

  6. 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

  7. Depression after traumatic brain injury: a biopsychosocial cultural perspective.

    Science.gov (United States)

    Roy, Durga; Jayaram, Geetha; Vassila, Alex; Keach, Shari; Rao, Vani

    2015-02-01

    There are several challenges in diagnosing and treating mental illness amongst South Asians. Often times, formulating a patient's case presentation cannot adequately be accomplished strictly using a biopsychosocial model. The cultural components play an imperative role in explaining certain psychiatric symptoms and can guide treatment. With the growing population of immigrants coming to the United States, many of which require treatment for mental illness, it is essential that clinicians be cognizant in incorporating cultural perspectives when treating such patients. The authors describe the case of a 24-year old South Asian male who suffered an exacerbation of a depressive syndrome after a traumatic brain injury. Using a biopsychosocial cultural approach, this case highlights how South Asian cultural values can contribute to and incite psychiatric symptoms while simultaneously providing protective drivers for treatment outcomes.

  8. 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.

  9. 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.

  10. 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.

  11. Amniotic cells protect and repair mouse brain cells following ischemia-reperfusion injury%羊膜细胞可保护和修复缺血再灌注损伤小鼠脑组织细胞

    Institute of Scientific and Technical Information of China (English)

    郑彦涛; 刘斌; Robert Lodato; 李奇林; 蓝迪慧; 洪小英; 鲜华

    2014-01-01

    背景:羊膜细胞主要由羊膜上皮细胞和羊膜间充质细胞组成,均具有多分化潜能,可转化为神经元,且还有合成、释放生物活性物质和神经营养因子的功能。作者前期研究证实羊膜细胞移植入脑内后,能明显促进脑内神经元的再生。目的:探索羊膜细胞对小鼠缺血再灌注损伤脑细胞的作用。方法:将Balb/C小鼠通过夹闭双侧颈总动脉方法建立脑缺血再灌注损伤模型后,分离小鼠脑细胞。取孕鼠新鲜胎盘,分离羊膜细胞。将与羊膜细胞共培养的小鼠脑细胞作为实验组,以PBS培养的小鼠脑细胞作为对照组。结果与结论:实验组小鼠脑细胞活性较对照组明显增加(P0.05),而培养48 h后实验组小鼠脑细胞坏死率较对照组明显降低(P0.05);after 48 hours co-culture, however, the necrotic rate of brain cells was significantly lower in the experimental group than the control group (P<0.05). In cellcycle, the experiment group showed increased S phase cells;while, the control group exhibited increased G 1 phase cells and decreased S phase cells. G 2 phase cells had no changes in number in both two groups. Through the above results, amnion cells can be proved to protect and promote the regeneration of brain cells of Balb/C mice with ischemia-reperfusion injury, and inhibit cellnecrosis and apoptosis.

  12. 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.

  13. 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

  14. 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

  15. 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...

  16. 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 ...

  17. 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,...

  18. 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.

  19. 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 ...

  20. 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 ...

  1. 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.

  2. 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.

  3. 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

  4. 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.

  5. 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 ...

  6. 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 ...

  7. 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.

  8. 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.

  9. Role of microglia in a mouse model of paediatric traumatic brain injury.

    Science.gov (United States)

    Chhor, Vibol; Moretti, Raffaella; Le Charpentier, Tifenn; Sigaut, Stephanie; Lebon, Sophie; Schwendimann, Leslie; Oré, Marie-Virginie; Zuiani, Chiara; Milan, Valentina; Josserand, Julien; Vontell, Regina; Pansiot, Julien; Degos, Vincent; Ikonomidou, Chrysanthy; Titomanlio, Luigi; Hagberg, Henrik; Gressens, Pierre; Fleiss, Bobbi

    2016-11-04

    The cognitive and behavioural deficits caused by traumatic brain injury (TBI) to the immature brain are more severe and persistent than TBI in the mature brain. Understanding this developmental sensitivity is critical as children under four years of age sustain TBI more frequently than any other age group. Microglia (MG), resident immune cells of the brain that mediate neuroinflammation, are activated following TBI in the immature brain. However, the type and temporal profile of this activation and the consequences of altering it are still largely unknown. In a mouse model of closed head weight drop paediatric brain trauma, we characterized i) the temporal course of total cortical neuroinflammation and the phenotype of ex vivo isolated CD11B-positive microglia/macrophage (MG/MΦ) using a battery of 32 markers, and ii) neuropathological outcome 1 and 5days post-injury. We also assessed the effects of targeting MG/MΦ activation directly, using minocycline a prototypical microglial activation antagonist, on these processes and outcome. TBI induced a moderate increase in both pro- and anti-inflammatory cytokines/chemokines in the ipsilateral hemisphere. Isolated cortical MG/MΦ expressed increased levels of markers of endogenous reparatory/regenerative and immunomodulatory phenotypes compared with shams. Blocking MG/MΦ activation with minocycline at the time of injury and 1 and 2days post-injury had only transient protective effects, reducing ventricular dilatation and cell death 1day post-injury but having no effect on injury severity at 5days. This study demonstrates that, unlike in adults, the role of MG/MΦ in injury mechanisms following TBI in the immature brain may not be negative. An improved understanding of MG/MΦ function in paediatric TBI could support translational efforts to design therapeutic interventions.

  10. 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

  11. 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.

  12. 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…

  13. 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.

  14. 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

  15. 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.

  16. 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

  17. 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

  18. 褪黑素对细菌脂多糖导致的宫内感染脑损伤的保护作用%Protective effect of melatonin on brain injury of intrauterine infection induced by bacterial lipopolysaccharide

    Institute of Scientific and Technical Information of China (English)

    刘利芬; 钱志红; 史明

    2011-01-01

    Objective: To investigate the effect of melatonin on free radical in brain tissues of fetal rats with intrauterine infection,explore the protective effect of melatonin on brain tissues of fetal rats with intrauterine infection. Methods: The models of cerebral palsy rat induced by intrauterine infection were established by injecting bacterial lipopolysaccharide into pregnant rats, melatonin intervention was carried out; the SD rats on the 19th day after pregnancy were selected as blank control group, intrauterine infection group and melatonin treatment group; the pregnant rats in intrauterine infection group were treated with intraperitoneal injection of bacterial lipopolysaccharide (500 μg/kg), and the pregnant rats in melatonin treatment group were treated with intraperitoneal injection of bacterial lipopolysaccharide (500 μg/kg) and melatonin ( 10 mg/kg); then the rats in each group were divided into 2 - hour group, 6 - hour group and 12 - hour group according to different observing times, 4 pregnant rats in each group; the pregnant rats in each group were executed at corresponding time points, then the brain tissues of fetal rats were obtained; the superoxide dismutase (SOD) activity, glutathione peroxidase (GSH -Px) activity and malondialdehyde (MDA) content in the brain tissues of fetal rats after homogenate were detected; HE staining was used to observe the pathological changes of brain tissues, and the differences among different groups were compared. Results: Compared with blank control group, SOD activity and GSH- Px activity of brain tissues of fetal rats in intrauterine infection group decreased, MDA content increased;with the extension of infection time, the above - mentioned changes became more obvious, there was significant difference; compared with intrauterine infection group, SOD activity and GSH - Px activity of brain tissues of fetal rats in melatonin treatment group increased, MDA content decreased. Conclusion: Brain injury of fetal rats with

  19. A TIGAR-regulated metabolic pathway is critical for protection of brain ischemia.

    Science.gov (United States)

    Li, Mei; Sun, Meiling; Cao, Lijuan; Gu, Jin-hua; Ge, Jianbin; Chen, Jieyu; Han, Rong; Qin, Yuan-Yuan; Zhou, Zhi-Peng; Ding, Yuqiang; Qin, Zheng-Hong

    2014-05-28

    TP53-induced glycolysis and apoptosis regulator (TIGAR) inhibits glycolysis and increases the flow of pentose phosphate pathway (PPP), which generates NADPH and pentose. We hypothesized that TIGAR plays a neuroprotective role in brain ischemia as neurons do not rely on glycolysis but are vulnerable to oxidative stress. We found that TIGAR was highly expressed in brain neurons and was rapidly upregulated in response to ischemia/reperfusion insult in a TP53-independent manner. Overexpression of TIGAR in normal mice with lentivirus reduced ischemic neuronal injury, whereas lentivirus-mediated TIGAR knockdown aggravated it. In cultured primary neurons, increasing TIGAR expression reduced oxygen and glucose deprivation (OGD)/reoxygenation-induced injury, whereas decreasing its expression worsened the injury. The glucose 6-phosphate dehydrogenase was upregulated in mouse and cellular models of stroke, and its upregulation was further enhanced by overexpression of TIGAR. Supplementation of NADPH also reduced ischemia/reperfusion brain injury and alleviated TIGAR knockdown-induced aggravation of ischemic injury. In animal and cellular stroke models, ischemia/reperfusion increased mitochondrial localization of TIGAR. OGD/reoxygenation-induced elevation of ROS, reduction of GSH, dysfunction of mitochondria, and activation of caspase-3 were rescued by overexpression of TIGAR or supplementation of NADPH, while knockdown of TIGAR aggravated these changes. Together, our results show that TIGAR protects ischemic brain injury via enhancing PPP flux and preserving mitochondria function, and thus may be a valuable therapeutic target for ischemic brain injury.

  20. [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.

  1. 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.

  2. 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.

  3. Protective Effects of HDL Against Ischemia/Reperfusion Injury.

    Science.gov (United States)

    Gomaraschi, Monica; Calabresi, Laura; Franceschini, Guido

    2016-01-01

    Several lines of evidence suggest that, besides being a strong independent predictor of the occurrence of primary coronary events, a low plasma high density lipoprotein (HDL) cholesterol level is also associated with short- and long-term unfavorable prognosis in patients, who have recovered from a myocardial infarction, suggesting a direct detrimental effect of low HDL on post-ischemic myocardial function. Experiments performed in ex vivo and in vivo models of myocardial ischemia/reperfusion (I/R) injury have clearly shown that HDL are able to preserve cardiac function when given before ischemia or at reperfusion; the protective effects of HDL against I/R injury have been also confirmed in other tissues and organs, as brain and hind limb. HDL were shown to act on coronary endothelial cells, by limiting the increase of endothelium permeability and promoting vasodilation and neoangiogenesis, on white blood cells, by reducing their infiltration into the ischemic tissue and the release of pro-inflammatory and matrix-degrading molecules, and on cardiomyocytes, by preventing the activation of the apoptotic cascade. Synthetic HDL retains the cardioprotective activity of plasma-derived HDL and may become a useful adjunctive therapy to improve clinical outcomes in patients with acute coronary syndromes or undergoing coronary procedures.

  4. 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...

  5. 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

  6. 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.

  7. 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

  8. [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.

  9. Brain neuropeptides in gastric mucosal protection.

    Science.gov (United States)

    Gyires, Klára; Zádori, Zoltán S

    2014-12-01

    The centrally induced gastroprotective effect of neuropeptides has been intensively studied. Besides many similarities, however, differences can also be observed in their gastroprotective actions. The gastroprotective dose-response curve proved to be either sigmoid, or bell-shaped. Additional gastrointestinal effects of neuropeptides can contribute to their mucosal protective effect. Part of the neuropeptides induces gastroprotection by peripheral administration as well. Besides vagal nerve the sympathetic nervous system may also be involved in conveying the central effect to the periphery. Better understanding of the complex mechanism of the maintenance of gastric mucosal integrity may result in the development of new strategy to enhance gastric mucosal resistance against injury.

  10. 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.

  11. 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

  12. 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.

  13. 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

  14. 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.

  15. 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.

  16. Neuroprotective efficacy of a proneurogenic compound after traumatic brain injury.

    Science.gov (United States)

    Blaya, Meghan O; Bramlett, Helen M; Naidoo, Jacinth; Pieper, Andrew A; Dietrich, W Dalton

    2014-03-01

    Traumatic brain injury (TBI) is characterized by histopathological damage and long-term sensorimotor and cognitive dysfunction. Recent studies have reported the discovery of the P7C3 class of aminopropyl carbazole agents with potent neuroprotective properties for both newborn neural precursor cells in the adult hippocampus and mature neurons in other regions of the central nervous system. This study tested, for the first time, whether the highly active P7C3-A20 compound would be neuroprotective, promote hippocampal neurogenesis, and improve functional outcomes after experimental TBI. Sprague-Dawley rats subjected to moderate fluid percussion brain injury were evaluated for quantitative immunohistochemical and behavioral changes after trauma. P7C3-A20 (10 mg/kg) or vehicle was initiated intraperitoneally 30 min postsurgery and twice per day every day thereafter for 7 days. Administration of P7C3-A20 significantly reduced overall contusion volume, preserved vulnerable anti-neuronal nuclei (NeuN)-positive pericontusional cortical neurons, and improved sensorimotor function 1 week after trauma. P7C3-A20 treatment also significantly increased both bromodeoxyuridine (BrdU)- and doublecortin (DCX)-positive cells within the subgranular zone of the ipsilateral dentate gyrus 1 week after TBI. Five weeks after TBI, animals treated with P7C3-A20 showed significantly increased BrdU/NeuN double-labeled neurons and improved cognitive function in the Morris water maze, compared to TBI-control animals. These results suggest that P7C3-A20 is neuroprotective and promotes endogenous reparative strategies after TBI. We propose that the chemical scaffold represented by P7C3-A20 provides a basis for optimizing and advancing new pharmacological agents for protecting patients against the early and chronic consequences of TBI.

  17. 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."

  18. Traumatic Brain Injury Studies in Britain during World War II.

    Science.gov (United States)

    Lanska, Douglas J

    2016-01-01

    As a result of the wartime urgency to understand, prevent, and treat patients with traumatic brain injury (TBI) during World War II (WWII), clinicians and basic scientists in Great Britain collaborated on research projects that included accident investigations, epidemiologic studies, and development of animal and physical models. Very quickly, investigators from different disciplines shared information and ideas that not only led to new insights into the mechanisms of TBI but also provided very practical approaches for preventing or ameliorating at least some forms of TBI. Neurosurgeon Hugh Cairns (1896-1952) conducted a series of influential studies on the prevention and treatment of head injuries that led to recognition of a high rate of fatal TBI among motorcycle riders and subsequently to demonstrations of the utility of helmets in lowering head injury incidence and case fatality. Neurologists Derek Denny-Brown (1901-1981) and (William) Ritchie Russell (1903-1980) developed an animal model of TBI that demonstrated the fundamental importance of sudden acceleration (i.e., jerking) of the head in causing concussion and forced a distinction between head injury associated with sudden acceleration/deceleration and that associated with crush or compression. Physicist A.H.S. Holbourn (1907-1962) used theoretical arguments and simple physical models to illustrate the importance of shear stress in TBI. The work of these British neurological clinicians and scientists during WWII had a strong influence on subsequent clinical and experimental studies of TBI and also eventually resulted in effective (albeit controversial) public health campaigns and legislation in several countries to prevent head injuries among motorcycle riders and others through the use of protective helmets. Collectively, these studies accelerated our understanding of TBI and had subsequent important implications for both military and civilian populations. As a result of the wartime urgency to understand

  19. 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

  20. Protective effects of N-acetylcysteine on brain-dead rat liver

    Institute of Scientific and Technical Information of China (English)

    Shui-Jun Zhang; Ting-Wu Ma; Xiu-Xian Ma; Jian-Jun Gou; Ji-Hua Shi; Wen-Zhi Guo

    2006-01-01

    BACKGROUND: Brain-dead donors have been the main sources in organ transplantation. But many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in rats and the protective effects of N-acetyleysteine (NAC) on liver injury. METHODS: A total of 30 Wistar rats were randomized into 3 groups: normal control group (C), brain-dead group (B), and NAC pretreatment group (N). At 4 hours after the establishment of a brain-dead model, serum was collected to determine the levels of ALT, AST, TNF-α and hyaluronic acid (HA). Hepatic tissue was obtained for electron microscopic examination. RESULTS:At 4 hours, the levels of ALT, AST, TNF-α, and HA in group N were signiifcantly higher than those in group C, but these parameters were signiifcantly lower than those in group B. Electron microscopy showed activated Kupffer cells, denuded sinusoidal endothelial cells (SECs), and widened fenestration in group B, but eliminated activation of Kupffer cells and intact SECs in group N. CONCLUSION: Brain death can cause liver injury, and N-acetyleysteine can protect the liver from the injury.

  1. 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.

  2. 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.

  3. Effects of estradiol on cognition and hippocampal pathology after lateral fluid percussion brain injury in female rats.

    Science.gov (United States)

    Lebesgue, Diane; LeBold, David G; Surles, Nathan O; Morales, Diego M; Etgen, Anne M; Zukin, R Suzanne; Saatman, Kathryn E

    2006-12-01

    Studies involving animal models of acute central nervous system (CNS) stroke and trauma strongly indicate that sex and/or hormonal status are important determinants of outcome after brain injury. The present study was undertaken to examine the ability of estradiol to protect hippocampal neurons from lateral fluid percussion brain injury. Sprague-Dawley female rats (211-285 g; n = 119) were ovariectomized, and a subset (n = 66) were implanted with 17beta-estradiol pellets to provide near physiological levels of estradiol. Animals were subjected to lateral fluid percussion brain injury or sham injury 1 week later. Activation of caspase-3 (n = 26) and TUNEL staining (n = 21) were assessed at 3 and 12 h after injury, respectively, in surviving control and estradiol-treated animals. Memory retention was examined using a Morris water maze test in a separate subset of animals (n = 43) at 8 days after injury. Activated caspase-3 and TUNEL staining were observed in the dentate hilus, granule cell layer, and CA3 regions in all injured rats, indicative of selective hippocampal cell apoptosis in the acute posttraumatic period. Estradiol did not significantly alter the number of hippocampal neurons exhibiting caspase-3 activity or TUNEL staining. Brain injury impaired cognitive ability, assessed at 1 week post-injury (p < 0.001). However, estradiol at physiological levels did not significantly alter injury-induced loss of memory. These data indicate that estradiol at physiological levels does not ameliorate trauma-induced hippocampal injury or cognitive deficits in ovariectomized female rats.

  4. Antioxidant and antitranspirant protection of apple foliage against ozone injury

    Energy Technology Data Exchange (ETDEWEB)

    Elfving, D.C.; Gilbert, M.D.; Edgerton, L.J.; Wilde, M.H.; Lisk, D.J.

    1976-01-01

    Visible injury to apple foliage from exposure to ozone includes brown stippling on lower leaf surfaces and a light yellow mosaic on upper surfaces. Histologically, chlorophyll is destroyed and palisade and spongy mesophyll cells collapse following disintegration of their protoplasm. Foliar spray applications of the antioxidant, diphenylamine (DPA) or the antitranspirant, Wilt Pruf offer protection against this visible and histological injury. Superior protection results from application of both agents in combination.

  5. Copper exposure induces oxidative injury, disturbs the antioxidant system and changes the Nrf2/ARE (CuZnSOD) signaling in the fish brain: protective effects of myo-inositol.

    Science.gov (United States)

    Jiang, Wei-Dan; Liu, Yang; Hu, Kai; Jiang, Jun; Li, Shu-Hong; Feng, Lin; Zhou, Xiao-Qiu

    2014-10-01

    The brain is the center of the nervous system in all vertebrates, and homeostasis of the brain is crucial for fish survival. Copper (Cu) is essential for normal cellular processes in most eukaryotic organisms but is toxic in excess. Although Cu is indicated as a potent neurotoxicant, information regarding its threat to fish brain and underlying mechanisms is still scarce. In accordance, the objective of this study was to assess the effects and the potential mechanism of Cu toxicity by evaluating brain oxidative status, the enzymatic and mRNA levels of antioxidant genes, as well as the Nrf2/ARE signaling in the brain of fish after Cu exposure. The protective effects of myo-inositol (MI) against subsequent Cu exposure were also investigated. The results indicate that induction of oxidative stress by Cu is shown by increases in brain ROS production, lipid peroxidation and protein oxidation, which are accompanied by depletions of antioxidants, including total superoxide dismutase (T-SOD), CuZnSOD, glutathione-S-transferase (GST) and glutathione reductase (GR) activities and glutathione (GSH) content. Cu exposure increased the catalase (CAT) and glutathione peroxidase (GPx) activities. Further molecular results showed that Cu exposure up-regulated CuZnSOD, GPx1a and GR mRNA levels, suggesting an adaptive mechanism against stress. Moreover, Cu exposure increased fish brain Nrf2 nuclear accumulation and increased its ability of binding to ARE (CuZnSOD), which supported the increased CuZnSOD mRNA levels. In addition, Cu exposure caused increases of the expression of the Nrf2, Maf G1 (rather than Maf G2 gene) and PKCd genes, suggesting that de novo synthesis of those factors is required for the protracted induction of such antioxidant genes. However, the modulation of Keap1a (rather than Keap1b) of fish brain under Cu exposure might be used to turn off of the signaling cascade and avoid harmful effects. Interestingly, pre-treatment of fish with MI prevented the fish brain

  6. 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

  7. 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

  8. Copper exposure induces oxidative injury, disturbs the antioxidant system and changes the Nrf2/ARE (CuZnSOD) signaling in the fish brain: Protective effects of myo-inositol

    Energy Technology Data Exchange (ETDEWEB)

    Jiang, Wei-Dan; Liu, Yang [Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Hu, Kai [Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Jiang, Jun [Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Li, Shu-Hong [Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Feng, Lin, E-mail: fenglin@sicau.edu.cn [Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Zhou, Xiao-Qiu, E-mail: xqzhouqq@tom.com [Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, Sichuan (China); Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Sichuan Agricultural University, Chengdu 611130, Sichuan (China)

    2014-10-15

    Highlights: • Cu exposure increased ROS production, lipid and protein oxidation of fish brain. • Cu exposure caused depletion of some antioxidants in the brain of fish. • Cu exposure up-regulated mRNA levels of brain CuZnSOD, GPx1a and GR genes in fish. • Cu exposure induced Nrf2 nuclear translocation and binding to ARE in fish brain. • Myo-inositol can inhibit Cu-induced toxic effects in the brain of fish. - Abstract: The brain is the center of the nervous system in all vertebrates, and homeostasis of the brain is crucial for fish survival. Copper (Cu) is essential for normal cellular processes in most eukaryotic organisms but is toxic in excess. Although Cu is indicated as a potent neurotoxicant, information regarding its threat to fish brain and underlying mechanisms is still scarce. In accordance, the objective of this study was to assess the effects and the potential mechanism of Cu toxicity by evaluating brain oxidative status, the enzymatic and mRNA levels of antioxidant genes, as well as the Nrf2/ARE signaling in the brain of fish after Cu exposure. The protective effects of myo-inositol (MI) against subsequent Cu exposure were also investigated. The results indicate that induction of oxidative stress by Cu is shown by increases in brain ROS production, lipid peroxidation and protein oxidation, which are accompanied by depletions of antioxidants, including total superoxide dismutase (T-SOD), CuZnSOD, glutathione-S-transferase (GST) and glutathione reductase (GR) activities and glutathione (GSH) content. Cu exposure increased the catalase (CAT) and glutathione peroxidase (GPx) activities. Further molecular results showed that Cu exposure up-regulated CuZnSOD, GPx1a and GR mRNA levels, suggesting an adaptive mechanism against stress. Moreover, Cu exposure increased fish brain Nrf2 nuclear accumulation and increased its ability of binding to ARE (CuZnSOD), which supported the increased CuZnSOD mRNA levels. In addition, Cu exposure caused increases of

  9. 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.

  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. Inhibition of neuronal ferroptosis protects hemorrhagic brain

    Science.gov (United States)

    Li, Qian; Han, Xiaoning; Lan, Xi; Gao, Yufeng; Wan, Jieru; Durham, Frederick; Cheng, Tian; Yang, Jie; Wang, Zhongyu; Jiang, Chao; Ying, Mingyao; Stockwell, Brent R.

    2017-01-01

    Intracerebral hemorrhage (ICH) causes high mortality and morbidity, but our knowledge of post-ICH neuronal death and related mechanisms is limited. In this study, we first demonstrated that ferroptosis, a newly identified form of cell death, occurs in the collagenase-induced ICH model in mice. We found that administration of ferrostatin-1, a specific inhibitor of ferroptosis, prevented neuronal death and reduced iron deposition induced by hemoglobin in organotypic hippocampal slice cultures (OHSCs). Mice treated with ferrostatin-1 after ICH exhibited marked brain protection and improved neurologic function. Additionally, we found that ferrostatin-1 reduced lipid reactive oxygen species production and attenuated the increased expression level of PTGS2 and its gene product cyclooxygenase-2 ex vivo and in vivo. Moreover, ferrostatin-1 in combination with other inhibitors that target different forms of cell death prevented hemoglobin-induced cell death in OHSCs and human induced pluripotent stem cell–derived neurons better than any inhibitor alone. These results indicate that ferroptosis contributes to neuronal death after ICH, that administration of ferrostatin-1 protects hemorrhagic brain, and that cyclooxygenase-2 could be a biomarker of ferroptosis. The insights gained from this study will advance our knowledge of the post-ICH cell death cascade and be essential for future preclinical studies.

  12. 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...

  13. 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.

  14. A Hypothesis: Hydrogen Sulfide Might Be Neuroprotective against Subarachnoid Hemorrhage Induced Brain Injury

    Directory of Open Access Journals (Sweden)

    Yong-Peng Yu

    2014-01-01

    Full Text Available Gases such as nitric oxide (NO and carbon monoxide (CO play important roles both in normal physiology and in disease. Recent studies have shown that hydrogen sulfide (H2S protects neurons against oxidative stress and ischemia-reperfusion injury and attenuates lipopolysaccharides (LPS induced neuroinflammation in microglia, exhibiting anti-inflammatory and antiapoptotic activities. The gas H2S is emerging as a novel regulator of important physiologic functions such as arterial diameter, blood flow, and leukocyte adhesion. It has been known that multiple factors, including oxidative stress, free radicals, and neuronal nitric oxide synthesis as well as abnormal inflammatory responses, are involved in the mechanism underlying the brain injury after subarachnoid hemorrhage (SAH. Based on the multiple physiologic functions of H2S, we speculate that it might be a promising, effective, and specific therapy for brain injury after SAH.

  15. 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

  16. Astrocytes require insulin-like growth factor I to protect neurons against oxidative injury.

    Science.gov (United States)

    Genis, Laura; Dávila, David; Fernandez, Silvia; Pozo-Rodrigálvarez, Andrea; Martínez-Murillo, Ricardo; Torres-Aleman, Ignacio

    2014-01-01

    Oxidative stress is a proposed mechanism in brain aging, making the study of its regulatory processes an important aspect of current neurobiological research. In this regard, the role of the aging regulator insulin-like growth factor I (IGF-I) in brain responses to oxidative stress remains elusive as both beneficial and detrimental actions have been ascribed to this growth factor. Because astrocytes protect neurons against oxidative injury, we explored whether IGF-I participates in astrocyte neuroprotection and found that blockade of the IGF-I receptor in astrocytes abrogated their rescuing effect on neurons. We found that IGF-I directly protects astrocytes against oxidative stress (H 2O 2). Indeed, in astrocytes but not in neurons, IGF-I decreases the pro-oxidant protein thioredoxin-interacting protein 1 and normalizes the levels of reactive oxygen species. Furthermore, IGF-I cooperates with trophic signals produced by astrocytes in response to H 2O 2 such as stem cell factor (SCF) to protect neurons against oxidative insult. After stroke, a condition associated with brain aging where oxidative injury affects peri-infarcted regions, a simultaneous increase in SCF and IGF-I expression was found in the cortex, suggesting that a similar cooperative response takes place in vivo. Cell-specific modulation by IGF-I of brain responses to oxidative stress may contribute in clarifying the role of IGF-I in brain aging.

  17. 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.

  18. 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

  19. 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

  20. 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

  1. 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.

  2. Protection of the Transplant Kidney from Preservation Injury by Inhibition of Matrix Metalloproteinases.

    Directory of Open Access Journals (Sweden)

    Michael A J Moser

    Full Text Available Matrix metalloproteinases (MMPs, particularly MMP-2 and MMP-9, play an important role in ischemic injury to the heart, yet it is not known if these MMPs are involved in the injury that occurs to the transplant kidney. We therefore studied the pharmacologic protection of transplant kidneys during machine cold perfusion.Human kidney perfusates were analyzed for the presence of injury markers such as cytochrome c oxidase, lactate dehydrogenase, and neutrophil-gelatinase associated lipocalin (NGAL, and MMP-2 and MMP-9 were measured. The effects of MMP inhibitors MMP-2 siRNA and doxycycline were studied in an animal model of donation after circulatory determination of death (DCDD.Markers of injury were present in all analyzed perfusates, with higher levels seen in perfusates from human kidneys donated after controlled DCDD compared to brain death and in perfusate from kidneys with delayed graft function. When rat kidneys were perfused at 4°C for 22 hours with the addition of MMP inhibitors, this resulted in markedly reduced levels of MMP-2, MMP-9 and analyzed injury markers.Based on our study, MMPs are involved in preservation injury and the supplementation of preservation solution with MMP inhibitors is a potential novel strategy in protecting the transplant kidney from preservation injury.

  3. 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.

  4. 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.

  5. 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.

  6. 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

  7. [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...

  8. 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.

  9. 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.

  10. 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...

  11. 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.

  12. 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.

  13. 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.

  14. 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...

  15. Interaction between anesthesia, gender, and functional outcome task following diffuse traumatic brain injury in rats.

    Science.gov (United States)

    O'Connor, Christine A; Cernak, Ibolja; Vink, Robert

    2003-06-01

    A number of experimental and clinical studies have demonstrated that functional outcome following traumatic brain injury differs between males and females. Some studies report that females have a better outcome than males following trauma while others report the opposite. In experimental studies, some of the contradictory results may be due to the different experimental conditions, including type of anesthesia and the outcome measures employed. In the present study we have used three different anesthetic protocols and four different outcome measures to determine how these parameters interact and affect functional outcome following traumatic brain injury in male and female rats. Diffuse traumatic brain injury was induced in adult male and female animals using the impact-acceleration brain injury model. Mortality in female animals was no different than males when using halothane anesthesia, slightly better than males when using isoflurane anesthesia, but significantly worse than males under pentobarbital anesthesia. Female animals always performed better than males on rotarod tests of motor outcome, with this effect being unrelated to anesthetic effects. Conversely, in cognitive tests using the Barnes Maze, only isoflurane-anesthetized females performed better than their male counterparts. Similarly, in an open field activity task, females always performed better than males after trauma, with isoflurane-anesthetized females also performing significantly better than the halothane-anesthetized female group after injury. Our results suggest that female animals do better than males after diffuse traumatic brain injury, although this observation is dependent upon the type of anesthesia and the functional task employed. Isoflurane is particularly protective in females, pentobarbital is deleterious to female outcome, while halothane anesthesia has the least influence on gender-related outcome.

  16. Preventive administration of cromakalim reduces aquaporin-4 expression and blood-brain barrier permeability in a rat model of cerebral ischemia/reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Shilei Wang; Yanting Wang; Yan Jiang; Qingxian Chang; Peng Wang; Shiduan Wang

    2011-01-01

    Cromakalim, an adenosine triphosphate-sensitive potassium channel opener, exhibits protective effects on cerebral ischemia/reperfusion injury. However, there is controversy as to whether this effect is associated with aquaporin-4 and blood-brain barrier permeability. Immunohistochemistry results show that preventive administration of cromakalim decreased aquaporin-4 and IgG protein expression in rats with ischemia/reperfusion injury; it also reduced blood-brain barrier permeability, and alleviated brain edema, ultimately providing neuroprotection.

  17. Implications of astrocytes in mediating the protective effects of Selective Estrogen Receptor Modulators upon brain damage

    Directory of Open Access Journals (Sweden)

    George E. Barreto

    2015-04-01

    Full Text Available Selective Estrogen Receptor Modulators (SERMs are steroidal or non-steroidal compounds that are already used in clinical practice for the treatment of breast cancer, osteoporosis and menopausal symptoms. While SERMs actions in the breast, bone, and uterus have been well characterized, their actions in the brain are less well understood. Previous works have demonstrated the beneficial effects of SERMs in different chronic neurodegenerative diseases like Alzheimer, Parkinson’s disease and Multiple sclerosis, as well as acute degeneration as stroke and traumatic brain injury. Moreover, these compounds exhibit similar protective actions as those of estradiol in the Central Nervous System, overt any secondary effect. For these reasons, in the past few years, there has been a growing interest in the neuroprotective effects exerted directly or indirectly by SERMs in the SNC. In this context, astrocytes play an important role in the maintenance of brain metabolism, and antioxidant support to neurons, thus indicating that better protection of astrocytes are an important asset targeting neuronal protection. Moreover, various clinical and experimental studies have reported that astrocytes are essential for the neuroprotective effects of SERMs during neuronal injuries, as these cells express different estrogen receptors in cell membrane, demonstrating that part of SERMs effects upon injury may be mediated by astrocytes. The present work highlights the current evidence on the protective mechanisms of SERMs, such as tamoxifen and raloxifene, in the SNC, and their modulation of astrocytic properties as promising therapeutic targets during brain damage.

  18. 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.

  19. 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

  20. 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 ...

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. The effects of different hyperbaric oxygen manipulations in rats after traumatic brain injury.

    Science.gov (United States)

    Yang, Yang; Zhang, Yong-Gang; Lin, Guo-An; Xie, He-Qiu; Pan, Hai-Tao; Huang, Ben-Qing; Liu, Ji-Dong; Liu, Hui; Zhang, Nan; Li, Li; Chen, Jian-Hua

    2014-03-20

    The protective effects of hyperbaric oxygenation following traumatic brain injury have been widely investigated; however, few studies have made systematic comparisons between the different hyperbaric oxygenation manipulations and their corresponding effects. In this study, male Sprague-Dawley rats were observed at 4h, 15d and 75d after traumatic brain injury. The effects of the different hyperbaric oxygenation manipulations on the rats were compared based on morphological, molecular biological and behavioral tests. Our results showed that hyperbaric oxygenation inhibited cell apoptosis in the rat hippocampus and improved their physiological functions. The effects observed in the hyperbaric oxygen-early group were better than the hyperbaric oxygen-delayed group, and the hyperbaric oxygen-early-delayed group demonstrated the best effects among all the groups. Our results showed the hyperbaric oxygenation was recommended early and delayed post-traumatic brain injury and exposure to hyperbaric oxygenation should be prolonged. These findings provide new ideal therapeutic insight for the clinical treatment of traumatic brain injury.

  7. Protective effect of recombinant human brain natriuretic peptide on acute renal injury induced by endotoxin in canines%rhB NP对内毒素介导的犬急性肾损伤的保护作用

    Institute of Scientific and Technical Information of China (English)

    李牧; 刘岩; 李辉

    2014-01-01

    干预组比较,血清HMGB-1水平显著性减少(P<0.05)。结论 rhBNP可以有效减轻内毒素介导的犬肾组织损伤,改善肾功能,并降低SVRI,且其治疗作用呈剂量-效应关系;rhBNP还能有效降低脓毒症犬血清HMGB-1水平,可能与晚期炎症因子HMGB1水平的降低有关。%Objective To observe the influence of recombinant human brain natriuretic peptide(rhBNP)on serum HMGB1 levels in canines'acute renal injury induced by endotoxin and explore its protective role of rhBNP in protecting canines'kidney against acute renal injury.Methods A total of 20 healthy dogs were randomly divided into four groups:blank group,sepsis shock group,low-dose intervention group and high dose intervention group, and there were 5 rats in each group.After establishing the model of canines'sepsis shock induced by endotoxin,15 canines (besides blank group)were randomly divided into 3 groups.As follows,5 μg/kg rhBNP was given to the low-dose intervention group,10μg/kg rhBNP was given to the high-dose intervention group.But nothing was given to control group.Systemic vascular resistance index(SVRI)at 0 h,2 h,4 h,8 h,12 h were observed by PICCO instrument.High mobility group box 1 protein (HMGB-1)and creatinine(CR)in blood samples at each time point were detected.After 12 hours,kidney samples were taken for histological examination.Results The results revealed that some renal tubulars epithelial cell were swelled,some epithelial cells were atrophy and interstitial cells swelled in control group under the light microscope.Kidney pathology score was 2-3.But these changes were improved in low-and high-dose intervention groups,and there were no significant difference in the latter two groups,kidney of both groups pathology score were 1-2.Compared with control group at the same point,CR of blood serum were significantly decreased in low-dose intervention group at 8 h,12 h(P<0.01), and high-dose intervention group significantly decreased at 4 h,8 h,12 h(P<0.01).Compared with

  8. 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 ...

  9. 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.

  10. Effects of therapeutic hypothermia on inflammasome signaling after traumatic brain injury.

    Science.gov (United States)

    Tomura, Satoshi; de Rivero Vaccari, Juan Pablo; Keane, Robert W; Bramlett, Helen M; Dietrich, W Dalton

    2012-10-01

    Traumatic brain injury (TBI) activates the NALP1/NLRP1 inflammasome, which is an important component of the early innate inflammatory response to injury. We investigated the influence of therapeutic hypothermia on inflammasome activation after TBI. Adult male Sprague-Dawley rats were subjected to moderate fluid percussion brain injury. Temperature manipulation (33°C or 37°C) was initiated 30 minutes after TBI and maintained for 4 hours. At 4 or 24 hours after TBI, traumatized cortex and hippocampus were prepared for immunoblot or immunohistochemical analysis. In the normothermic groups, caspase-1, caspase-11 and expression of the purinergic receptor P2X7 increased at 24 hours after TBI. Posttraumatic hypothermia lead to decreased expression of these proteins at 24 hours compared with normothermic levels. Immunocytochemical studies showed that posttraumatic hypothermia also decreased caspase-1 staining in cerebral cortical neurons compared with normothermic TBI. Cultured cortical neurons subjected to stretch injury demonstrated significant secretion of caspase-1 into the culture medium and caspase-3 activation, both results reduced by hypothermic treatment. Posttraumatic hypothermia decreases inflammasome signaling in neurons and reduces the innate immune response to TBI at 24 hours after injury. Therapeutic hypothermia may protect the injured central nervous system by targeting the detrimental consequences of the innate immune response to injury.

  11. 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.

  12. For Parents, Teachers and Coaches: About Sports Eye Injury and Protective Eyewear

    Science.gov (United States)

    ... Protection Resources for Adults Resources for Children About Sports Eye Injury and Protective Eyewear Parents and coaches play an ... activities and protective eyewear, visit: Coalition to Prevent Sports Eye Injuries Vision Council of America Prevent Blindness America Photo ...

  13. 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.

  14. 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.

  15. 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

  16. 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.

  17. 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…

  18. 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…

  19. [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.

  20. 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

  1. 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.

  2. 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…

  3. 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.

  4. 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…

  5. 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…

  6. 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

  7. 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.

  8. Protect Your Brain (A Cup of Health with CDC)

    Centers for Disease Control (CDC) Podcasts

    2013-03-21

    Recent high-profile cases among professional athletes have called attention to the serious problem of traumatic brain injuries, or TBI, but the problem isn’t limited to playing fields. In 2009, at least three and a half million people in the U.S. sustained a TBI, either with or without other injuries. In this podcast, Dr. Lisa McGuire discusses the importance of early diagnosis and treatment of brain injuries.  Created: 3/21/2013 by MMWR.   Date Released: 3/21/2013.

  9. 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.

  10. 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

  11. 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...

  12. 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.

  13. 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.

  14. 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......

  15. 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

  16. 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.

  17. 经鼻给予神经生长因子对创伤性脑外伤大鼠的脑保护作用%Protection effect of intranasal nerve growth factor on brain of rats with tramatic brain injury

    Institute of Scientific and Technical Information of China (English)

    郭芮兵; 吕秋石; 田利丽; 刘新峰

    2012-01-01

    Objective To investigate the protection effect of intranasal nerve growth factor on brain of rats with tramatic brain injury. Methods The rats were randomly divided into sham, control and treatment group. They were subjected to the modified Feeney's weight-drop model. The treatment group was treated with NGF administered by nasal route,and the control group was given phosphate-buffered saline( PBS). Beam walking test was performed in the three groups, lmmunohistochemistry was used to detect the β-APP and NSE positive cells near the region of injury in rats after TBI. Results NGF group traversed the beam significantly quicker than control group(P < 0.05). Immunohistot hemical staining showed that NSE was declined significantly in both control and NGF group compared to sham group(P<0.01) ,but it was higher in NGF group compared to control group(P<0. 01). p-APP was elevated significantly in both control and NGF group compared to sham group( P <0.01),but but it was lower in NGF group compared to control group( P <0.05). Conclusion Intranasal nerve growth factor after TBI in rats can improve neurol function, increasing NSE positive cells and decreasing β-APP positive cells.%目的 探讨经鼻给予神经生长因子(nerve growth factor,NGF)对实验性创伤性脑外伤(tramatic brain injury,TBI)大鼠大脑的保护作用.方法 将大鼠随机分为假手术组、对照组和NGF组,参照Feeney's自由落体法制作TBI大鼠模型,NGF组经鼻给予NGF治疗.采用平衡木方法评估3组TBI大鼠的神经功能恢复情况.行免疫组化染色检测各组TBI大鼠脑组织β-淀粉样蛋白前体蛋白(β-APP)和神经元特异性烯醇化酶(NSE)的表达情况.结果 NGF组TBI大鼠与对照组相比,运动协调功能恢复较快(P<0.05),免疫组化观察发现对照组和NGF组NSE阳性细胞均明显低于假手术组(P<0.01),NGF组NSE阳性细胞明显高于对照组(P<0.01);对照组和NGF组β-APP阳性表达均明显高于假手术组(P<0

  18. 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.

  19. 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.)

  20. 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.

  1. Cortical spreading depression in traumatic brain injuries: is there a role for astrocytes?

    Science.gov (United States)

    Torrente, Daniel; Cabezas, Ricardo; Avila, Marco Fidel; García-Segura, Luis Miguel; Barreto, George E; Guedes, Rubem Carlos Araújo

    2014-04-17

    Cortical spreading depression (CSD) is a presumably pathophysiological phenomenon that interrupts local cortical function for periods of minutes to hours. This phenomenon is important due to its association with different neurological disorders such as migraine, malignant stroke and traumatic brain injury (TBI). Glial cells, especially astrocytes, play an important role in the regulation of CSD and in the protection of neurons under brain trauma. The correlation of TBI with CSD and the astrocytic function under these conditions remain unclear. This review discusses the possible link of TBI and CSD and its implication for neuronal survival. Additionally, we highlight the importance of astrocytic function for brain protection, and suggest possible therapeutic strategies targeting astrocytes to improve the outcome following TBI-associated CSD.

  2. [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.

  3. 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.

  4. Preventive Effects of Safety Helmets on Traumatic Brain Injury after Work-Related Falls

    Directory of Open Access Journals (Sweden)

    Sang Chul Kim

    2016-10-01

    Full Text Available Introduction: Work-related traumatic brain injury (TBI caused by falls is a catastrophic event that leads to disabilities and high socio-medical costs. This study aimed to measure the magnitude of the preventive effect of safety helmets on clinical outcomes and to compare the effect across different heights of fall. Methods: We collected a nationwide, prospective database of work-related injury patients who visited the 10 emergency departments between July 2010 and October 2012. All of the adult patients who experienced work-related fall injuries were eligible, excluding cases with unknown safety helmet use and height of fall. Primary and secondary endpoints were intracranial injury and in-hospital mortality. We calculated adjusted odds ratios (AORs of safety helmet use and height of fall for study outcomes, and adjusted for any potential confounders. Results: A total of 1298 patients who suffered from work-related fall injuries were enrolled. The industrial or construction area was the most common place of fall injury occurrence, and 45.0% were wearing safety helmets at the time of fall injuries. The safety helmet group was less likely to have intracranial injury comparing with the no safety helmet group (the adjusted odds ratios (ORs (95% confidence interval (CI: 0.42 (0.24–0.73, however, there was no statistical difference of in-hospital mortality between two groups (the adjusted ORs (95% CI: 0.83 (0.34–2.03. In the interaction analysis, preventive effects of safety helmet on intracranial injury were significant within 4 m height of fall. Conclusions: A safety helmet is associated with prevention of intracranial injury resulting from work-related fall and the effect is preserved within 4 m height of fall. Therefore, wearing a safety helmet can be an intervention for protecting fall-related intracranial injury in the workplace.

  5. 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.

  6. 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

  7. Ecdysterone protects brain injury against free radical in rats%蜕皮甾酮对大鼠脑组织自由基损伤的保护作用

    Institute of Scientific and Technical Information of China (English)

    高诗豪; 唐政恒; 陈图南; 李飞; 单佑安; 冯华

    2012-01-01

    目的 观察蜕皮甾酮(ecdysterone,EDS)对大鼠脑损伤的治疗作用.方法 SD雄性大鼠120只,按随机数字表法分6组,每组20只.采用Feeney法自由落体打击鼠脑造模.假手术组动物只开颅,不打击;治疗组:分别采用4、8、16 mg/kg的EDS腹腔注射模型动物;阴性治疗对照组:模型动物腹腔注射生理盐水;阳性治疗对照组:模型动物腹腔注射3 mg/kg依达拉奉.伤后7d计算各组动物死亡率;检测各组动物脑组织含水量及丙二醛(MDA)、羟自由基能力及超(过)氧化物歧化酶(superoxide dismutase,SOD)等.HE染色观测各组大鼠脑组织海马病变情况.结果 伤后7d,16 mg/kg EDS治疗组的死亡率、脑组织含水量MDA与羟自由基含量较阴性治疗对照组明显降低(P<0.05),SOD活性显著升高(P<0.01),脑细胞损害明显减轻,大鼠海马CA1区正常神经元数量明显优于阴性治疗组(P<0.01).结论 蜕皮甾酮对脑损伤具有保护治疗作用.%Objective To investigate the effect of ecdysterone ( EDS) on traumatic brain injury (TBI) in rats. Methods A total of 120 male Sprague-Dawley rats were randomly and equally divided into 6 groups, sham-operation group, TBI group, edaravone treatment group and EDS treatment groups. Modified Feeney' s method was used to establish the rat model of experimental TBI with an impact of a weight of 30 g from 20 cm after craniotomy. Rats of EDS treatment groups were given EDS at 4, 8, and 16 mg/kg via peritoneal injection for 7 d. The other 3 groups were treated with normal saline or edaravone (3 mg/kg). The animal death rate was calculated, and the changes of the brain water content, malondialdehyde (MDA) , and superox-ide dismutase(SOD)in brain tissue were calculated and measured. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of brain hippocampus tissue. Results EDS (16 mg/kg) resulted in significant decreases in the death rate, brain water content, and MDA content (P <0

  8. Up-regulation of GBP2 is Associated with Neuronal Apoptosis in Rat Brain Cortex Following Traumatic Brain Injury.

    Science.gov (United States)

    Miao, Qi; Ge, Meihong; Huang, Lili

    2017-02-27

    Guanylate binding protein 2 (GBP2) is one member of GBP family. Recently, GBP2 has been proposed to be a novel target of anti-cancer drugs. However, the role of GBP2 in the traumatic brain injury (TBI) is very limited. In this study, we sought to define GBP2's role in brain injury. GBP2 protein levels were significantly increased in the brain 3 days after injury, suggesting a functional role for GBP2 in TBI. Neuronal cells overexpressing GBP2 exhibited up-regulation of co-location of GBP2 and NeuN following TBI, suggesting that GBP2 potentiates the neuron apoptosis. To confirm the role of GBP2 in neuron apoptosis process, we employed a highly potent inhibitor of GBP2 (GBP2 RNAi). In H2O2-stimulated PC12 cells, in vitro blockade of GBP2 activity using GBP2 RNAi markedly attenuated the neuron apoptosis number. GBP2 RNAi also inhibited the expression levels of active caspase3 and p-Stat1. Furthermore, we found the expression of p-Stat1 in line with GBP2 and GBP2 interacted with p-Stat1 following TBI. The Jak2 inhibitor, AG490 inhibited this interaction and decreased the active caspase3 expression as well as promoted the functional recovery. Taken together, these data suggest that GBP2 RNAi has a protective effect in a rat TBI. This study demonstrates that GBP2 is an important positive regulator of TBI and is a promising therapeutic target for brain injury.

  9. 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…

  10. Influence of physical exercise on traumatic brain injury deficits: scaffolding effect.

    Science.gov (United States)

    Archer, Trevor

    2012-05-01

    Traumatic brain injury (TBI) may be due to a bump, blow, or jolt to the head or a penetrating head injury that disrupts normal brain function; it presents an ever-growing, serious public health problem that causes a considerable number of fatalities and cases of permanent disability annually. Physical exercise restores the healthy homeostatic regulation of stress, affect and the regulation of hypothalamic-pituitary-adrenal axis. Physical activity attenuates or reverses the performance deficits observed in neurocognitive tasks. It induces anti-apoptotic effects and buttresses blood-brain barrier intactness. Exercise offers a unique non-pharmacologic, non-invasive intervention that incorporates different regimes, whether dynamic or static, endurance, or resistance. Exercise intervention protects against vascular risk factors that include hypertension, diabetes, cellular inflammation, and aortic rigidity. It induces direct changes in cerebrovasculature that produce beneficial changes in cerebral blood flow, angiogenesis and vascular disease improvement. The improvements induced by physical exercise regimes in brain plasticity and neurocognitive performance are evident both in healthy individuals and in those afflicted by TBI. The overlap and inter-relations between TBI effects on brain and cognition as related to physical exercise and cognition may provide lasting therapeutic benefits for recovery from TBI. It seems likely that some modification of the notion of scaffolding would postulate that physical exercise reinforces the adaptive processes of the brain that has undergone TBI thereby facilitating the development of existing networks, albeit possibly less efficient, that compensate for those lost through damage.

  11. 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

  12. 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....

  13. 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.

  14. 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.

  15. 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.

  16. 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.

  17. Skull Flexure from Blast Waves: A New Mechanism for Brain Injury with Implications for Helmet Design

    CERN Document Server

    Moss, William C; Blackman, Eric G

    2008-01-01

    Traumatic brain injury [TBI] has become the signature injury of current military conflicts. The debilitating effects of TBI on society are long-lasting and costly. Although the mechanisms by which impacts cause TBI have been well researched, the mechanisms by which blasts cause TBI are not understood. Various mechanisms, including impacts caused by the blast, have been investigated, but blast-induced deformation of the skull has been neglected. Through the use of hydrodynamical numerical simulations, we have discovered that non-lethal blasts can induce sufficient flexure of the skull to generate potentially damaging loads in the brain, even if no impact occurs. This mechanism has implications for the diagnosis of TBI in soldiers and the design of protective equipment such as helmets.

  18. Skull flexure from blast waves: a mechanism for brain injury with implications for helmet design

    Energy Technology Data Exchange (ETDEWEB)

    Moss, W C; King, M J; Blackman, E G

    2009-04-14

    Traumatic brain injury [TBI] has become a signature injury of current military conflicts. The debilitating effects of TBI are long-lasting and costly. Although the mechanisms by which impacts cause TBI have been well researched, the mechanisms by which blasts cause TBI are not understood. Various possibilities have been investigated, but blast-induced deformation of the skull has been neglected. From numerical hydrodynamic simulations, we have discovered that nonlethal blasts can induce sufficient flexure of the skull to generate potentially damaging loads in the brain, even if no impact occurs. The possibility that this mechanism may contribute to TBI has implications for the diagnosis of soldiers and the design of protective equipment such as helmets.

  19. Melatonin as Protection Against Radiation Injury

    DEFF Research Database (Denmark)

    Zetner, D; Andersen, L P H; Rosenberg, J

    2016-01-01

    -hormone melatonin is a free radical scavenger, and induces several anti-oxidative enzymes. This review investigates the scientific literature on the protective effects of melatonin against exposure to ionizing radiation, and discusses the clinical potential of melatonin as prophylactic treatment against ionizing...... radiation damage. Methods: A systematic literature search was performed and included experimental or clinical studies written in English that investigated the protective effects of melatonin against gamma or X-ray irradiation in vivo. Studies were excluded if patients were treated with chemotherapy...... concomitantly. Results: 37 studies were included in the review. All were of experimental case-control design and employed animals. The studies demonstrated that exogenous melatonin reduced oxidative stress and inflammation in all investigated tissues. Furthermore, melatonin increased 30-day survival...

  20. 38 CFR 9.20 - Traumatic injury protection.

    Science.gov (United States)

    2010-07-01

    ... loss of voluntary movement resulting from damage to the spinal cord or associated nerves, or to the... and 38 CFR 9.13. (j) Who will be paid the traumatic injury protection benefit? The injured member who... weapon means chemical substances intended to kill, seriously injure, or incapacitate humans through...

  1. 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.

  2. 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.

  3. [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.

  4. 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.

  5. 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...

  6. 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.

  7. Protective effects of mangiferin on cerebral ischemia-reperfusion injury and its mechanisms.

    Science.gov (United States)

    Yang, Zhang; Weian, Chen; Susu, Huang; Hanmin, Wang

    2016-01-15

    The aim of our study was to investigate the protective properties of mangiferin, a natural glucosyl xanthone found in both mango and papaya on the cerebral ischemia-reperfusion injury and the underlying mechanism. Wistar male rats were subjected to middle cerebral artery occlusion for 2h followed by 24h of reperfusion. Mangiferin (25, 50, and 100mg/kg, ig) or 0.5% carboxymethyl cellulose sodium was administered three times before ischemia and once at 2h after the onset of ischemia. Neurological score, infarct volume, and brain water content, some oxidative stress markers and inflammatory cytokines were evaluated after 24h of reperfusion. Treatment with mangiferin significantly ameliorated neurologic deficit, infarct volume and brain water content after cerebral ischemia reperfusion. Mangiferin also reduced the content of malondialdehyde (MDA), IL-1β and TNF-α, and up-regulated the activities of superoxide dismutase (SOD), glutathione (GSH) and IL-10 levels in the brain tissue of rats with the cerebral ischemia-reperfusion injury. Moreover, mangiferin up-regulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream anti-oxidant protein heme oxygenase-1 (HO-1). The results indicate that mangiferin can play a certain protective role in the cerebral ischemia-reperfusion injury, and the protective effect of mangiferin may be related to the improvement on the antioxidant capacity of brain tissue and the inhibition of overproduction of inflammatory cytokines. The mechanisms are associated with enhancing the oxidant defense systems via the activation of Nrf2/HO-1 pathway.

  8. Protective effect of ginkgo proanthocyanidins against cerebral ischemia/reperfusion injury associated with its antioxidant effects

    Science.gov (United States)

    Cao, Wang-li; Huang, Hai-bo; Fang, Ling; Hu, Jiang-ning; Jin, Zhu-ming; Wang, Ru-wei

    2016-01-01

    Proanthocyanidins have been shown to effectively protect ischemic neurons, but its mechanism remains poorly understood. Ginkgo proanthocyanidins (20, 40, 80 mg/kg) were intraperitoneally administered 1, 24, 48 and 72 hours before reperfusion. Results showed that ginkgo proanthocyanidins could effectively mitigate neurological disorders, shorten infarct volume, increase superoxide dismutase activity, and decrease malondialdehyde and nitric oxide contents. Simultaneously, the study on grape seed proanthocyanidins (40 mg/kg) confirmed that different sources of proanthocyanidins have a similar effect. The neurological outcomes of ginkgo proanthocyanidins were similar to that of nimodipine in the treatment of cerebral ischemia/reperfusion injury. Our results suggest that ginkgo proanthocyanidins can effectively lessen cerebral ischemia/reperfusion injury and protect ischemic brain tissue and these effects are associated with antioxidant properties. PMID:28123420

  9. D-Cycloserine improves functional outcome after traumatic brain injury with wide therapeutic window

    Energy Technology Data Exchange (ETDEWEB)

    Adeleye, A.; Biegon, A.; Adeleye, A.; Shohami, E.; Nachman, D.; Alexandrovich, A.; Trembovler, V.; Yaka, R.; Shoshan, Y.; Dhawan, J.; Biegon, A.

    2009-12-01

    It has been long thought that hyperactivation of N-methyl-D-aspartate (NMDA) receptors underlies neurological decline after traumatic brain injury. However, all clinical trials with NMDA receptor antagonists failed. Since NMDA receptors are down-regulated from 4 h to 2 weeks after brain injury, activation at 24 h, rather than inhibition, of these receptors, was previously shown to be beneficial in mice. Here, we tested the therapeutic window, dose regimen and mechanism of action of the NMDA receptor partial agonist d-cycloserine (DCS) in traumatic brain injury. Male mice were subjected to trauma using a weight-drop model, and administered 10 mg/kg (i.p.) DCS or vehicle once (8, 16, 24, or 72 h) twice (24 and 48 h) or three times (24, 48 and 72 h). Functional recovery was assessed for up to 60 days, using a Neurological Severity Score that measures neurobehavioral parameters. In all groups in which treatment was begun at 24 or 72 h neurobehavioral function was significantly better than in the vehicle-treated groups. Additional doses, on days 2 and 3 did not further improve recovery. Mice treated at 8 h or 16 h post injury did not differ from the vehicle-treated controls. Co-administration of the NMDA receptor antagonist MK-801 completely blocked the protective effect of DCS given at 24 h. Infarct volume measured by 2,3,5-triphenyltetrazolium chloride staining at 48 h or by cresyl violet at 28 days was not affected by DCS treatment. Since DCS is used clinically for other indications, the present study offers a novel approach for treating human traumatic brain injury with a therapeutic window of at least 24 h.

  10. 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.

  11. 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.

  12. 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.

  13. 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.

  14. 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.

  15. 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

  16. 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

  17. The effects of ultrasound on BBB integration in ischemic brain injury model

    Directory of Open Access Journals (Sweden)

    Shuaib A.

    2008-06-01

    Full Text Available Background: Ultrasound (US has been used in neuroprotection after cerebral ischemia, however the mechanism of action remains unclearly. We have previously shown the protective effect of ultrasound on infarction volume and brain edema in ischemic brain injured at normothermic condition. Ultrasound may also amplify the effect of fibrinolytic medications in thrombolysis process .We have also shown that hyperthermia can exacerbate cerebral ischemic injury and that the efficacy of tissue plasminogen activator (tPA is reduced in the presence of hyperthermia. In this study, the effects of US alone or in combination with tPA on brain ischemic injury were evaluated.Methods: Focal ischemic brain injury was induced by emblazing a pre-formed clot into the middle cerebral artery in rats. Principally, we examined whether US can reduce the perfusion deficits and, the damage of blood- brain barrier (BBB in the ischemic injured brain. There are two series of experiments at this study .in the first series, animals were randomly assigned to four groups (n=7 per group as follows: 1-control (saline, 2-US (1W/cm2, 10 duty cycle , 3- US+high- tPA (1W/cm2, 10 duty cycle +20 mg/kg and 4- high -tPA (20 mg/kg. We also examined the effects of US and tPA on BBB integrity after ischemic injury. The animals were assigned into four groups (n=7 per group, treatment is the same as above. BBB permeability was assessed by the Evans blue (EB extravasations method at 8 h after MCA occlusion. BBB permeability was evaluated by fluorescent detection of extravagated Evans blue dye and Perfusion deficits were analyzed using an Evans blue staining procedure. The perfused microvessels in the brain were visualized using fluorescent microscopy. Areas of perfusion deficits in the brain were traced, calculated and expressed in mm2.Results: The results showed that US improved neurological deficits significantly (p<0.05. The administration of US significantly decreased perfusion deficits and BBB

  18. 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.

  19. 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

  20. 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...

  1. 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.

  2. 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.

  3. 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.

  4. 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 ...

  5. 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

  6. 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

  7. 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...

  8. 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...

  9. 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.

  10. 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.

  11. Early protective effects of Iloprost after experimental spinal cord injury.

    Science.gov (United States)

    Attar, A; Tuna, H; Sargon, M F; Yüceer, N; Türker, R K; Egemen, N

    1998-06-01

    This investigation was undertaken to study the early protective effects of Iloprost, a stable analogue of prostacyclin, after spinal cord injury in rabbit. Sixteen adult male rabbits (New Zealand Albino) were injured by application of epidural aneurysm clip. Eight rabbits received an intravenous (i.v.) infusion of 30 micrograms kg-1 Iloprost, and eight rabbits received an infusion of saline (SF). Treatment with Iloprost started immediately after spinal cord injury and continued for one hour. Evoked potentials were recorded for each rabbit at one, 15, and 60 minutes after the spinal cord injury. Twenty-four hours later, all the rabbits were deeply anesthetized and spinal cords were removed for histopathological examinations. There was no meaningful statistical difference between cortical somatosensorial evoked potentials (CSEP) of the saline and Iloprost group. However, light and electron microscopic studies showed that the Iloprost treated group had moderate protection of myelin and axons; and limited edema. These results suggest that intravenous Iloprost treatment after spinal cord injury has a highly protective effect without any side effects.

  12. 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.

  13. 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

  14. 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.

  15. 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.

  16. 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.

  17. 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.

  18. 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.

  19. IMPACT OF SEVOFLURANE AND ACETYLCYSTEINE ON ISCHEMIA-REPERFUSION INJURY OF THE LIVER FROM BRAIN-DEAD DONOR

    Directory of Open Access Journals (Sweden)

    A. E. Shcherba

    2013-01-01

    Full Text Available Aim. The purpose of our work was to estimate the impact of preconditioning with acetylcysteine and sevoflurane on ischemia-reperfusion injury of cadaveric donor liver with marginal features. Methods and results. In this prospective randomized controlled trial we recruited 21 heart beating donors with brain death. We assigned 11 donors to the study group, and 10 donors to the control group. Morphological characteristics of ischemia- reperfusion injury in both groups were analyzed. Conclusion. Use of pharmacological preconditioning with acetylcysteine and sevoflurane resulted in necrosis and hepatocyte apoptosis reduction as compared to the control group, thereby had a protective effect against ischemia-reperfusion injury

  20. Suramin protects from cisplatin-induced acute kidney injury.

    Science.gov (United States)

    Dupre, Tess V; Doll, Mark A; Shah, Parag P; Sharp, Cierra N; Kiefer, Alex; Scherzer, Michael T; Saurabh, Kumar; Saforo, Doug; Siow, Deanna; Casson, Lavona; Arteel, Gavin E; Jenson, Alfred Bennett; Megyesi, Judit; Schnellmann, Rick G; Beverly, Levi J; Siskind, Leah J

    2016-02-01

    Cisplatin, a commonly used cancer chemotherapeutic, has a dose-limiting side effect of nephrotoxicity. Approximately 30% of patients administered cisplatin suffer from kidney injury, and there are limited treatment options for the treatment of cisplatin-induced kidney injury. Suramin, which is Federal Drug Administration-approved for the treatment of trypanosomiasis, improves kidney function after various forms of kidney injury in rodent models. We hypothesized that suramin would attenuate cisplatin-induced kidney injury. Suramin treatment before cisplatin administration reduced cisplatin-induced decreases in kidney function and injury. Furthermore, suramin attenuated cisplatin-induced expression of inflammatory cytokines and chemokines, endoplasmic reticulum stress, and apoptosis in the kidney cortex. Treatment of mice with suramin 24 h after cisplatin also improved kidney function, suggesting that the mechanism of protection is not by inhibition of tubular cisplatin uptake or its metabolism to nephrotoxic species. If suramin is to be used in the context of cancer, then it cannot prevent cisplatin-induced cytotoxicity of cancer cells. Suramin did not alter the dose-response curve of cisplatin in lung adenocarcinoma cells in vitro. In addition, suramin pretreatment of mice harboring lung adenocarcinomas did not alter the initial cytotoxic effects of cisplatin (DNA damage and apoptosis) on tumor cells. These results provide evidence that suramin has potential as a renoprotective agent for the treatment/prevention of cisplatin-induced acute kidney injury and justify future long-term preclinical studies using cotreatment of suramin and cisplatin in mouse models of cancer.

  1. 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.

  2. 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.

  3. 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

  4. 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.

  5. Ultra Low Dose Delta 9-Tetrahydrocannabinol Protects Mouse Liver from Ischemia Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Edith Hochhauser

    2015-07-01

    Full Text Available Background/Aims: Ischemia/reperfusion (I/R injury is the main cause of both primary graft dysfunction and primary non-function of liver allografts. Cannabinoids has been reported to attenuate myocardial, cerebral and hepatic I/R oxidative injury. Delta-9-tetrahydrocannabinol (THC, a cannabinoid agonist, is the active components of marijuana. In this study we examined the role of ultralow dose THC (0.002mg/kg in the protection of livers from I/R injury. This extremely low dose of THC was previously found by us to protect the mice brain and heart from a variety of insults. Methods: C57Bl Mice were studied in in vivo model of hepatic segmental (70% ischemia for 60min followed by reperfusion for 6 hours. Results: THC administration 2h prior to the induction of hepatic I/R was associated with significant attenuated elevations of: serum liver transaminases ALT and AST, the hepatic oxidative stress (activation of the intracellular signaling CREB pathway, the acute proinflammatory response (TNF-α, IL-1α, IL-10 and c-FOS hepatic mRNA levels, and ERK signaling pathway activation. This was followed by cell death (the cleavage of the pro-apoptotic caspase 3, DNA fragmentation and TUNEL after 6 hours of reperfusion. Significantly less hepatic injury was detected in the THC treated I/R mice and fewer apoptotic hepatocytes cells were identified by morphological criteria compared with untreated mice. Conclusion: A single ultralow dose THC can reduce the apoptotic, oxidative and inflammatory injury induced by hepatic I/R injury. THC may serve as a potential target for therapeutic intervention in hepatic I/R injury during liver transplantation, liver resection and trauma.

  6. 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.

  7. Amine-modified single-walled carbon nanotubes protect neurons from injury in a rat stroke model

    Science.gov (United States)

    Lee, Hyun Jung; Park, Jiae; Yoon, Ok Ja; Kim, Hyun Woo; Lee, Do Yeon; Kim, Do Hee; Lee, Won Bok; Lee, Nae-Eung; Bonventre, Joseph V.; Kim, Sung Su

    2011-02-01

    Stroke results in the disruption of tissue architecture and is the third leading cause of death in the United States. Transplanting scaffolds containing stem cells into the injured areas of the brain has been proposed as a treatment strategy, and carbon nanotubes show promise in this regard, with positive outcomes when used as scaffolds in neural cells and brain tissues. Here, we show that pretreating rats with amine-modified single-walled carbon nanotubes can protect neurons and enhance the recovery of behavioural functions in rats with induced stroke. Treated rats showed less tissue damage than controls and took longer to fall from a rotating rod, suggesting better motor functions after injury. Low levels of apoptotic, angiogenic and inflammation markers indicated that amine-modified single-walled carbon nanotubes protected the brains of treated rats from ischaemic injury.

  8. 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...

  9. 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.

  10. 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.

  11. 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.

  12. 77 FR 32397 - Servicemembers' Group Life Insurance Traumatic Injury Protection Program-Genitourinary Losses

    Science.gov (United States)

    2012-06-01

    ... AFFAIRS 38 CFR Part 9 RIN 2900-AO20 Servicemembers' Group Life Insurance Traumatic Injury Protection... Servicemembers' Group Life Insurance Traumatic Injury Protection (TSGLI) program by adding certain genitourinary... Servicemembers' Group Life Insurance Traumatic Injury Protection (TSGLI) program to add certain genitourinary...

  13. Publication trends in studies examining radix notoginseng as a treatment for ischemic brain injury

    Institute of Scientific and Technical Information of China (English)

    Haiping Li; Luo Qiang; Chunyang Zhang; Chaohui Wang; Zhenxing Mu; Ligang Jiang

    2014-01-01

    Acute ischemic stroke has become a major disease burden with high mortality and morbidity rates. There is a lack of evidence-based medicine conifrming the efifcacy of common treatments. Panax notoginseng saponins, the main active ingredient of radix notoginseng, have a neuro-protective role in ischemic brain injury, and have been popularized as a maintenance treatment for acute cerebral infarction and its sequelae. We conducted literature searches on the Web of Science, ClinicalTrials.gov, Cochrane Collaboration, CNKI, Wanfang and the China Scientific&Technological Achievements Database and analyzed the experimental and clinical outcomes of studies investigating the use of radix notoginseng in the treatment of ischemic brain injury to improve the understanding of relevant research trends and existing problems. We found that over the past 10 years, China has maintained its interest in Panax notoginseng research, while such studies are scarce on the Web of Science. However, Chinese researchers often focus on the neuroprotective role of radix notoginseng in ischemic brain injury, but there are no large-scale clinical data to conifrm its efifcacy and safety. There remains a need for more rigorous large-sam-ple randomized controlled clinical trials with long-term follow-up, to determine whether radix notoginseng lowers stroke recurrence and improves patient’s quality of life.

  14. 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.

  15. Green tea may protect brain cells against Parkinson's

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    @@ Does the consumption of green tea, widely touted to have beneficial effects on health, also protect brain cells? As reported in the 15 December, 2007 issue of Biological Psychiatry, studies by CAS researchers indicate this may be the case.

  16. 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.

  17. 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

  18. 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…

  19. 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

  20. 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

  1. 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.

  2. Isoflurane anesthesia initiated at the onset of reperfusion attenuates oxidative and hypoxic-ischemic brain injury.

    Directory of Open Access Journals (Sweden)

    Sergey A Sosunov

    Full Text Available This study demonstrates that in mice subjected to hypoxia-ischemia (HI brain injury isoflurane anesthesia initiated upon reperfusion limits a release of mitochondrial oxidative radicals by inhibiting a recovery of complex-I dependent mitochondrial respiration. This significantly attenuates an oxidative stress and reduces the extent of HI brain injury. Neonatal mice were subjected to HI, and at the initiation of reperfusion were exposed to isoflurane with or without mechanical ventilation. At the end of HI and isoflurane exposure cerebral mitochondrial respiration, H2O2 emission rates were measured followed by an assessment of cerebral oxidative damage and infarct volumes. At 8 weeks after HI navigational memory and brain atrophy were assessed. In vitro, direct effect of isoflurane on mitochondrial H2O2 emission was compared to that of complex-I inhibitor, rotenone. Compared to controls, 15 minutes of isoflurane anesthesia inhibited recovery of the compex I-dependent mitochondrial respiration and decreased H2O2 production in mitochondria supported with succinate. This was associated with reduced oxidative brain injury, superior navigational memory and decreased cerebral atrophy compared to the vehicle-treated HI-mice. Extended isoflurane anesthesia was associated with sluggish recovery of cerebral blood flow (CBF and the neuroprotection was lost. However, when isoflurane anesthesia was supported with mechanical ventilation the CBF recovery improved, the event associated with further reduction of infarct volume compared to HI-mice exposed to isoflurane without respiratory support. Thus, in neonatal mice brief isoflurane anesthesia initiated at the onset of reperfusion limits mitochondrial release of oxidative radicals and attenuates an oxidative stress. This novel mechanism contributes to neuroprotective action of isoflurane. The use of mechanical ventilation during isoflurane anesthesia counterbalances negative effect of isoflurane anesthesia on

  3. 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.

  4. Brain-protecting effect of β2-adrenoceptor antagonist in rats with traumatic brain injury%β2肾上腺素能受体阻断剂对外伤性脑损伤大鼠的脑保护作用

    Institute of Scientific and Technical Information of China (English)

    杜立武; 吴晶; 袁红梅; 谭远辉; 胡益民; 杨建军

    2012-01-01

    目的 外伤性脑损伤后促炎细胞因子释放增多,并引起脑损伤.文中观察β2肾上腺素能受体(简称β2受体)阻断剂ICI 118551对外伤性脑损伤大鼠促炎细胞因子释放的影响,并研究其是否具有脑保护作用.方法 成年雄性SD大鼠18只,随机均分为3组(n=6):假手术组(S组)、外伤性脑损伤组(T组)及ICI 118551治疗组(I组).T组和I组分别静脉注射等容等渗盐水或ICI 118551 20mg/kg,20min 后建立外伤性脑损伤模型.6h后抽血检测各组大鼠血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)及神经元特异性烯醇化酶(neuronespecificenolase,NSE)水平.结果 与S组相比,T组及I组TNF-α、IL-6和NSE水平升高(P<0.05);与T组相比,I组TNF-α、IL-6 和NSE水平降低(P<0.05).结论 β2受体阻断剂ICI 118551具有脑保护作用,这可能与抑制外伤性脑损伤后炎症反应有关.%Objective Proinflammatory cytokines increase after traumatic brain injury ( TBI ) and result in brain damage. Recent studies suggest that β-adrenoceptor antagonist can reduce proinflammatory cytokines. This study aims to observe the effects of β2 -adrenoceptor antagonist ICI 118551 on proinflammatory cytokine release and to investigate whether ICI 118551 has neuroprotective effect. Methods Eighteen Sprague-Dawley male rats were equally randomized into a sham-operation group, a TBI group and an ICI 118551 treatment group, the latter two injected intravenously with equal volume of normal saline and ICI 118551 at 20mg/kg, respectively , and the TBI model was established 20 min later. Blood samples were obtained 6 h after TBI for the determination of the levels of tumor necrosis factor-alpha ( TNF-a ), Interleukin-6 ( IL-6 ) and neuronespecificenolase ( NSE ). Results The levels of TNF-a, IL-6 and NSE were significantly increased in the TBI and ICI 118551 groups as compared with the sham-operation group ( P<0.05 ),but remarkably decreased in the

  5. Platelets protect lung from injury induced by systemic inflammatory response

    Science.gov (United States)

    Luo, Shuhua; Wang, Yabo; An, Qi; Chen, Hao; Zhao, Junfei; Zhang, Jie; Meng, Wentong; Du, Lei

    2017-01-01

    Systemic inflammatory responses can severely injure lungs, prompting efforts to explore how to attenuate such injury. Here we explored whether platelets can help attenuate lung injury in mice resulting from extracorporeal circulation (ECC)-induced systemic inflammatory responses. Mice were subjected to ECC for 30 min, then treated with phosphate-buffered saline, platelets, the GPIIb/IIIa inhibitor Tirofiban, or the combination of platelets and Tirofiban. Blood and lung tissues were harvested 60 min later, and lung injury and inflammatory status were assessed. As expected, ECC caused systemic inflammation and pulmonary dysfunction, and platelet transfusion resulted in significantly milder lung injury and higher lung function. It also led to greater numbers of circulating platelet-leukocyte aggregates and greater platelet accumulation in the lung. Platelet transfusion was associated with higher production of transforming growth factor-β and as well as lower levels of tumour necrosis factor-α and neutrophil elastase in plasma and lung. None of these platelet effects was observed in the presence of Tirofiban. Our results suggest that, at least under certain conditions, platelets can protect lung from injury induced by systemic inflammatory responses. PMID:28155889

  6. Neuroendocrine abnormalities in patients with traumatic brain injury

    Science.gov (United States)

    Yuan, X. Q.; Wade, C. E.

    1991-01-01

    This article provides an overview of hypothalamic and pituitary alterations in brain trauma, including the incidence of hypothalamic-pituitary damage, injury mechanisms, features of the hypothalamic-pituitary defects, and major hypothalamic-pituitary disturbances in brain trauma. While hypothalamic-pituitary lesions have been commonly described at postmortem examination, only a limited number of clinical cases of traumatic hypothalamic-pituitary dysfunction have been reported, probably because head injury of sufficient severity to cause hypothalamic and pituitary damage usually leads to early death. With the improvement in rescue measures, an increasing number of severely head-injured patients with hypothalamic-pituitary dysfunction will survive to be seen by clinicians. Patterns of endocrine abnormalities following brain trauma vary depending on whether the injury site is in the hypothalamus, the anterior or posterior pituitary, or the upper or lower portion of the pituitary stalk. Injury predominantly to the hypothalamus can produce dissociated ACTH-cortisol levels with no response to insulin-induced hypoglycemia and a limited or failed metopirone test, hypothyroxinemia with a preserved thyroid-stimulating hormone response to thyrotropin-releasing hormone, low gonadotropin levels with a normal response to gonadotropin-releasing hormone, a variable growth hormone (GH) level with a paradoxical rise in GH after glucose loading, hyperprolactinemia, the syndrome of inappropriate ADH secretion (SIADH), temporary or permanent diabetes insipidus (DI), disturbed glucose metabolism, and loss of body temperature control. Severe damage to the lower pituitary stalk or anterior lobe can cause low basal levels of all anterior pituitary hormones and eliminate responses to their releasing factors. Only a few cases showed typical features of hypothalamic or pituitary dysfunction. Most severe injuries are sufficient to damage both structures and produce a mixed endocrine picture

  7. Does Dexpantenol Protect the Kidney from Ischemia-Reperfusion Injury?

    Directory of Open Access Journals (Sweden)

    Sezen ÖZKISACIK

    2011-05-01

    Full Text Available OBJECTIVES: Tissue injury occurs following reperfusion after creation of ischemia. Plenty of chemical agents have been shown to protect from such an injury. We planned to evaluate the protective effect of dexpanthenol (dxp in ischemia-reperfusion injury. MATERIAL and METHODS: 24 adult rats were used and divided into 3 groups. A right nephrectomy was performed through a median laparotomy incision in all groups. Additionally, in group 1 (sham group, left nephrectomy was made 6 hours later without creation of ischemia. In group 2 (Saline group, the left kidney was left ischemic for 1 hour and reperfusion was established for 6 hours. Saline was administered intraperitoneally thirty minutes before creation of ischemia and just before reperfusion. In group 3 (Dexpanthenol group, the left kidney was left ischemic for 1 hour and reperfusion was established for 6 hours. Dxp (500 mg/kg was administered intraperitoneally thirty minutes before creation of ischemia and just before reperfusion. A left nephrectomy was performed at the end of the 6 hours of reperfusion. Nephrectomy specimens were histopathologically analysed for congestion, inflammation and necrosis. Tissue NO, glutathione reductase, catalase and MDA levels were measured. RESULTS: There was no significant differences between the groups histopathologically or biochemically. CONCLUSION: Dexpanthenol is the biologically active form of pantothenic acid and has an antioxidant effect. Our study was not in correlation with the literature regarding a protective effect of dxp on various organs via its antioxidant effect.

  8. Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury

    Science.gov (United States)

    Sturdivant, Nasya M.; Smith, Sean G.; Ali, Syed F.; Wolchok, Jeffrey C.; Balachandran, Kartik

    2016-09-01

    Non-penetrating or mild traumatic brain injury (mTBI) is commonly experienced in accidents, the battlefield and in full-contact sports. Astrocyte cellular edema is one of the major factors that leads to high morbidity post-mTBI. Various studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following brain injury. AZA is an antiepileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the drug as a therapeutic to mitigate the extent of mTBI induced cellular edema. We hypothesized that mTBI-mediated astrocyte dysfunction, initiated by increased intracellular volume, could be reduced when treated with AZA. We tested our hypothesis in a three-dimensional in vitro astrocyte model of mTBI. Samples were subject to no stretch (control) or one high-speed stretch (mTBI) injury. AQP4 expression was significantly increased 24 hours after mTBI. mTBI resulted in a significant increase in the cell swelling within 30 min of mTBI, which was significantly reduced in the presence of AZA. Cell death and expression of S100B was significantly reduced when AZA was added shortly before mTBI stretch. Overall, our data point to occurrence of astrocyte swelling immediately following mTBI, and AZA as a promising treatment to mitigate downstream cellular mortality.

  9. Neuroimaging in adult penetrating brain injury: a guide for radiographers

    Energy Technology Data Exchange (ETDEWEB)

    Temple, Nikki; Donald, Cortny; Skora, Amanda [Discipline of Medical Radiation Sciences, The University of Sydney, Lidcombe, New South Wales (Australia); Reed, Warren, E-mail: warren.reed@sydney.edu.au [Medical Image Optimisation and Perception Group, Discipline of Medical Radiation Sciences, The University of Sydney, Lidcombe, New South Wales (Australia)

    2015-06-15

    Penetrating brain injuries (PBI) are a medical emergency, often resulting in complex damage and high mortality rates. Neuroimaging is essential to evaluate the location and extent of injuries, and to manage them accordingly. Currently, a myriad of imaging modalities are included in the diagnostic workup for adult PBI, including skull radiography, computed tomography (CT), magnetic resonance imaging (MRI) and angiography, with each modality providing their own particular benefits. This literature review explores the current modalities available for investigating PBI and aims to assist in decision making for the appropriate use of diagnostic imaging when presented with an adult PBI. Based on the current literature, the authors have developed an imaging pathway for adult penetrating brain injury that functions as both a learning tool and reference guide for radiographers and other health professionals. Currently, CT is recommended as the imaging modality of choice for the initial assessment of PBI patients, while MRI is important in the sub-acute setting where it aids prognosis prediction and rehabilitation planning, Additional follow-up imaging, such as angiography, should be dependent upon clinical findings.

  10. Fatal Hyperammonemic Brain Injury from Valproic Acid Exposure

    Directory of Open Access Journals (Sweden)

    Danny Bega

    2012-12-01

    Full Text Available Background: Hyperammonemia is known to cause neuronal injury, and can result from valproic acid exposure. Prompt reduction of elevated ammonia levels may prevent permanent neurological injury. We report a case of fatal hyperammonemic brain injury in a woman exposed to valproic acid. Case: A 38-year-old woman with schizoaffective disorder and recent increase in valproic acid dosage presented with somnolence and confusion and rapidly progressed to obtundation. Brain MRI showed diffuse bilateral restricted diffusion in nearly the entire cerebral cortex. She had normal liver function tests but serum ammonia level was severely elevated at 288 µmol/l. Genetic testing showed no mutation in urea cycle enzymes. Despite successful elimination of ammonia with hemodialysis she developed fatal cerebral edema. Conclusion: Cerebral edema secondary to hyperammonemia is potentially reversible if recognized early. Ammonia excretion can be facilitated by initiation of hemodialysis and administration of scavenging agents (sodium phenylacetate and sodium benzoate. Severe hyperammonemia can result from valproic acid exposure even in the absence of hepatotoxicity or inborn errors of metabolism. It is important to check serum ammonia in any patient with encephalopathy who has had recent valproic acid exposure.

  11. Epidemiology, Severity Classification, and Outcome of Moderate and Severe Traumatic Brain Injury: A Prospective Multicenter Study

    NARCIS (Netherlands)

    T.M.J.C. Andriessen; J. Horn; G. Franschman; J. van der Naalt; I. Haitsma; B. Jacobs; E.W. Steyerberg; P.E. Vos

    2011-01-01

    Changes in the demographics, approach, and treatment of traumatic brain injury (TBI) patients require regular evaluation of epidemiological profiles, injury severity classification, and outcomes. This prospective multicenter study provides detailed information on TBI-related variables of 508 moderat

  12. Epidemiology, severity classification, and outcome of moderate and severe traumatic brain injury: a prospective multicenter study

    NARCIS (Netherlands)

    Andriessen, T.M.J.C.; Horn, J.; Franschman, G.; Naalt, J. van der; Haitsma, I.; Jacobs, B.; Steyerberg, E.W.; Vos, P.E.

    2011-01-01

    Changes in the demographics, approach, and treatment of traumatic brain injury (TBI) patients require regular evaluation of epidemiological profiles, injury severity classification, and outcomes. This prospective multicenter study provides detailed information on TBI-related variables of 508 moderat

  13. Epidemiology, Severity Classification, and Outcome of Moderate and Severe Traumatic Brain Injury : A Prospective Multicenter Study

    NARCIS (Netherlands)

    Andriessen, Teuntje M. J. C.; Horn, Janneke; Franschman, Gaby; van der Naalt, Joukje; Haitsma, Iain; Jacobs, Bram; Steyerberg, Ewout W.; Vos, Pieter E.

    2011-01-01

    Changes in the demographics, approach, and treatment of traumatic brain injury (TBI) patients require regular evaluation of epidemiological profiles, injury severity classification, and outcomes. This prospective multicenter study provides detailed information on TBI-related variables of 508 moderat

  14. Metabolic alterations in developing brain after injury – knowns and unknowns

    Science.gov (United States)

    McKenna, Mary C.; Scafidi, Susanna; Robertson, Courtney L.

    2016-01-01

    Brain development is a highly orchestrated complex process. The developing brain utilizes many substrates including glucose, ketone bodies, lactate, fatty acids and amino acids for energy, cell division and the biosynthesis of nucleotides, proteins and lipids. Metabolism is crucial to provide energy for all cellular processes required for brain development and function including ATP formation, synaptogenesis, synthesis, release and uptake of neurotransmitters, maintaining ionic gradients and redox status, and myelination. The rapidly growing population of infants and children with neurodevelopmental and cognitive impairments and life-long disability resulting from developmental brain injury is a significant public health concern. Brain injury in infants and children can have devastating effects because the injury is superimposed on the high metabolic demands of the developing brain. Acute injury in the pediatric brain can derail, halt or lead to dysregulation of the complex and highly regulated normal developmental processes. This paper provides a brief review of metabolism in developing brain and alterations found clinically and in animal models of developmental brain injury. The metabolic changes observed in three major categories of injury that can result in life-long cognitive and neurological disabilities, including neonatal hypoxia-ischemia, pediatric traumatic brain injury, and brain injury secondary to prematurity are reviewed. PMID:26148530

  15. 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.

  16. 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.

  17. Contribution of psychological trauma to outcomes after traumatic brain injury: assaults versus sporting injuries.

    Science.gov (United States)

    Mathias, Jane L; Harman-Smith, Yasmin; Bowden, Stephen C; Rosenfeld, Jeffrey V; Bigler, Erin D

    2014-04-01

    Clinical research into outcomes after traumatic brain injury (TBI) frequently combines injuries that have been sustained through different causes (e.g., car accidents, assaults, and falls), the effect of which is not well understood. This study examined the contribution of injury-related psychological trauma—which is more commonly associated with specific types of injuries—to outcomes after nonpenetrating TBI in order to determine whether it may be having a differential effect in samples containing mixed injuries. Data from three groups that were prospectively recruited for two larger studies were compared: one that sustained a TBI as a result of physical assaults (i.e., psychologically traumatizing) and another as a result of sporting injuries (i.e., nonpsychologically traumatizing), as well as an orthopedic control group (OC). Psychosocial and emotional (postconcussion symptoms, injury-related stress, and depression), cognitive (memory, abstract reasoning, problem solving, and verbal fluency), and functional (general outcome; resumption of home, social, and work roles) outcomes were all assessed. The TBI(assault) group reported significantly poorer psychosocial and emotional outcomes and higher rates of litigation (criminal rather than civil) than both the TBI(sport) and OC groups approximately 6 months postinjury, but there were no differences in the cognitive or functional outcomes of the three groups. The findings suggest that the cause of a TBI may assist in explaining some of the differences in outcomes of people who have seemingly comparable injuries. Involvement in litigation and the cause of an injury may also be confounded, which may lead to the erroneous conclusion that litigants have poorer outcomes.

  18. Peripheral nerve injury induces adult brain neurogenesis and remodelling.

    Science.gov (United States)

    Rusanescu, Gabriel; Mao, Jianren

    2017-02-01

    Unilateral peripheral nerve chronic constriction injury (CCI) has been widely used as a research model of human neuropathic pain. Recently, CCI has been shown to induce spinal cord adult neurogenesis, which may contribute to the chronic increase in nociceptive sensitivity. Here, we show that CCI also induces rapid and profound asymmetrical anatomical rearrangements in the adult rodent cerebellum and pons. This remodelling occurs throughout the hindbrain, and in addition to regions involved in pain processing, also affects other sensory modalities. We demonstrate that these anatomical changes, partially reversible in the long term, result from adult neurogenesis. Neurogenic markers Mash1, Ngn2, doublecortin and Notch3 are widely expressed in the rodent cerebellum and pons, both under normal and injured conditions. CCI-induced hindbrain structural plasticity is absent in Notch3 knockout mice, a strain with impaired neuronal differentiation, demonstrating its dependence on adult neurogenesis. Grey matter and white matter structural changes in human brain, as a result of pain, injury or learned behaviours have been previously detected using non-invasive neuroimaging techniques. Because neurogenesis-mediated structural plasticity is thought to be restricted to the hippocampus and the subventricular zone, such anatomical rearrangements in other parts of the brain have been thought to result from neuronal plasticity or glial hypertrophy. Our findings suggest the presence of extensive neurogenesis-based structural plasticity in the adult mammalian brain, which may maintain a memory of basal sensory levels, and act as an adaptive mechanism to changes in sensory inputs.

  19. 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.

  20. 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....

  1. A Danish national strategy for treatment and rehabilitation after acquired brain injury

    DEFF Research Database (Denmark)

    Engberg, Aase W

    2007-01-01

    This study describes the establishment of a Danish national strategy for treatment and rehabilitation of acquired brain injury, particularly traumatic brain injury, in 1997. The vision was to create a system of tax-financed continuous treatment, restoration of function, and outpatient...... rehabilitation. Recommendations and their fulfillment are described. Focus is on the establishment and function of early intensive interdisciplinary rehabilitation after severe traumatic brain injury, centralized as 2 units since the year 2000, each with half the country as uptake area, corresponding...

  2. Alteration and reorganization of functional networks: a new perspective in brain injury study

    Directory of Open Access Journals (Sweden)

    Nazareth P. Castellanos

    2011-09-01

    Full Text Available Plasticity is the mechanism underlying brain’s potential capability to compensate injury. Recently several studies have shown that functional connections among brain areas are severely altered by brain injury and plasticity leading to a reorganization of the networks. This new approach studies the impact of brain injury by means of alteration of functional interactions. The concept of functional connectivity refers to the statistical interdependencies between physiological time series simultaneously recorded in various brain areas and it could be an essential tool for brain function studies, being its deviation from healthy reference an indicator for damage. In this article, we review studies investigating functional connectivity changes after brain injury and subsequent recovery, providing an accessible introduction to common mathematical methods to infer functional connectivity, exploring their capabilities, future perspectives and clinical uses in brain injury studies.

  3. Temporal and spatial characterization of neuronal injury following lateral fluid-percussion brain injury in the rat.

    Science.gov (United States)

    Hicks, R; Soares, H; Smith, D; McIntosh, T

    1996-01-01

    The pattern of neuronal injury following lateral fluid-percussion (FP) brain injury in the rat was systematically characterized at sequential time points to identify selectively vulnerable regions and to determine the temporal contribution of primary and delayed neuropathological events. Male Sprague-Dawley rats (n = 28) were killed 10 min, 2 h, 12 h, 24 h, 4 days, and 7 days following a lateral FP brain injury of moderate severity (2.2 atm), or 24 h after a sham injury. Brain sections were stained and analyzed using Nissl, acid fuchsin, and silver staining methods to identify regions with injured neurons or with visible lesions. Extensive numbers of acid fuchsin or silver-stained neurons were observed as early as 10 min after the FP brain injury in regions extending from the caudate/putamen to the pons. The frequency of injured neurons was greatest in the ipsilateral cortex, hippocampus, and thalamus, and a visible loss of Nissl-stained neurons was observed in these regions beginning at 12 h after the FP brain injury. Acid fuchsin-stained neurons were restricted to the same brain regions for all of the survival periods and gradually decreased in numbers between 24 h and 7 days after injury. These findings suggest that lateral FP brain injury in the rat produces a combination of focal cortical contusion and diffuse subcortical neuronal injury, which is present within minutes of the impact, progresses to a loss of neurons by 12 h, and does not markedly expand into other brain regions with survival periods up to 7 days. Furthermore, the acute onset and rapid evolution of the neuronal injury process may have important implications when considering a window of opportunity for pharmacological intervention.

  4. Head motions while riding roller coasters: implications for brain injury.

    Science.gov (United States)

    Pfister, Bryan J; Chickola, Larry; Smith, Douglas H

    2009-12-01

    The risk of traumatic brain injury (TBI) while riding roller coasters has received substantial attention. Case reports of TBI around the time of riding roller coasters have led many medical professionals to assert that the high gravitational forces (G-forces) induced by roller coasters pose a significant TBI risk. Head injury research, however, has shown that G-forces alone cannot predict TBI. Established head injury criterions and procedures were employed to compare the potential of TBI between daily activities and roller coaster riding. Three-dimensional head motions were measured during 3 different roller coaster rides, a pillow fight, and car crash simulations. Data was analyzed and compared with published data, using similar analyses of head motions. An 8.05 m/s car crash lead to the largest head injury criterion measure of 28.1 and head impact power of 3.41, over 6 times larger than the roller coaster rides of 4.1 and 0.36. Notably, the linear and rotational components of head acceleration during roller coaster rides were milder than those induced by many common activities. As such, there appears to be an extremely low risk of TBI due to the head motions induced by roller coaster rides.

  5. 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.

  6. Traumatic brain injury impairs synaptic plasticity in hippocampus in rats

    Institute of Scientific and Technical Information of China (English)

    ZHANG Bao-liang; CHEN Xin; TAN Tao; YANG Zhuo; CARLOS Dayao; JIANG Rong-cai; ZHANG Jian-ning

    2011-01-01

    Background Traumatic brain injury (TBl) often causes cognitive deficits and remote symptomatic epilepsy.Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBl may impair the cellular circuit in the hippocampus.Methods Forty male Wistar rats were randomized into control (n=20) and TBl groups (n=20). Long-term potentiation,extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.Results TBI resulted in a significantly increased excitability in the dentate gyrus (DG), but a significantly decreased excitability in the cornu ammonis 1 (CA1) area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area.Conclusions TBl leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.

  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. Dynamic pituitary hormones change after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Ping Zheng

    2014-01-01

    Full Text Available Objective: To study the dynamic changes of pituitary hormones in traumatic brain injury (TBI and to correlate the severity and neurological outcome. Patients and Methods: Dynamic changes in the pituitary hormones were evaluated in 164 patients with TBI on day-1, day-7, day-14, day-21, and day-28 post injury. Admission TBI severity and long-term outcome were assessed with Glasgow Coma Scale (GCS score and Glasgow Outcome Scale (GOS score. The pituitary hormonal changes were correlated with TBI severity and outcome. Results: Of the 164 patients included in the study, pituitary dysfunction was found in 84 patients and in the remaining 80 patients pituitary function was normal. Most of the pituitary hormone deficiencies observed resolved over time; however, a significant proportion of patients had pituitary dysfunction at one month post injury. The hormones associated with poor outcome included growth hormone, thyrotropic hormone, and gonadotropic hormone. Conclusion: Dynamic changes of pituitary hormones in patients with TBI may reflect the severity of injury and also determine the outcome. Deficiency of growth hormone, gonadotropic hormone, and thyrotropic hormone can adversely affect neurological outcome.

  9. 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

  10. Structural Neuroimaging Findings in Mild Traumatic Brain Injury.

    Science.gov (United States)

    Bigler, Erin D; Abildskov, Tracy J; Goodrich-Hunsaker, Naomi J; Black, Garrett; Christensen, Zachary P; Huff, Trevor; Wood, Dawn-Marie G; Hesselink, John R; Wilde, Elisabeth A; Max, Jeffrey E

    2016-09-01

    Common neuroimaging findings in mild traumatic brain injury (mTBI), including sport-related concussion (SRC), are reviewed based on computed tomography and magnetic resonance imaging (MRI). Common abnormalities radiologically identified on the day of injury, typically a computed tomographic scan, are in the form of contusions, small subarachnoid or intraparenchymal hemorrhages as well as subdural and epidural collections, edema, and skull fractures. Common follow-up neuroimaging findings with MRI include white matter hyperintensities, hypointense signal abnormalities that reflect prior hemorrhage, focal encephalomalacia, presence of atrophy and/or dilated Virchow-Robins perivascular space. The MRI findings from a large pediatric mTBI study show low frequency of positive MRI findings at 6 months postinjury. The review concludes with an examination of some of the advanced MRI-based image analysis methods that can be performed in the patient who has sustained an mTBI.

  11. Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management

    Science.gov (United States)

    ARAKI, Takashi; YOKOTA, Hiroyuki; MORITA, Akio

    2017-01-01

    Traumatic brain injury (TBI) is the leading cause of death and disability in children. Pediatric TBI is associated with several distinctive characteristics that differ from adults and are attributable to age-related anatomical and physiological differences, pattern of injuries based on the physical ability of the child, and difficulty in neurological evaluation in children. Evidence suggests that children exhibit a specific pathological response to TBI with distinct accompanying neurological symptoms, and considerable efforts have been made to elucidate their pathophysiology. In addition, recent technical advances in diagnostic imaging of pediatric TBI has facilitated accurate diagnosis, appropriate treatment, prevention of complications, and helped predict long-term outcomes. Here a review of recent studies relevant to important issues in pediatric TBI is presented, and recent specific topics are also discussed. This review provides important updates on the pathophysiology, diagnosis, and age-appropriate acute management of pediatric TBI. PMID:28111406

  12. Dose- and time-dependent neuroprotective effects of Pycnogenol following traumatic brain injury.

    Science.gov (United States)

    Ansari, Mubeen A; Roberts, Kelly N; Scheff, Stephen W

    2013-09-01

    After traumatic brain injury (TBI), both primary and secondary injury cascades are initiated, leading to neuronal death and cognitive dysfunction. We have previously shown that the combinational bioflavonoid, Pycnogenol (PYC), alters some secondary injury cascades and protects synaptic proteins when administered immediately following trauma. The purpose of the present study was to explore further the beneficial effects of PYC and to test whether it can be used in a more clinically relevant fashion. Young adult male Sprague-Dawley rats were subjected to a unilateral moderate/severe cortical contusion. Subjects received a single intravenous (i.v.) injection of PYC (1, 5, or 10 mg/kg) or vehicle, with treatment initiated at 15 min, 2 h, or 4 h post injury. All rats were killed at 96 h post TBI. Both the cortex and hippocampus ipsilateral and contralateral to the injury were evaluated for possible changes in oxidative stress (thiobarbituric acid reactive species; TBARS) and both pre- and post-synaptic proteins (synapsin-I, synaptophysin, drebrin, post synaptic density protein-95, and synapse associated protein-97). Following TBI, TBARS were significantly increased in both the injured cortex and ipsilateral hippocampus. Regardless of the dose and delay in treatment, PYC treatment significantly lowered TBARS. PYC treatment significantly protected both the cortex and hippocampus from injury-related declines in pre- and post-synaptic proteins. These results demonstrate that a single i.v. treatment of PYC is neuroprotective after TBI with a therapeutic window of at least 4 h post trauma. The natural bioflavonoid PYC may provide a possible therapeutic intervention in neurotrauma.

  13. Hypothermic protection in rat focal ischemia models: strain differences and relevance to "reperfusion injury".

    Science.gov (United States)

    Ren, Yubo; Hashimoto, Megumi; Pulsinelli, William A; Nowak, Thaddeus S

    2004-01-01

    Hypothermic protection was compared in Long-Evans and spontaneously hypertensive rat (SHR) strains using transient focal ischemia, and in Wistar and SHR strains using permanent focal ischemia. Focal ischemia was produced by distal surgical occlusion of the middle cerebral artery and tandem occlusion of the ipsilateral common carotid artery (MCA/CCAO). Moderate hypothermia of 2 hours' duration was produced by systemic cooling to 32 degrees C, with further cooling of the brain achieved by reducing to 30 degrees C the temperature of the saline drip superfusing the exposed occlusion site. Infarct volume was determined from serial hematoxylin and eosin-stained frozen sections obtained routinely at 24 hours, or in some cases after 3 days' survival. In the SHR, moderate hypothermia was only effective when initiated before recirculation after a 90-minute occlusion period. In contrast, the same intervention was strikingly effective in the Long-Evans rat even when initiated after as long as 30-minute reperfusion after a 3-hour occlusion. This magnitude and duration of cooling was not protective in permanent MCA/CCAO in the SHR, but such transient hypothermia did effectively reduce infarct volume after permanent occlusions in Wistar rats. These results show striking differences in the temporal window for hypothermic protection among rat focal ischemia models. As expected, "reperfusion injury" in the Long-Evans strain is particularly responsive to delayed cooling. The finding that the SHR can be protected by hypothermia initiated immediately before recirculation suggests a rapidly evolving component of injury occurs subsequent to reperfusion in this model as well. Hypothermic protection after permanent occlusion in Wistar rats identifies a transient, temperature-sensitive phase of infarct evolution that is not evident in the unreperfused SHR. These observations confirm that distinct mechanisms can underlie the temporal progression of injury in rat stroke models, and emphasize

  14. Magnetic resonance imaging and cell-based neurorestorative therapy after brain injury

    Directory of Open Access Journals (Sweden)

    Quan Jiang

    2016-01-01

    Full Text Available Restorative cell-based therapies for experimental brain injury, such as stroke and traumatic brain injury, substantially improve functional outcome. We discuss and review state of the art magnetic resonance imaging methodologies and their applications related to cell-based treatment after brain injury. We focus on the potential of magnetic resonance imaging technique and its associated challenges to obtain useful new information related to cell migration, distribution, and quantitation, as well as vascular and neuronal remodeling in response to cell-based therapy after brain injury. The noninvasive nature of imaging might more readily help with translation of cell-based therapy from the laboratory to the clinic.

  15. Magnetic resonance imaging and cell-based neurorestorative therapy after brain injury

    Institute of Scientific and Technical Information of China (English)

    Quan Jiang

    2016-01-01

    Restorative cell-based therapies for experimental brain injury, such as stroke and traumatic brain injury, substantially improve functional outcome. We discuss and review state of the art magnetic resonance im-aging methodologies and their applications related to cell-based treatment after brain injury. We focus on the potential of magnetic resonance imaging technique and its associated challenges to obtain useful new information related to cell migration, distribution, and quantitation, as well as vascular and neuronal remodeling in response to cell-based therapy after brain injury. The noninvasive nature of imaging might more readily help with translation of cell-based therapy from the laboratory to the clinic.

  16. Coagulopathy as prognostic marker in acute traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Gaurav Chhabra

    2013-01-01

    Full Text Available Context: Coagulopathy frequently occurs following traumatic brain injury (TBI and usually occurs 6-72 hour post-trauma. The incidence and the probable risk factors for development of coagulopathy and poor outcome following TBI are largely unknown and vary considerably. Aims: To assess the incidence and probable risk factors for development of coagulopathy and to identify the risk factors for poor outcome in terms of median survival time following TBI. Materials and Methods: In this prospective study over two years, patients of isolated moderate and severe traumatic brain injury (GCS≤12 admitted to trauma center had coagulation profile (PT, APTT, thrombin time, fibrinogen and D-dimer, arterial lactate and ABG analysis done on day of admission and on day three. Coagulopathy was defined as prothrombin time (PT or/and activated partial thromboplastin time (APTT more than 1.5 times the normal control. Incidence of in-hospital mortality was assessed in all cases. Statistical Analysis: A stepwise logistic regression analysis was performed to identify risk factors for coagulopathy and mortality in these patients. Results: A total of 208 patients were enrolled in the study. The mean age was 32 ± 12 years and mean GCS was 7.1 ± 2.8. Coagulopathy was present in 46% ( n = 96 of patients. Risk factors for development of coagulopathy were found out to be severity of head injury (OR: 2.81, elevated D-dimer (OR: 3.43, low hemoglobin (OR: 3.13, and effaced cisterns in the CT scan (OR: 2.72. Presence of coagulopathy (OR: 2.97 and severity of head injury (OR: 5.70 strongly predicted poor outcome, and were associated with a decreased median survival time. Conclusions: There is a high incidence of coagulopathy following TBI. The presence of coagulopathy as well as of severity of TBI are strong predictors of in-hospital mortality in these patients.

  17. Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    YANG Xiao-feng; LIU Wei-guo; SHEN Hong; GONG Jiang-biao; YU Jun; HU Wei-wei; L(U) Shi-ting; ZHENG Xiu-jue; FU Wei-ming

    2005-01-01

    Objective: To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI). Methods: In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain. Results: Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP. Conclusions: In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.

  18. Neuroprotection of GST, an extract of traditional Chinese herb, against ischemic brain injury induced by transient brain ischemia and reperfusion in rat hippocampus.

    Science.gov (United States)

    Sun, Ya-Feng; Pei, Dong-Sheng; Zhang, Qing-Xiu; Zhang, Guang-Yi

    2008-06-01

    In this study, we investigated the effect of GST, an extract of Chinese traditional herb, on transient brain ischemia/reperfusion-induced neuronal cell death. Immunoblotting was used to detect the phosphorylation of MLK, JNK and c-jun. Transient (15 minutes) brain ischemia was induced by the four-vessel occlusion in Sprague-Dawley rats. GST was administrated to the SD rats 20 minutes before ischemia or 1 hour after ischemia. Our data showed that the pretreatment of GST could inhibit phosphorylation of MLK, JNK and c-jun. Moreover, GST showed potent neuroprotective effects on ischemic brain damage in vivo and administration of it 1 hour after ischemia also achieved the protective effects. These results indicate that GST has a prominent neuroprotection action against brain ischemic damage and provides a promising therapeutic approach for ischemic brain injury.

  19. Protective effect of cocaine-and amphetamine-regulated transcript peptide in ischemic brain injury%可卡因-苯丙胺调节转录肽在缺血性脑损伤中的保护作用

    Institute of Scientific and Technical Information of China (English)

    金佳丽; 徐运

    2010-01-01

    可卡因-苯丙胺调节转录肽(cocaine-and amphetamine-regulated transcript,CART)是一种内源性神经肽,广泛分布于脑、胃肠道和胰腺等器官组织,具有多种重要的生理功能,包括进食与肥胖、应激、精神焦虑行为、药物成瘾和内分泌调节等.前期研究提示,CART在中枢神经系统广泛分布,并且参与调节多种生理学过程,具有一定的中枢保护作用,是一种很有潜力的神经保护剂.文章就CART对卒中以及神经变性疾病的神经保护作用及其机制,以及其在中枢神经系统疾病治疗作用等方面的研究进展进行了综述.%Cocaine-and amphetamine-regulated transcript (CART), an endogenous neuropeptide, is widely distributed in human organs and tissues, such as brain, gastrointestinal tract and pancreas. It has a variety of important physiological functions, including eating and obesity, stress, mental anxiety, drug addition, and endocrine regulation. Previous studies have suggested that CART is widely distributed in the central nervous system, and it involves in the regulation of a variety of physiological processes and has some central protective effects. It is a potential neuroprotective agent. This article reviews the recent progress in research on the neuroprotective effect of CART on stroke and neurodegenerative disease and its mechanisms, as well as its therapeutic effect in central nervous system diseases.

  20. Alteration in synaptic junction proteins following traumatic brain injury.

    Science.gov (United States)

    Merlo, Lucia; Cimino, Francesco; Angileri, Filippo Flavio; La Torre, Domenico; Conti, Alfredo; Cardali, Salvatore Massimiliano; Saija, Antonella; Germanò, Antonino

    2014-08-15

    Extensive research and scientific efforts have been focused on the elucidation of the pathobiology of cellular and axonal damage following traumatic brain injury (TBI). Conversely, few studies have specifically addressed the issue of synaptic dysfunction. Synaptic junction proteins may be involved in post-TBI alterations, leading to synaptic loss or disrupted plasticity. A Synapse Protein Database on synapse ontology identified 109 domains implicated in synaptic activities and over 5000 proteins, but few of these demonstrated to play a role in the synaptic dysfunction after TBI. These proteins are involved in neuroplasticity and neuromodulation and, most importantly, may be used as novel neuronal markers of TBI for specific intervention.