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Sample records for blast-induced traumatic brain

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

    Science.gov (United States)

    2014-10-28

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

  2. 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.

  3. 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...

  4. Hyperbaric Oxygen Therapy in the Treatment of Chronic Mild-Moderate Blast-Induced Traumatic Brain Injury PCS and PTSD

    Science.gov (United States)

    2015-10-01

    Award Number: W81XWH-10-1-0962 TITLE: Hyperbaric Oxygen therapy in the Treatment of Chronic Mild-Moderate Blast-Induced Traumatic Brain Injury...Annual 3. DATES COVERED (From – To) 30Sep2014 - 29Sep2015 4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER W81XWH-10-1-0962 Hyperbaric Oxygen therapy in...post- hyperbaric oxygen treatment. Four additional subjects have been screened in October 2015 and nine are awaiting first appointment for

  5. Molecular mechanisms of increased cerebral vulnerability after repeated mild blast-induced traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Alaa Kamnaksh

    2014-06-01

    Full Text Available The consequences of a mild traumatic brain injury can be especially severe if it is repeated within the period of increased cerebral vulnerability (ICV that follows the initial insult. To better understand the molecular mechanisms that contribute to ICV, we exposed rats to different levels of mild blast overpressure (5 exposures; total pressure range: 15.54–19.41 psi or 107.14–133.83 kPa at a rate of 1 per 30 min, monitored select physiological parameters, and assessed behavior. Two days post-injury or sham, we determined changes in protein biomarkers related to various pathologies in behaviorally relevant brain regions and in plasma. We found that oxygen saturation and heart rate were transiently depressed following mild blast exposure and that injured rats exhibited significantly increased anxiety- and depression-related behaviors. Proteomic analyses of the selected brain regions showed evidence of substantial oxidative stress and vascular changes, altered cell adhesion, and inflammation predominantly in the prefrontal cortex. Importantly, these pathological changes as well as indications of neuronal and glial cell loss/damage were also detected in the plasma of injured rats. Our findings illustrate some of the complex molecular changes that contribute to the period of ICV in repeated mild blast-induced traumatic brain injury. Further studies are needed to determine the functional and temporal relationship between the various pathomechanisms. The validation of these and other markers can help to diagnose individuals with ICV using a minimally invasive procedure and to develop evidence-based treatments for chronic neuropsychiatric conditions.

  6. A multi-mode shock tube for investigation of blast-induced traumatic brain injury.

    Science.gov (United States)

    Reneer, Dexter V; Hisel, Richard D; Hoffman, Joshua M; Kryscio, Richard J; Lusk, Braden T; Geddes, James W

    2011-01-01

    Blast-induced mild traumatic brain injury (bTBI) has become increasingly common in recent military conflicts. The mechanisms by which non-impact blast exposure results in bTBI are incompletely understood. Current small animal bTBI models predominantly utilize compressed air-driven membrane rupture as their blast wave source, while large animal models use chemical explosives. The pressure-time signature of each blast mode is unique, making it difficult to evaluate the contributions of the different components of the blast wave to bTBI when using a single blast source. We utilized a multi-mode shock tube, the McMillan blast device, capable of utilizing compressed air- and compressed helium-driven membrane rupture, and the explosives oxyhydrogen and cyclotrimethylenetrinitramine (RDX, the primary component of C-4 plastic explosives) as the driving source. At similar maximal blast overpressures, the positive pressure phase of compressed air-driven blasts was longer, and the positive impulse was greater, than those observed for shockwaves produced by other driving sources. Helium-driven shockwaves more closely resembled RDX blasts, but by displacing air created a hypoxic environment within the shock tube. Pressure-time traces from oxyhydrogen-driven shockwaves were very similar those produced by RDX, although they resulted in elevated carbon monoxide levels due to combustion of the polyethylene bag used to contain the gases within the shock tube prior to detonation. Rats exposed to compressed air-driven blasts had more pronounced vascular damage than those exposed to oxyhydrogen-driven blasts of the same peak overpressure, indicating that differences in blast wave characteristics other than peak overpressure may influence the extent of bTBI. Use of this multi-mode shock tube in small animal models will enable comparison of the extent of brain injury with the pressure-time signature produced using each blast mode, facilitating evaluation of the blast wave components

  7. A Novel Preclinical Model of Moderate Primary Blast-Induced Traumatic Brain Injury.

    Science.gov (United States)

    Divani, Afshin A; Murphy, Amanda J; Meints, Joyce; Sadeghi-Bazargani, Homayoun; Nordberg, Jessica; Monga, Manoj; Low, Walter C; Bhatia, Prerana M; Beilman, Greg J; SantaCruz, Karen S

    2015-07-15

    Blast-induced traumatic brain injury (bTBI) is the "signature" injury of the recent Iraq and Afghanistan wars. Here, we present a novel method to induce bTBI using shock wave (SW) lithotripsy. Using a lithotripsy machine, Wistar rats (N = 70; 408.3 ± 93 g) received five SW pulses to the right side of the frontal cortex at 24 kV and a frequency of 60 Hz. Animals were then randomly divided into three study endpoints: 24 h (n = 25), 72 h (n = 19) and 168 h (n = 26). Neurological and behavioral assessments (Garcia's test, beam walking, Rotarod, and elevated plus maze) were performed at the baseline, and further assessments followed at 3, 6, 24, 72, and 168 h post-injury, if applicable. We performed digital subtraction angiography (DSA) to assess presence of cerebral vasospasm due to induced bTBI. Damage to brain tissue was assessed by an overall histological severity (OHS) score based on depth of injury, area of hemorrhage, and extent of axonal injury. Except for beam walking, OHS was significantly correlated with the other three outcome measures with at least one of their assessments during the first 6 h after the experiment. OHS manifested the highest absolute correlation coefficients with anxiety at the baseline and 6 h post-injury (r(baseline) = -0.75, r(6hrs) = 0.85; p<0.05). Median hemispheric differences for contrast peak values (obtained from DSA studies) for 24, 72, and 168 h endpoints were 3.45%, 3.05% and 0.2%, respectively, with statistically significant differences at 1 versus 7 d (p<0.05) and 3 versus 7 d (p<0.01). In this study, we successfully established a preclinical rat model of bTBI with characteristics similar to those observed in clinical cases. This new method may be useful for future investigations aimed at understanding bTBI pathophysiology.

  8. Experimental study of blast-induced traumatic brain injury using a physical head model.

    Science.gov (United States)

    Zhang, Jiangyue; Pintar, Frank A; Yoganandan, Narayan; Gennarelli, Thomas A; Son, Steven F

    2009-11-01

    This study was conducted to quantify intracranial biomechanical responses and external blast overpressures using physical head model to understand the biomechanics of blast traumatic brain injury and to provide experimental data for computer simulation of blast-induced brain trauma. Ellipsoidal-shaped physical head models, made from 3-mm polycarbonate shell filled with Sylgard 527 silicon gel, were used. Six blast tests were conducted in frontal, side, and 45 degrees oblique orientations. External blast overpressures and internal pressures were quantified with ballistic pressure sensors. Blast overpressures, ranging from 129.5 kPa to 769.3 kPa, were generated using a rigid cannon and 1.3 to 3.0 grams of pentaerythritol tetranitrate (PETN) plastic sheet explosive (explosive yield of 13.24 kJ and TNT equivalent mass of 2.87 grams for 3 grams of material). The PETN plastic sheet explosive consisted of 63% PETN powder, 29% plasticizer, and 8% nitrocellulose with a density of 1.48 g/cm3 and detonation velocity of 6.8 km/s. Propagation and reflection of the shockwave was captured using a shadowgraph technique. Shockwave speeds ranging from 423.3 m/s to 680.3 m/s were recorded. The model demonstrated a two-stage response: a pressure dominant (overpressure) stage followed by kinematic dominant (blast wind) stage. Positive pressures in the brain simulant ranged from 75.1 kPa to 1095 kPa, and negative pressures ranged from -43.6 kPa to -646.0 kPa. High- and normal-speed videos did not reveal observable deformations in the brain simulant from the neutral density markers embedded in the midsagittal plane of the head model. Amplitudes of the internal positive and negative pressures were found to linearly correlate with external overpressure. Results from the current study suggested a pressure-dominant brain injury mechanism instead of strain injury mechanism under the blast severity of the current study. These quantitative results also served as the validation and calibration

  9. Combined Effects of Primary and Tertiary Blast on Rat Brain: Characterization of a Model of Blast-induced Mild Traumatic Brain Injury

    Science.gov (United States)

    2014-03-01

    R) asymmetry . Since none of the brain regions exhibited a significant Blast x No. of Events x Side (L/R) interaction, the effect of side was...AD Award Number: W81XWH-11-2-0127 TITLE: Combined Effects of Primary and Tertiary Blast on Rat Brain : Characterization of a Model of...Blast-induced Mild Traumatic Brain Injury PRINCIPAL INVESTIGATOR: Dr. Joseph Long CONTRACTING ORGANIZATION: The Geneva Foundation, Tacoma, WA

  10. An open air research study of blast-induced traumatic brain injury to goats

    Institute of Scientific and Technical Information of China (English)

    Hui-Jun Chen; Chuan Xu; Yue Li; Zhi-Qiang Chen; Guan-Hua Li; Zhao-Xia Duan; Xiao-Xia Li

    2015-01-01

    Purpose:We once reported blast-induced traumatic brain injury (bTBI) in confined space.Here,bTBI was studied again on goats in the open air using 3.0 kg trinitrotoluene.Methods:The goats were placed at 2,4,6 and 8 m far from explosion center.Trinitrotoluene (TNT) was used as the source of the blast wave and the pressure at each distance was recorded.The systemic physiology,electroencephalogram,serum level of S-100beta,and neuron specific enolase (NSE) were determined pre and post the exposure.Neuroanatomy and neuropathology were observed 4 h after the exposure.Results:Simple blast waveforms were recorded with parameters of 702.8 kPa-0,442 ms,148.4 kPa-2.503 ms,73.9 kPa-3.233 ms,and 41.9 kPa-5.898 ms at 2,4,6 and 8 m respectively.Encephalic blast overpressure was on the first time recorded in the literature by us at 104.2 kPa-0.60 ms at 2 m,where mortality and burn rate were 44% and 44%.Gross examination showed that bTBI was mainly manifested as congestive expansion of blood vessels and subarachnoid hemorrhage,which had a total incidence of 25% and 19% in 36 goats.Microscopical observation found that the main pathohistological changes were enlarged perivascular space (21/36,58%),small hemorrhages (9/36,25%),vascular dilatation and congestion (8/36,22%),and less subarachnoid hemorrhage (2/36,6%).After explosion,serum levels of S100β and NSE were elevated,and EEG changed into slow frequency with declined amplitude.The results indicated that severity and incidence of bTBI is related to the intensity of blast overpressure.Conclusion:Blast wave can pass through the skull to directly injure brain tissue.

  11. The complexity of biomechanics causing primary blast-induced traumatic brain injury: a review of potential mechanisms.

    Directory of Open Access Journals (Sweden)

    Amy eCourtney

    2015-10-01

    Full Text Available Primary blast induced traumatic brain injury (bTBI is a prevalent battlefield injury in recent conflicts, yet biomechanical mechanisms of bTBI remain unclear. Elucidating specific biomechanical mechanisms is essential to developing animal models for testing candidate therapies and for improving protective equipment. Three hypothetical mechanisms of primary bTBI have received the most attention. Because translational and rotational head accelerations are primary contributors to TBI from non-penetrating blunt force head trauma, the acceleration hypothesis suggests that blast-induced head accelerations may cause bTBI. The hypothesis of direct cranial transmission suggests that a pressure transient traverses the skull into the brain and directly injures brain tissue. The thoracic hypothesis of bTBI suggests that some combination of a pressure transient reaching the brain via the thorax and a vagally mediated reflex result in bTBI. These three mechanisms may not be mutually exclusive, and quantifying exposure thresholds (for blasts of a given duration is essential for determining which mechanisms may be contributing for a level of blast exposure. Progress has been hindered by experimental designs which do not effectively expose animal models to a single mechanism and by over-reliance on poorly validated computational models. The path forward should be predictive validation of computational models by quantitative confirmation with blast experiments in animal models, human cadavers, and biofidelic human surrogates over a range of relevant blast magnitudes and durations coupled with experimental designs which isolate a single injury mechanism.

  12. 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.

  13. Distinguishing Realistic Military Blasts from Firecrackers in Mitigation Studies of Blast Induced Traumatic Brain Injury

    Energy Technology Data Exchange (ETDEWEB)

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

    2011-01-21

    In their Contributed Article, Nyein et al. (1,2) present numerical simulations of blast waves interacting with a helmeted head and conclude that a face shield may significantly mitigate blast induced traumatic brain injury (TBI). A face shield may indeed be important for future military helmets, but the authors derive their conclusions from a much smaller explosion than typically experienced on the battlefield. The blast from the 3.16 gm TNT charge of (1) has the following approximate peak overpressures, positive phase durations, and incident impulses (3): 10 atm, 0.25 ms, and 3.9 psi-ms at the front of the head (14 cm from charge), and 1.4 atm, 0.32 ms, and 1.7 psi-ms at the back of a typical 20 cm head (34 cm from charge). The peak pressure of the wave decreases by a factor of 7 as it traverses the head. The blast conditions are at the threshold for injury at the front of the head, but well below threshold at the back of the head (4). The blast traverses the head in 0.3 ms, roughly equal to the positive phase duration of the blast. Therefore, when the blast reaches the back of the head, near ambient conditions exist at the front. Because the headform is so close to the charge, it experiences a wave with significant curvature. By contrast, a realistic blast from a 2.2 kg TNT charge ({approx} an uncased 105 mm artillery round) is fatal at an overpressure of 10 atm (4). For an injury level (4) similar to (1), a 2.2 kg charge has the following approximate peak overpressures, positive phase durations, and incident impulses (3): 2.1 atm, 2.3 ms, and 18 psi-ms at the front of the head (250 cm from charge), and 1.8 atm, 2.5 ms, and 16.8 psi-ms at the back of the head (270 cm from charge). The peak pressure decreases by only a factor of 1.2 as it traverses the head. Because the 0.36 ms traversal time is much smaller than the positive phase duration, pressures on the head become relatively uniform when the blast reaches the back of the head. The larger standoff implies

  14. Expression of galanin and its receptors are perturbed in a rodent model of mild, blast-induced traumatic brain injury.

    Science.gov (United States)

    Kawa, Lizan; Barde, Swapnali; Arborelius, Ulf P; Theodorsson, Elvar; Agoston, Denes; Risling, Mårten; Hökfelt, Tomas

    2016-05-01

    The symptomatology, mood and cognitive disturbances seen in post-traumatic stress disorder (PTSD) and mild blast-induced traumatic brain injury (mbTBI) overlap considerably. However the pathological mechanisms underlying the two conditions are currently unknown. The neuropeptide galanin has been suggested to play a role in the development of stress and mood disorders. Here we applied bio- and histochemical methods with the aim to elucidate the nature of any changes in the expression of galanin and its receptors in a rodent model of mbTBI. In situ hybridization and quantitative polymerase chain reaction studies revealed significant, injury-induced changes, in some cases lasting at least for one week, in the mRNA levels of galanin and/or its three receptors, galanin receptor 1-3 (GalR1-3). Such changes were seen in several forebrain regions, and the locus coeruleus. In the ventral periaqueductal gray GalR1 mRNA levels were increased, while GalR2 were decreased. Analysis of galanin peptide levels using radioimmunoassay demonstrated an increase in several brain regions including the locus coeruleus, dorsal hippocampal formation and amygdala. These findings suggest a role for the galanin system in the endogenous response to mbTBI, and that pharmacological studies of the effects of activation or inhibition of different galanin receptors in combination with functional assays of behavioral recovery may reveal promising targets for new therapeutic strategies in mbTBI.

  15. Simulation of blast-induced, early-time intracranial wave physics leading to traumatic brain injury.

    Energy Technology Data Exchange (ETDEWEB)

    Taylor, Paul Allen; Ford, Corey C. (University of New Mexico, Albuquerque, NM)

    2008-04-01

    U.S. soldiers are surviving blast and impacts due to effective body armor, trauma evacuation and care. Blast injuries are the leading cause of traumatic brain injury (TBI) in military personnel returning from combat. Understanding of Primary Blast Injury may be needed to develop better means of blast mitigation strategies. The objective of this paper is to investigate the effects of blast direction and strength on the resulting mechanical stress and wave energy distributions generated in the brain.

  16. 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

  17. 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.

  18. Investigation of cavitation as a possible damage mechanism in blast-induced traumatic brain injury.

    Science.gov (United States)

    Goeller, Jacques; Wardlaw, Andrew; Treichler, Derrick; O'Bruba, Joseph; Weiss, Greg

    2012-07-01

    Cavitation was investigated as a possible damage mechanism for war-related traumatic brain injury (TBI) due to an improvised explosive device (IED) blast. When a frontal blast wave encounters the head, a shock wave is transmitted through the skull, cerebrospinal fluid (CSF), and tissue, causing negative pressure at the contrecoup that may result in cavitation. Numerical simulations and shock tube experiments were conducted to determine the possibility of cranial cavitation from realistic IED non-impact blast loading. Simplified surrogate models of the head consisted of a transparent polycarbonate ellipsoid. The first series of tests in the 18-inch-diameter shock tube were conducted on an ellipsoid filled with degassed water to simulate CSF and tissue. In the second series, Sylgard gel, surrounded by a layer of degassed water, was used to represent the tissue and CSF, respectively. Simulated blast overpressure in the shock tube tests ranged from a nominal 10-25 pounds per square inch gauge (psig; 69-170 kPa). Pressure in the simulated CSF was determined by Kulite thin line pressure sensors at the coup, center, and contrecoup positions. Using video taken at 10,000 frames/sec, we verified the presence of cavitation bubbles at the contrecoup in both ellipsoid models. In all tests, cavitation at the contrecoup was observed to coincide temporally with periods of negative pressure. Collapse of the cavitation bubbles caused by the surrounding pressure and elastic rebound of the skull resulted in significant pressure spikes in the simulated CSF. Numerical simulations using the DYSMAS hydrocode to predict onset of cavitation and pressure spikes during cavity collapse were in good agreement with the tests. The numerical simulations and experiments indicate that skull deformation is a significant factor causing cavitation. These results suggest that cavitation may be a damage mechanism contributing to TBI that requires future study.

  19. Screening of biochemical and molecular mechanisms of secondary injury and repair in the brain after experimental blast-induced traumatic brain injury in rats.

    Science.gov (United States)

    Kochanek, Patrick M; Dixon, C Edward; Shellington, David K; Shin, Samuel S; Bayır, Hülya; Jackson, Edwin K; Kagan, Valerian E; Yan, Hong Q; Swauger, Peter V; Parks, Steven A; Ritzel, David V; Bauman, Richard; Clark, Robert S B; Garman, Robert H; Bandak, Faris; Ling, Geoffrey; Jenkins, Larry W

    2013-06-01

    Abstract Explosive blast-induced traumatic brain injury (TBI) is the signature insult in modern combat casualty care and has been linked to post-traumatic stress disorder, memory loss, and chronic traumatic encephalopathy. In this article we report on blast-induced mild TBI (mTBI) characterized by fiber-tract degeneration and axonal injury revealed by cupric silver staining in adult male rats after head-only exposure to 35 psi in a helium-driven shock tube with head restraint. We now explore pathways of secondary injury and repair using biochemical/molecular strategies. Injury produced ∼25% mortality from apnea. Shams received identical anesthesia exposure. Rats were sacrificed at 2 or 24 h, and brain was sampled in the hippocampus and prefrontal cortex. Hippocampal samples were used to assess gene array (RatRef-12 Expression BeadChip; Illumina, Inc., San Diego, CA) and oxidative stress (OS; ascorbate, glutathione, low-molecular-weight thiols [LMWT], protein thiols, and 4-hydroxynonenal [HNE]). Cortical samples were used to assess neuroinflammation (cytokines, chemokines, and growth factors; Luminex Corporation, Austin, TX) and purines (adenosine triphosphate [ATP], adenosine diphosphate, adenosine, inosine, 2'-AMP [adenosine monophosphate], and 5'-AMP). Gene array revealed marked increases in astrocyte and neuroinflammatory markers at 24 h (glial fibrillary acidic protein, vimentin, and complement component 1) with expression patterns bioinformatically consistent with those noted in Alzheimer's disease and long-term potentiation. Ascorbate, LMWT, and protein thiols were reduced at 2 and 24 h; by 24 h, HNE was increased. At 2 h, multiple cytokines and chemokines (interleukin [IL]-1α, IL-6, IL-10, and macrophage inflammatory protein 1 alpha [MIP-1α]) were increased; by 24 h, only MIP-1α remained elevated. ATP was not depleted, and adenosine correlated with 2'-cyclic AMP (cAMP), and not 5'-cAMP. Our data reveal (1) gene-array alterations similar to disorders of

  20. Modulation of Cholinergic Pathways and Inflammatory Mediators in Blast-Induced Traumatic Brain Injury

    Science.gov (United States)

    2013-01-01

    Neuroinflammation including cross-talk between central and peripheral immune systems is considered to be a primary event after blast exposure...cholinergic anti-inflammatory pathway has been proposed as a link in neuroimmunomodulation, especially during stress con- ditions [8–11]. Neuroinflammation is...BINT) elicits early complement activation and tumor necrosis factor alpha (TNFalpha) release in a rat brain, J. Neurol. Sci. 318 (2012) 146–154. [8

  1. Modeling and simulation of blast-induced, early-time intracranial wave physics leading to traumatic brain injury.

    Energy Technology Data Exchange (ETDEWEB)

    Ford, Corey C. (University of New Mexico, Albuquerque, NM); Taylor, Paul Allen

    2008-02-01

    The objective of this modeling and simulation study was to establish the role of stress wave interactions in the genesis of traumatic brain injury (TBI) from exposure to explosive blast. A high resolution (1 mm{sup 3} voxels), 5 material model of the human head was created by segmentation of color cryosections from the Visible Human Female dataset. Tissue material properties were assigned from literature values. The model was inserted into the shock physics wave code, CTH, and subjected to a simulated blast wave of 1.3 MPa (13 bars) peak pressure from anterior, posterior and lateral directions. Three dimensional plots of maximum pressure, volumetric tension, and deviatoric (shear) stress demonstrated significant differences related to the incident blast geometry. In particular, the calculations revealed focal brain regions of elevated pressure and deviatoric (shear) stress within the first 2 milliseconds of blast exposure. Calculated maximum levels of 15 KPa deviatoric, 3.3 MPa pressure, and 0.8 MPa volumetric tension were observed before the onset of significant head accelerations. Over a 2 msec time course, the head model moved only 1 mm in response to the blast loading. Doubling the blast strength changed the resulting intracranial stress magnitudes but not their distribution. We conclude that stress localization, due to early time wave interactions, may contribute to the development of multifocal axonal injury underlying TBI. We propose that a contribution to traumatic brain injury from blast exposure, and most likely blunt impact, can occur on a time scale shorter than previous model predictions and before the onset of linear or rotational accelerations traditionally associated with the development of TBI.

  2. Altering endoplasmic reticulum stress in a model of blast-induced traumatic brain injury controls cellular fate and ameliorates neuropsychiatric symptoms

    Directory of Open Access Journals (Sweden)

    Aric Flint Logsdon

    2014-12-01

    Full Text Available Neuronal injury following blast-induced traumatic brain injury (bTBI increases the risk for neuropsychiatric disorders, yet the pathophysiology remains poorly understood. Blood-brain-barrier (BBB disruption, endoplasmic reticulum (ER stress, and apoptosis have all been implicated in bTBI. Microvessel compromise is a primary effect of bTBI and is postulated to cause subcellular secondary effects such as ER stress. What remains unclear is how these secondary effects progress to personality disorders in humans exposed to head trauma. To investigate this we exposed male rats to a clinically relevant bTBI model we have recently developed. The study examined initial BBB disruption using Evan’s blue, ER stress mechanisms, apoptosis and impulsive-like behavior measured with elevated plus maze (EPM. Large BBB openings were observed immediately following bTBI, and persisted for at least 6 h. Data showed increased mRNA abundance of stress response genes at 3 h, with subsequent increases in the ER stress markers C/EBP homologous protein (CHOP and growth arrest and DNA damage-inducible protein 34 (GADD34 at 24 h. Caspase-12 and Caspase-3 were both cleaved at 24 h following bTBI. The ER stress inhibitor, salubrinal (SAL, was administered (1mg/kg i.p. to investigate its’ effects on neuronal injury and impulsive-like behavior associated with bTBI. SAL reduced CHOP protein expression, and diminished Caspase-3 cleavage, suggesting apoptosis attenuation. Interestingly, SAL also ameliorated impulsive-like behavior indicative of head trauma. These results suggest SAL plays a role in apoptosis regulation and the pathology of chronic disease. These observations provide evidence that bTBI involves ER stress and that the UPR is a promising molecular target for the attenuation of neuronal injury.

  3. Amelioration of acute sequelae of blast induced mild traumatic brain injury by N-acetyl cysteine: a double-blind, placebo controlled study.

    Directory of Open Access Journals (Sweden)

    Michael E Hoffer

    Full Text Available BACKGROUND: Mild traumatic brain injury (mTBI secondary to blast exposure is the most common battlefield injury in Southwest Asia. There has been little prospective work in the combat setting to test the efficacy of new countermeasures. The goal of this study was to compare the efficacy of N-acetyl cysteine (NAC versus placebo on the symptoms associated with blast exposure mTBI in a combat setting. METHODS: This study was a randomized double blind, placebo-controlled study that was conducted on active duty service members at a forward deployed field hospital in Iraq. All symptomatic U.S. service members who were exposed to significant ordnance blast and who met the criteria for mTBI were offered participation in the study and 81 individuals agreed to participate. Individuals underwent a baseline evaluation and then were randomly assigned to receive either N-acetyl cysteine (NAC or placebo for seven days. Each subject was re-evaluated at 3 and 7 days. Outcome measures were the presence of the following sequelae of mTBI: dizziness, hearing loss, headache, memory loss, sleep disturbances, and neurocognitive dysfunction. The resolution of these symptoms seven days after the blast exposure was the main outcome measure in this study. Logistic regression on the outcome of 'no day 7 symptoms' indicated that NAC treatment was significantly better than placebo (OR = 3.6, p = 0.006. Secondary analysis revealed subjects receiving NAC within 24 hours of blast had an 86% chance of symptom resolution with no reported side effects versus 42% for those seen early who received placebo. CONCLUSION: This study, conducted in an active theatre of war, demonstrates that NAC, a safe pharmaceutical countermeasure, has beneficial effects on the severity and resolution of sequelae of blast induced mTBI. This is the first demonstration of an effective short term countermeasure for mTBI. Further work on long term outcomes and the potential use of NAC in civilian m

  4. Design and Analysis of Blast Induced Traumatic Brain Injury Mechanism Using a Surrogate Headform: Instrumentation and Outcomes

    Science.gov (United States)

    2011-05-01

    of twenty cases. London : s.n., 1961. OCLC: 603454539. 6. University of Toronto. Workshop on Brain Biomechanics . Presentation Notes. Toronto, Canada...Strain Gauge Technology; 2nd edition. New York : Springer , 1993. ISBN: 978-1-85166-864-9. 36. Vishay Micro-Measurements. MR-Series Bridge Completion...38. Books LLC (Editor). Accelerometers: Accelerometer, Piezoelectric Accelerometer, Piga Accelerometer, Gravimeter, Liquid Capacitive Inclinometers

  5. Combined Effects of Primary and Tertiary Blast on Rat Brain: Characterization of a Model of Blast-induced Mild Traumatic Brain Injury

    Science.gov (United States)

    2015-03-01

    changes in protein biomarker levels in functionally -relevant brain regions Two days following injury (or sham), we dissected the PFC, AD, DHC, and VHC and...period. Neuropathological changes are temporally and anatomically closely associated with neuroinflammation, prompting interest in the latter as...known function of TNAP in dephosphorylating pTau, the accumulation of pTau after brain injury could be attributed to the decreased TNAP

  6. Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

    Science.gov (United States)

    2013-01-01

    10 mM ThioGloTM-1 (Calbiochem, SanDiego, CA), a maleimid reagent that produces a highly fluorescent product upon its reaction with thiol groups.21...GSH concentrations were determined by addition of GSH peroxidase and cumene hydro peroxide to the brain homogenates with ThioGloTM-1 working solution...cAMP, 5’- AMP, 3’-AMP, 2’-AMP, adenosine and inosine using our standard LC-MS/MS purine assay with selected reaction monitoring (SRM).24 The brain

  7. Increase in Blood-Brain Barrier Perrmeability, Oxidative Stress, and Activated Microglia in a Rat Model of Blast-Induced Traumatic Brain Injury

    Science.gov (United States)

    2010-01-01

    3 X 3 min), followed by dipping in ict> cold water. The sections were exposed to Kodax BioMax Autoradiography Film (Kodak, Rochester, NY) for 55...days. All films were developed using a Kodak D-19 developer and analyzed in NIH Image v1.59 on a Power Macintosh connected to a Sony XC-77 CCD...matic brain injury in rats: an evJluation of sckcted measurcs. J Neuro- trauma 18:1207-1216. Hastings TG. 2tlO<J. The role of dopamine oxidation in

  8. A Novel Method for Inducing Therapeutic Hypothermia in a Swine Model of Blast-Induced Traumatic Brain Injury with Associated Hemorrhagic Shock

    Science.gov (United States)

    2012-05-01

    BURR HOLE  LOCATTION  NEUROLOGIC  DEFICIT   MACROSCOPIC  BRAIN INJURY  SERUM ENOLASE (NSE) LEVEL  ng/ml    0hr  3hr  6hr  24hr  3 ATM  Left Parietal...have not completed this task. Data regarding rate of brain cooling, changes in vital signs, neurological deficits , rise in intracranial pressure...helium and the vaporization of PFC produce rapid cooling of the alveolar gases. The thin alveolar membrane and the large surface area of contact between

  9. Blast-induced Mild Traumatic Brain Injury

    Science.gov (United States)

    2010-01-01

    may worsen TBI-related cognitive complaints, and agents that improve cognitive function, such as methylphenidate , may exacerbate PTSD symptoms. It is...for management of depression, PTSD, and anxiety; (7) referrals to substance abuse treatment specialists as needed; (8) teaching of sleep manage- ment

  10. 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

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

    Institute of Scientific and Technical Information of China (English)

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

    2015-01-01

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

  12. A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder.

    Science.gov (United States)

    Harch, Paul G; Andrews, Susan R; Fogarty, Edward F; Amen, Daniel; Pezzullo, John C; Lucarini, Juliette; Aubrey, Claire; Taylor, Derek V; Staab, Paul K; Van Meter, Keith W

    2012-01-01

    This is a preliminary report on the safety and efficacy of 1.5 ATA hyperbaric oxygen therapy (HBOT) in military subjects with chronic blast-induced mild to moderate traumatic brain injury (TBI)/post-concussion syndrome (PCS) and post-traumatic stress disorder (PTSD). Sixteen military subjects received 40 1.5 ATA/60 min HBOT sessions in 30 days. Symptoms, physical and neurological exams, SPECT brain imaging, and neuropsychological and psychological testing were completed before and within 1 week after treatment. Subjects experienced reversible middle ear barotrauma (5), transient deterioration in symptoms (4), and reversible bronchospasm (1); one subject withdrew. Post-treatment testing demonstrated significant improvement in: symptoms, neurological exam, full-scale IQ (+14.8 points; pPTSD symptoms (PCL-M: pself-report of percent of normal (pPTSD. Significant improvements occurred in symptoms, abnormal physical exam findings, cognitive testing, and quality-of-life measurements, with concomitant significant improvements in SPECT.

  13. 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 ...

  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. Blast-induced electromagnetic fields in the brain from bone piezoelectricity.

    Science.gov (United States)

    Lee, Ka Yan Karen; Nyein, Michelle K; Moore, David F; Joannopoulos, J D; Socrate, Simona; Imholt, Timothy; Radovitzky, Raul; Johnson, Steven G

    2011-01-01

    In this paper, we show that bone piezoelectricity-a phenomenon in which bone polarizes electrically in response to an applied mechanical stress and produces a short-range electric field-may be a source of intense blast-induced electric fields in the brain, with magnitudes and timescales comparable to fields with known neurological effects. We compute the induced charge density in the skull from stress data on the skull from a finite-element full-head model simulation of a typical IED-scale blast wave incident on an unhelmeted human head as well as a human head protected by a kevlar helmet, and estimate the resulting electric fields in the brain in both cases to be on the order of 10 V/m in millisecond pulses. These fields are more than 10 times stronger than the IEEE safety guidelines for controlled environments (IEEE Standards Coordinating Committee 28, 2002) and comparable in strength and timescale to fields from repetitive Transcranial Magnetic Stimulation (rTMS) that are designed to induce neurological effects (Wagner et al., 2006a). They can be easily measured by RF antennas, and may provide the means to design a diagnostic tool that records a quantitative measure of the head's exposure to blast insult.

  16. Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor α (TNFα) release in a rat brain.

    Science.gov (United States)

    Dalle Lucca, Jurandir J; Chavko, Mikulas; Dubick, Michael A; Adeeb, Saleena; Falabella, Michael J; Slack, Jessica L; McCarron, Richard; Li, Yansong

    2012-07-15

    Blast-induced neurotrauma (BINT) is a major medical concern yet its etiology is largely undefined. Complement activation may play a role in the development of secondary injury following traumatic brain injury; however, its role in BINT is still undefined. The present study was designed to characterize the complement system and adaptive immune-inflammatory responses in a rat model of moderate BINT. Anesthetized rats were exposed to a moderate blast (120 kPa) using an air-driven shock tube. Brain tissue injury, systemic and local complement, cerebral edema, inflammatory cell infiltration, and pro-inflammatory cytokine production were measured at 0.5, 3, 48, 72, 120, and 168 h. Injury to brain tissue was evaluated by histological evaluation. Systemic complement was measured via ELSIA. The remaining measurements were determined by immunohistoflourescent staining. Moderate blast triggers moderate brain injuries, elevated levels of local brain C3/C5b-9 and systemic C5b-9, increased leukocyte infiltration, unregulated tumor necrosis factor alpha (TNFα), and aquaporin-4 in rat brain cortex at 3- and 48-hour post blast. Early immune-inflammatory response to BINT involves complement and TNFα, which correlates with hippocampus and cerebral cortex damage. Complement and TNFα activation may be a novel therapeutic target for reducing the damaging effects of BINT inflammation.

  17. 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 ...

  18. 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...

  19. 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…

  20. 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 ...

  1. 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 ...

  2. 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.

  3. 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…

  4. 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…

  5. 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

  6. Traumatic Brain Injury

    Science.gov (United States)

    2010-03-01

    symptoms which delays treatment and may lead to worse outcomes of care. The military culture values and esteems physical and mental toughness. In this...culture service members suffering mental health problems fear being ostracized , humiliated, and belittled. They also fear negative career... self regulate and inhibit behavioral responses. The individual’s ability to emotionally cope with a traumatic event in the immediate aftermath of a

  7. Neuroimaging in Traumatic Brain Imaging

    OpenAIRE

    Lee, Bruce; Newberg, Andrew

    2005-01-01

    Summary: Traumatic brain injury (TBI) is a common and potentially devastating clinical problem. Because prompt proper management of TBI sequelae can significantly alter the clinical course especially within 48 h of the injury, neuroimaging techniques have become an important part of the diagnostic work up of such patients. In the acute setting, these imaging studies can determine the presence and extent of injury and guide surgical planning and minimally invasive interventions. Neuroimaging a...

  8. 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.

  9. Severe cerebral vasospasm after traumatic brain injury.

    Science.gov (United States)

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

    2014-07-01

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

  10. 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.

  11. 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

  12. 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

  13. Computational and in vitro studies of blast-induced blood-brain barrier disruption

    CERN Document Server

    Del Razo, Mauricio J; Meabon, James S; Huber, B Russell; Peskind, Elaine R; Banks, William A; Mourad, Pierre D; Leveque, Randall J; Cook, David G

    2015-01-01

    There is growing concern that blast-exposed individuals are at risk of developing neurological disorders later in life. Therefore, it is important to understand the dynamic properties of blast forces on brain cells, including the endothelial cells that maintain the blood-brain barrier (BBB), which regulates the passage of nutrients into the brain and protects it from toxins in the blood. To better understand the effect of shock waves on the BBB we have investigated an {\\em in vitro} model in which BBB endothelial cells are grown in transwell vessels and exposed in a shock tube, confirming that BBB integrity is directly related to shock wave intensity. It is difficult to directly measure the forces acting on these cells in the transwell container during the experiments, and so a computational tool has been developed and presented in this paper. Two-dimensional axisymmetric Euler equations with the Tammann equation of state were used to model the transwell materials, and a high-resolution finite volume method b...

  14. 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

  15. 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.

  16. 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.

  17. 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.

  18. 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 ...

  19. 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

  20. 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.

  1. 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...

  2. Research progress in traumatic brain penumbra

    Institute of Scientific and Technical Information of China (English)

    Wang Kai; Liu Baiyun; Ma Jun

    2014-01-01

    Objective Following traumatic brain injury (TBI),brain tissue that surrounding the regional primary lesion is known as traumatic penumbra; this region may undergo secondary injury and is considered to have the potential to recover.This review aimed to reveal the existence and significance of traumatic penumbra by analyzing all relevant studies concerning basic pathologic changes and brain imaging after TBI.Data sources We collected all relevant studies about TBI and traumatic penumbra in Medline (1995 to June 2013) and ISI (1997 to March 2013),evaluated their quality and relevance,then extracted and synthesized the information.Study selection We included all relevant studies concerning TBI and traumatic penumbra (there was no limitation of research design and article language) and excluded the duplicated articles.Results The crucial pathological changes after TBI include cerebral blood flow change,cerebral edema,blood-brain barrier damage,cell apoptosis and necrosis.Besides,traditional imaging method cannot characterize the consequences of CBF reduction at an early stage and provides limited insights into the underlying pathophysiology.While advanced imaging technique,such as diffusion tensor imaging (DTI) and positron emission tomography (PET),may provide better characterization of such pathophysiology.Conclusions The future of traumatic brain lesions depends to a large extent on the evolution of the penumbra.Therefore,understanding the formation and pathophysiologic process of the traumatic penumbra and its imaging research progress is of great significant for early clinical determination and timely brain rescue.

  3. A Blast Headform Surrogate for the Assessment of Blast-Induced Traumatic Brain Injury

    Science.gov (United States)

    2012-11-27

    Correct fit of headwear , Representative blast diffraction around headform – Biofidelic wrt internal geometry and material selection: Stress transmission...overpressure histories • With and without protective headwear BI2PED – Recent results Introduction Strategy Facilities Iterations BI2PED & results

  4. 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...

  5. 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.

  6. 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…

  7. Aquaporin-4 and traumatic brain edema

    Institute of Scientific and Technical Information of China (English)

    XU Miao; SU Wei; XU Qiu-ping

    2010-01-01

    Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortal-ity following traumatic brain injury as it increases intracra-nial pressure, impairs cerebral perfusion and oxygenation,and contributes to additional ischemic injuries.Classically,two major types of traumatic brain edema exist: "vasogenic"and "cytotoxic/cellular".However, the cellular and molecu-lar mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no ef-fective drugs can be used now.Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, pre-dominantly in astrocyte foot processes at the borders be-tween the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood.This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma.In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma.AQP4 has been proposed as a novel drug target in brain edema.These findings sug-gest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.

  8. Neurotransmitter Systems in a Mild Blast Traumatic Brain Injury Model: Catecholamines and Serotonin.

    Science.gov (United States)

    Kawa, Lizan; Arborelius, Ulf P; Yoshitake, Takashi; Kehr, Jan; Hökfelt, Tomas; Risling, Mårten; Agoston, Denes

    2015-08-15

    Exposure to improvised explosive devices can result in a unique form of traumatic brain injury--blast-induced traumatic brain injury (bTBI). At the mild end of the spectrum (mild bTBI [mbTBI]), there are cognitive and mood disturbances. Similar symptoms have been observed in post-traumatic stress disorder caused by exposure to extreme psychological stress without physical injury. A role of the monoaminergic system in mood regulation and stress is well established but its involvement in mbTBI is not well understood. To address this gap, we used a rodent model of mbTBI and detected a decrease in immobility behavior in the forced swim test at 1 d post-exposure, coupled with an increase in climbing behavior, but not after 14 d or later, possibly indicating a transient increase in anxiety-like behavior. Using in situ hybridization, we found elevated messenger ribonucleic acid levels of both tyrosine hydroxylase and tryptophan hydroxylase 2 in the locus coeruleus and the dorsal raphe nucleus, respectively, as early as 2 h post-exposure. High-performance liquid chromatography analysis 1 d post-exposure primarily showed elevated noradrenaline levels in several forebrain regions. Taken together, we report that exposure to mild blast results in transient changes in both anxiety-like behavior and brain region-specific molecular changes, implicating the monoaminergic system in the pathobiology of mbTBI.

  9. 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

  10. 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.

  11. Studies on blast traumatic brain injury using in-vitro model with shock tube.

    Science.gov (United States)

    Arun, Peethambaran; Spadaro, John; John, Jennifer; Gharavi, Robert B; Bentley, Timothy B; Nambiar, Madhusoodana P

    2011-06-11

    One of the major limitations in studying the mechanisms of blast-induced traumatic brain injury (bTBI) or screening therapeutics for protection is the lack of suitable laboratory model systems that can closely mimic the complex blast exposure. Although animal models of bTBI that use shock tubes to mimic blast exposure are available, no high throughput shock tube-based in-vitro models have been reported. Here, we report an in-vitro bTBI model using a compressed air-driven shock tube and mouse neuroblastoma/rat glioblastoma hybrid cells (NG108-15) or SH-SY5Y human neuroblastoma cells in tissue culture plates. Our data showed significant neurobiological effects with decreased adenosine triphosphate levels, increased cellular injury, lactate dehydrogenase release, and reactive oxygen species formation after blast exposure.

  12. 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...

  13. 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...

  14. 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...

  15. 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.

  16. 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

  17. 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.

  18. 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'.

  19. 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…

  20. 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…

  1. 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,…

  2. 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.

  3. 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.

  4. Traumatic Brain Injury: Nuclear Medicine Neuroimaging

    NARCIS (Netherlands)

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

    2014-01-01

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

  5. Narrative Language in Traumatic Brain Injury

    Science.gov (United States)

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

    2011-01-01

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

  6. Perioperative Management of Adult Traumatic Brain Injury

    OpenAIRE

    Sharma, Deepak; Vavilala, Monica S.

    2012-01-01

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

  7. Traumatic brain injury and olfactory deficits

    DEFF Research Database (Denmark)

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

    2010-01-01

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

  8. Anesthesia for Patients with Traumatic Brain Injuries.

    Science.gov (United States)

    Bhattacharya, Bishwajit; Maung, Adrian A

    2016-12-01

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

  9. 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. Mathematical models of blast induced TBI: current status, challenges and prospects

    Directory of Open Access Journals (Sweden)

    Raj K Gupta

    2013-05-01

    Full Text Available Blast induced traumatic brain injury (TBI has become a signature wound of recent military activities and is the leading cause of death and long-term disability among U.S. soldiers. The current limited understanding of brain injury mechanisms impedes the development of protection, diagnostic and treatment strategies. We believe mathematical models of blast wave brain injury biomechanics and neurobiology, complemented with in vitro and in vivo experimental studies, will enable a better understanding of injury mechanisms and accelerate the development of both protective and treatment strategies. The goal of this paper is to review the current state of the art in mathematical and computational modeling of blast induced TBI, identify research gaps and recommend future developments. A brief overview of blast wave physics, injury biomechanics and the neurobiology of brain injury is used as a foundation for a more detailed discussion of multiscale mathematical models of primary biomechanics and secondary injury and repair mechanisms. The paper also presents a discussion of model development strategies, experimental approaches to generate benchmark data for model validation and potential applications of the model for prevention and protection against blast wave TBI.

  13. 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.

  14. 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.

  15. 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.

  16. 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...

  17. 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...

  18. 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...

  19. 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.

  20. 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.

  1. 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...

  2. 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 ...

  3. 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.

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

    Science.gov (United States)

    2012-08-01

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

  5. Chronic caffeine exposure attenuates blast-induced memory deficit in mice

    Institute of Scientific and Technical Information of China (English)

    Ya-Lei Ning; Nan Yang; Xing Chen; Zi-Ai Zhao; Xiu-Zhu Zhang; Xing-Yun Chen; Ping Li

    2015-01-01

    Objective:To investigate the effects of three different ways of chronic caffeine administration on blastinduced memory dysfunction and to explore the underlying mechanisms.Methods:Adult male C57BL/6 mice were used and randomly divided into five groups:control:without blast exposure,con-water:administrated with water continuously before and after blast-induced traumatic brain injury (bTBI),con-caffeine:administrated with caffeine continuously for 1 month before and after bTBI,pre-caffeine:chronically administrated with caffeine for 1 month before bTBI and withdrawal after bTBI,post-caffeine:chronically administrated with caffeine after bTBI.After being subjected to moderate intensity of blast injury,mice were recorded for learning and memory performance using Morris water maze (MWM) paradigms at 1,4,and 8 weeks post-blast injury.Neurological deficit scoring,glutamate concentration,proinflammatory cytokines production,and neuropathological changes at 24 h,1,4,and 8 weeks post-bTBI were examined to evaluate the brain injury in early and prolonged stages.Adenosine A1 receptor expression was detected using qPCR.Results:All of the three ways of chronic caffeine exposure ameliorated blast-induced memory deficit,which is correlated with the neuroprotective effects against excitotoxicity,inflammation,astrogliosis and neuronal loss at different stages of injury.Continuous caffeine treatment played positive roles in both early and prolonged stages of bTBI;pre-bTBl and post-bTBl treatment of caffeine tended to exert neuroprotective effects at early and prolonged stages of bTBI respectively.Up-regulation of adenosine A1 receptor expression might contribute to the favorable effects of chronic caffeine consumption.Conclusion:Since caffeinated beverages are widely consumed in both civilian and military personnel and are convenient to get,the results may provide a promising prophylactic strategy for blast-induced neurotrauma and the consequent cognitive impairment.

  6. 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.

  7. 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.

  8. 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.

  9. Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury

    Science.gov (United States)

    Rubovitch, Vardit; Zilberstein, Yael; Chapman, Joab; Schreiber, Shaul; Pick, Chaim G.

    2017-01-01

    Blast induced traumatic brain injury (B-TBI) may cause various degrees of cognitive and behavioral disturbances but the exact brain pathophysiology involved is poorly understood. It was previously suggested that ganglioside alteration on the axon surface as well as axonal regenerating inhibitors (ARIs) such as myelin associated glycoprotein (MAG) were involved in axonal outgrowth inhibition (AOI), leading to brain damage. GM1 ganglioside content in the brain was significantly reduced while GD1 ganglioside was not affected. The axonal regeneration was also reduced as seen by the phosphorylated NF-H expression. Moreover, B-TBI induced a significant elevation in MAG expression in the brains of the injured mice. The blast injured mice exhibited a significant decline in spatial memory as seen by the Y-maze test. In addition, the injured mice showed pronounced damage to the visual memory (as evaluated by the Novel object recognition test). A single low dose of GM1 (2 mg/kg; IP), shortly after the injury, prevented both the cognitive and the cellular changes in the brains of the injured mice. These results enlighten part of the complicated mechanism that underlies the damage induced by B-TBI and may also suggest a potential new treatment strategy for brain injuries. PMID:28112258

  10. 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...

  11. 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.

  12. [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.

  13. 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...

  14. 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...

  15. 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...

  16. 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

  17. 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.

  18. 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.

  19. 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.

  20. 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

  1. 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.

  2. Classroom Strategies for Teaching Veterans with Post-Traumatic Stress Disorder and Traumatic Brain Injury

    Science.gov (United States)

    Sinski, Jennifer Blevins

    2012-01-01

    Postsecondary institutions currently face the largest influx of veteran students since World War II. As the number of veteran students who may experience learning problems caused by Post-Traumatic Stress Disorder and/or Traumatic Brain Injury continues to rise, the need for instructional strategies that address their needs increases. Educators may…

  3. Demyelination as a Target for Cell-Based Therapy of Chronic Blast-Induced Traumatic Brain Injury

    Science.gov (United States)

    2015-10-01

    disabling behavioral and cognitive abnormalities noted in significant number of combat veterans. These clinical phenotypes suggest impairment in...associated demyelination, with the goal of testing a therapeutic strategy to enhance remyelination using human glial restricted progenitors (hGRPs; Q... abnormalities noted in significant number of combat veterans. These clinical phenotypes suggest impairment in distributed cerebral functions dependent on the

  4. Demyelination as a Target for Cell-Based Therapy of Chronic Blast-Induced Traumatic Brain Injury

    Science.gov (United States)

    2015-10-01

    associated demyelination, with the goal of testing a therapeutic strategy to enhance remyelination using human glial restricted progenitors (hGRPs; Q...associated demyelination are explored, with the goal of testing a therapeutic strategy to enhance remyelination that uses glial restricted progenitors

  5. Demyelination as a Target for Cell-Based Therapy of Chronic Blast-Induced Traumatic Brain Injury

    Science.gov (United States)

    2014-10-01

    reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching...existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments...imaging and behavioral testing for a post-doctoral fellow – Sujith Sajja. He had also a chance to learn about exosomes , lipidomics and next generation

  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. 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

  8. 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

  9. 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.

  10. 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

  11. 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.

  12. 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.

  13. 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.

  14. 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...

  15. 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,...

  16. 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.

  17. 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 ...

  18. 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.

  19. 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

  20. 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.

  1. Effects of magnesium sulfate on traumatic brain edema in rats

    Institute of Scientific and Technical Information of China (English)

    冯东福; 朱志安; 卢亦成

    2004-01-01

    Objective: To investigate the effects of magnesium sulfate on traumatic brain edema and explore its possible mechanism.Methods: Forty-eight Sprague-Dawley ( SD ) rats were randomly divided into three groups: Control, Trauma and Treatment groups. In Treatment group, magnesium sulfate was intraperitoneally administered immediately after the induction of brain trauma. At 24 h after trauma, total tissue water content and Na + , K + , Ca2 + , Mg2+ contents were measured. Permeability of blood-brain barrier (BBB)was assessed quantitatively by Evans Blue (EB) dye technique. The pathological changes were also studied.Results: Water, Na + , Ca2 + and EB contents in Treatment group were significantly lower than those in Trauma group ( P < 0. 05 ). Results of light microscopy and electron microscopy confirmed that magnesium sulfate can attenuate traumatic brain injury and relieve BBB injury.Conclusions: Treatment with MgSO4 in the early stage can attenuate traumatic brain edema and prevent BBB injury.

  2. 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

  3. 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.

  4. 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.

  5. 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.

  6. 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

  7. 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.

  8. 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

  9. 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.

  10. 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.

  11. 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…

  12. 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

  13. Neurotherapy of Traumatic Brain Injury/Post-Traumatic Stress Symptoms in Vietnam Veterans.

    Science.gov (United States)

    Nelson, David V; Esty, Mary Lee

    2015-10-01

    Previous report suggested the beneficial effects of an adaptation of the Flexyx Neurotherapy System (FNS) for the amelioration of mixed traumatic brain injury/post-traumatic stress symptoms in veterans of the Afghanistan and Iraq wars. As a novel variant of electroencephalograph biofeedback, FNS falls within the bioenergy domain of complementary and alternative medicine. Rather than learning voluntary control over the production/inhibition of brain wave patterns, FNS involves offsetting stimulation of brain wave activity by means of an external energy source, specifically, the conduction of electromagnetic energy stimulation via the connecting electroencephalograph cables. Essentially, these procedures subliminally induce strategic distortion of ongoing brain wave activity to presumably facilitate resetting of more adaptive patterns of activity. Reported herein are two cases of Vietnam veterans with mixed traumatic brain injury/post-traumatic stress symptoms, each treated with FNS for 25 sessions. Comparisons of pre- and post-treatment questionnaire assessments revealed notable decreases for all symptoms, suggesting improvements across the broad domains of cognition, pain, sleep, fatigue, and mood/emotion, including post-traumatic stress symptoms, as well as for overall activity levels. Findings suggest FNS treatment may be of potential benefit for the partial amelioration of symptoms, even in some individuals for whom symptoms have been present for decades.

  14. 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...

  15. 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

  16. 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.

  17. 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.

  18. 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...

  19. 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. ...

  20. 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

  1. 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

  2. 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......

  3. 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

  4. 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

  5. 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 ...

  6. 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.

  7. 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...

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

    Institute of Scientific and Technical Information of China (English)

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

    2007-01-01

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

  9. 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.

  10. 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

  11. 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…

  12. 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…

  13. 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…

  14. 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

  15. 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…

  16. 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…

  17. 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…

  18. 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

  19. 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

  20. 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 ...

  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. 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.

  3. 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.

  4. Single-subject-based whole-brain MEG slow-wave imaging approach for detecting abnormality in patients with mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Ming-Xiong Huang

    2014-01-01

    Full Text Available Traumatic brain injury (TBI is a leading cause of sustained impairment in military and civilian populations. However, mild TBI (mTBI can be difficult to detect using conventional MRI or CT. Injured brain tissues in mTBI patients generate abnormal slow-waves (1–4 Hz that can be measured and localized by resting-state magnetoencephalography (MEG. In this study, we develop a voxel-based whole-brain MEG slow-wave imaging approach for detecting abnormality in patients with mTBI on a single-subject basis. A normative database of resting-state MEG source magnitude images (1–4 Hz from 79 healthy control subjects was established for all brain voxels. The high-resolution MEG source magnitude images were obtained by our recent Fast-VESTAL method. In 84 mTBI patients with persistent post-concussive symptoms (36 from blasts, and 48 from non-blast causes, our method detected abnormalities at the positive detection rates of 84.5%, 86.1%, and 83.3% for the combined (blast-induced plus with non-blast causes, blast, and non-blast mTBI groups, respectively. We found that prefrontal, posterior parietal, inferior temporal, hippocampus, and cerebella areas were particularly vulnerable to head trauma. The result also showed that MEG slow-wave generation in prefrontal areas positively correlated with personality change, trouble concentrating, affective lability, and depression symptoms. Discussion is provided regarding the neuronal mechanisms of MEG slow-wave generation due to deafferentation caused by axonal injury and/or blockages/limitations of cholinergic transmission in TBI. This study provides an effective way for using MEG slow-wave source imaging to localize affected areas and supports MEG as a tool for assisting the diagnosis of mTBI.

  5. 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.

  6. Neuroglobin-overexpression reduces traumatic brain lesion size in mice

    Directory of Open Access Journals (Sweden)

    Zhao Song

    2012-06-01

    Full Text Available Abstract Background Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb is neuroprotective against hypoxic/ischemic brain injuries. In this study we tested the neuroprotective effects of Ngb over-expression against traumatic brain injury (TBI in mice. Results Both Ngb over-expression transgenic (Ngb-Tg and wild-type (WT control mice were subjected to TBI induced by a controlled cortical impact (CCI device. TBI significantly increased Ngb expression in the brains of both WT and Ngb-Tg mice, but Ngb-Tg mice had significantly higher Ngb protein levels at the pre-injury baseline and post-TBI. Production of oxidative tissue damage biomarker 3NT in the brain was significantly reduced in Ngb-Tg mice compared to WT controls at 6 hours after TBI. The traumatic brain lesion volume was significantly reduced in Ngb Tg mice compared to WT mice at 3 weeks after TBI; however, there were no significant differences in the recovery of sensorimotor and spatial memory functional deficits between Ngb-Tg and WT control mice for up to 3 weeks after TBI. Conclusion Ngb over-expression reduced traumatic lesion volume, which might partially be achieved by decreasing oxidative stress.

  7. Pathophysiological links between traumatic brain injury and post-traumatic headaches [version 1; referees: 3 approved

    Directory of Open Access Journals (Sweden)

    Robert L. Ruff

    2016-08-01

    Full Text Available This article reviews possible ways that traumatic brain injury (TBI can induce migraine-type post-traumatic headaches (PTHs in children, adults, civilians, and military personnel. Several cerebral alterations resulting from TBI can foster the development of PTH, including neuroinflammation that can activate neural systems associated with migraine. TBI can also compromise the intrinsic pain modulation system and this would increase the level of perceived pain associated with PTH. Depression and anxiety disorders, especially post-traumatic stress disorder (PTSD, are associated with TBI and these psychological conditions can directly intensify PTH. Additionally, depression and PTSD alter sleep and this will increase headache severity and foster the genesis of PTH. This article also reviews the anatomic loci of injury associated with TBI and notes the overlap between areas of injury associated with TBI and PTSD.

  8. 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

  9. Deferoxamine attenuates acute hydrocephalus after traumatic brain injury in rats.

    Science.gov (United States)

    Zhao, Jinbing; Chen, Zhi; Xi, Guohua; Keep, Richard F; Hua, Ya

    2014-10-01

    Acute post-traumatic ventricular dilation and hydrocephalus are relatively frequent consequences of traumatic brain injury (TBI). Several recent studies have indicated that high iron levels in brain may relate to hydrocephalus development after intracranial hemorrhage. However, the role of iron in the development of post-traumatic hydrocephalus is still unclear. This study was to determine whether or not iron has a role in hydrocephalus development after TBI. TBI was induced by lateral fluid-percussion in male Sprague-Dawley rats. Some rats had intraventricular injection of iron. Acute hydrocephalus was measured by magnetic resonance T2-weighted imaging and brain hemorrhage was determined by T2* gradient-echo sequence imaging and brain hemoglobin levels. The effect of deferoxamine on TBI-induced hydrocephalus was examined. TBI resulted in acute hydrocephalus at 24 h (lateral ventricle volume: 24.1 ± 3.0 vs. 9.9 ± 0.2 mm(3) in sham group). Intraventricular injection of iron also caused hydrocephalus (25.7 ± 3.4 vs. 9.0 ± 0.6 mm(3) in saline group). Deferoxamine treatment attenuated TBI-induced hydrocephalus and heme oxygenase-1 upregulation. In conclusion, iron may contribute to acute hydrocephalus after TBI.

  10. [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.

  11. 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.

  12. Acute and long-term pituitary insufficiency in traumatic brain injury

    DEFF Research Database (Denmark)

    Klose, M; Juul, A; Struck, J

    2007-01-01

    To assess the prevalence of hypopituitarism following traumatic brain injury (TBI), describe the time-course and assess the association with trauma-related parameters and early post-traumatic hormone alterations.......To assess the prevalence of hypopituitarism following traumatic brain injury (TBI), describe the time-course and assess the association with trauma-related parameters and early post-traumatic hormone alterations....

  13. 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 ...

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

    NARCIS (Netherlands)

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

    2012-01-01

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

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

    Science.gov (United States)

    2009-04-01

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

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

    NARCIS (Netherlands)

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

    2012-01-01

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

  17. Brain 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

  18. Aqueous Date Fruit Efficiency as Preventing Traumatic Brain Deterioration and Improving Pathological Parameters after Traumatic Brain Injury in Male Rats

    Directory of Open Access Journals (Sweden)

    Hamze Badeli

    2016-09-01

    Full Text Available Objective: Following traumatic brain injury, disruption of blood-brain-barrier and consequent brain edema are critical events which might lead to increasing intracranial pressure (ICP, and nerve damage. The current study assessed the effects of aqueous date fruit extract (ADFE on the aforementioned parameters. Materials and Methods: In this experimental study, diffused traumatic brain injury (TBI was generated in adult male rats using Marmarou’s method. Experimental groups include two pre-treatment (oral ADFE, 4 and 8 mL/kg for 14 days, vehicle (distilled water, for 14 days and sham groups. Brain edema and neuronal injury were measured 72 hours after TBI. Veterinary coma scale (VCS and ICP were determined at -1, 4, 24, 48 and 72 hours after TBI. Differences among multiple groups were assessed using ANOVA. Turkey’s test was employed for the ANOVA post-hoc analysis. The criterion of statistical significance was sign at P<0.05. Results: Brain water content in ADFE-treated groups was decreased in comparison with the TBI+vehicle group. VCS at 24, 48 and 72 hours after TBI showed a significant increase in ADFE groups in comparison with the TBI+vehicle group. ICP at 24, 48 and 72 hours after TBI, was decreased in ADFE groups, compared to the TBI+vehicle. Brain edema, ICP and neuronal injury were also decreased in ADFE group, but VCS was increased following on TBI. Conclusion: ADFE pre-treatment demonstrated an efficient method for preventing traumatic brain deterioration and improving pathological parameters after TBI.

  19. The neuropathology and neurobiology of traumatic brain injury.

    Science.gov (United States)

    Blennow, Kaj; Hardy, John; Zetterberg, Henrik

    2012-12-06

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

  20. 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.

  1. 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

  2. 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.

  3. 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

  4. 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.

  5. Neuroendocrine Abnormalities in Patients with Traumatic Brain Injury

    Science.gov (United States)

    1991-01-01

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

  6. 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

  7. 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

  8. 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...

  9. 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...

  10. 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

  11. [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...

  12. Combined Effects of Primary and Tertiary Blast on Rat Brain: Characterization of a Model of Blast-induced Mild Traumatic Brain Injury

    Science.gov (United States)

    2013-03-01

    Basile AS, Huang JM, Xie C, Webster D, Berlin C, Skolnick P: N-methyl-D-aspartate antagonists limit aminoglycoside antibi- otic-induced hearing loss...specific biomarkers of tissue injury. Clin Chem 55: 1977–1983. clinchem.2009.131797 [pii];10.1373/clin- chem.2009.131797 [doi]. 25. Redell JB, Moore AN

  13. 78 FR 27036 - Final Priority. National Institute on Disability and Rehabilitation Research-Traumatic Brain...

    Science.gov (United States)

    2013-05-09

    ...--Traumatic Brain Injury Model Systems Centers Collaborative Research Project AGENCY: Office of Special... Rehabilitation Research Project (DRRP) on Traumatic Brain Injury Model Systems Centers Collaborative Research... Brain Injury Model Systems (TBIMS) multi-site collaborative research project. To be eligible under...

  14. 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…

  15. 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

  16. 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 ...

  17. Reducing Secondary Insults in Traumatic Brain Injury

    Science.gov (United States)

    2015-03-01

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

  18. Blast-Induced Moderate Neurotrauma (BINT) Elicits Early Complement Activation and Tumor Necrosis Factor Alpha (TNFalpha) Release in a Rat Brain

    Science.gov (United States)

    2012-04-25

    for the damaged tissue. Mol Psychiatry 1997;2:133–6. [20] Chavko M, Prusaczyk WK, McCarron RM. Lung injury and recovery after exposure to blast...complement pathways after contusion -induced spinal cord injury. J Neurotrauma2004;21:1831–46. [23] Bellander BM, von Holst H, Fredman P, Svensson M...Activation of the complement cascade and increase of clusterin in the brain following a cortical contusion in the adult rat. J Neurosurg 1996;85:468–75. [24

  19. 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

  20. 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.

  1. Clinical Phase IIB Trial of Oxycyte Perflurocarbon in Severe Human Traumatic Brain Injury

    Science.gov (United States)

    2013-10-01

    following traumatic brain and spinal cord injury. Any agent which might exacerbate thrombocytopenia in intracranial hemorrhage into traumatic contusions is...injury. Any agent which might exacerbate thrombocytopenia in intracranial hemorrhage into traumatic contusions is dangerous for obvious reasons. The...spleen or lungs , Oxygen Biotherapeutics presented at Military Health System Research Symposium (MHSRS) 2013 Ft. Lauderdale, that radio labeled platelets

  2. 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.

  3. [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.

  4. 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

  5. The Effects of Mild Traumatic Brain Injury, Post-Traumatic Stress Disorder, and Combined Mild Traumatic Brain Injury/Post-Traumatic Stress Disorder on Returning Veterans.

    Science.gov (United States)

    Combs, Hannah L; Berry, David T R; Pape, Theresa; Babcock-Parziale, Judith; Smith, Bridget; Schleenbaker, Randal; Shandera-Ochsner, Anne; Harp, Jordan P; High, Walter M

    2015-07-01

    United States veterans of the Iraqi (Operation Iraqi Freedom [OIF]) and Afghanistan (Operation Enduring Freedom [OEF]) conflicts have frequently returned from deployment after sustaining mild traumatic brain injury (mTBI) and enduring stressful events resulting in post-traumatic stress disorder (PTSD). A large number of returning service members have been diagnosed with both a history of mTBI and current PTSD. Substantial literature exists on the neuropsychological factors associated with mTBI and PTSD occurring separately; far less research has explored the combined effects of PTSD and mTBI. The current study employed neuropsychological and psychological measures in a sample of 251 OIF/OEF veterans to determine whether participants with a history of mTBI and current PTSD (mTBI+PTSD) have poorer cognitive and psychological outcomes than participants with mTBI only (mTBI-o), PTSD only (PTSD-o), or veteran controls (VC), when groups are comparable on intelligence quotient, education, and age. The mTBI+PTSD group performed more poorly than VC, mTBI-o, and PTSD-o groups on several neuropsychological measures. Effect size comparisons suggest small deleterious effects for mTBI-o on measures of processing speed and visual attention and small effects for PTSD-o on measures of verbal memory, with moderate effects for mTBI+PTSD on the same variables. Additionally, the mTBI+PTSD group was significantly more psychologically distressed than the PTSD-o group, and PTSD-o group was more distressed than VC and mTBI-o groups. These findings suggest that veterans with mTBI+PTSD perform significantly lower on neuropsychological and psychiatric measures than veterans with mTBI-o or PTSD-o. The results also raise the possibility of mild but persisting cognitive changes following mTBI sustained during deployment.

  6. 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.

  7. The military's approach to traumatic brain injury and post-traumatic stress disorder

    Science.gov (United States)

    Ling, Geoffrey S. F.; Grimes, Jamie; Ecklund, James M.

    2014-06-01

    Traumatic brain injury (TBI) and Post Traumatic Stress Disorder (PTSD) are common conditions. In Iraq and Afghanistan, explosive blast related TBI became prominent among US service members but the vast majority of TBI was still due to typical causes such as falls and sporting events. PTS has long been a focus of the US military mental health providers. Combat Stress Teams have been integral to forward deployed units since the beginning of the Global War on Terror. Military medical management of disease and injury follows standard of care clinical practice guidelines (CPG) established by civilian counterparts. However, when civilian CPGs do not exist or are not applicable to the military environment, new practice standards are created. Such is the case for mild TBI. In 2009, the VA-DoD CPG for management of mild TBI/concussion was published and a system-wide clinical care program for mild TBI/concussion was introduced. This was the first large scale effort on an entire medical care system to address all severities of TBI in a comprehensive organized way. In 2010, the VA-DoD CPG for management of PTSD was published. Nevertheless, both TBI and PTS are still incompletely understood. Investment in terms of money and effort has been committed by the DoD to their study. 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 are prominent examples of this effort. These are just beginnings, a work in progress ready to leverage advances made scientifically and always striving to provide the very best care to its military beneficiaries.

  8. 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.

  9. 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.

  10. Development of Magnetic Resonance Imaging Biomarkers for Traumatic Brain Injury

    Science.gov (United States)

    2012-07-01

    properties of human blood at 1.5 Tesla : magnetic susceptibility, T(1), T(2), T*(2), and non-Lorentzian signal behavior. Magn Reson Med 2001;45:533–542. 32...Reichenbach, J.R., Rombouts, S.A., Haacke, E.M., 1999. Sub-millimeter fMRI at 1.5 Tesla : correlation of high resolution with low resolution measurements...noninvasively following severe traumatic brain injury. Acta Neurochir (Wien) 152(6):965–972 Catherine R, Sophie L, Nicolas B, Bernard V (2007) Transcranial

  11. 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...

  12. HYPOPITUITARISM FOLLOWING TRAUMATIC BRAIN INJURY: DETERMINING FACTORS FOR DIAGNOSIS

    Directory of Open Access Journals (Sweden)

    FELIPE F eCASANUEVA

    2011-08-01

    Full Text Available Neuroendocrine dysfunction, long recognised as a consequence of traumatic brain injury (TBI, is a major cause of disability that includes physical and psychological involvement with long-term cognitive, behavioural and social changes.There is no standard procedure regarding at what time after trauma the diagnosis should be made. Also there is uncertainty on defining the best methods for diagnosis and testing and what types of patients should be selected for screening. Common criteria for evaluating these patients are required on account of the high prevalence of TBI worldwide and the potential new cases of hypopituitarism.

  13. Agitation, aggression, and disinhibition syndromes after traumatic brain injury.

    Science.gov (United States)

    Kim, Edward

    2002-01-01

    Traumatic brain injury (TBI) is frequently complicated by disinhibition and aggression. These often profound changes in personality, present obstacles to rehabilitative treatments and community reentry. Syndromal presentations may involve a loss of impulse control, spontaneous aggression, and dysphoric bipolar states. Common neuropathological findings of inferior frontal lobe dysfunction support both disinhibition and kindling models of TBI-induced aggression. Assessment of these highly disruptive symptoms requires detailed historical, clinical, and neuropsychological information to formulate appropriate strategies. Management of TBI-related aggression may involve pharmacological, environmental, and psychotherapeutic strategies that incorporate caregiver training and support.

  14. 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.

  15. 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.

  16. 78 FR 28546 - Secondary Service Connection for Diagnosable Illnesses Associated With Traumatic Brain Injury

    Science.gov (United States)

    2013-05-15

    ... Traumatic Brain Injury Correction In proposed rule document 2012-29709 beginning on page 73366 in the issue...: Structural imaging of the brain. LOC--Loss of consciousness. AOC--Alteration of consciousness/mental...

  17. 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 ...

  18. 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

  19. Resilience Is Associated with Outcome from Mild Traumatic Brain Injury.

    Science.gov (United States)

    Losoi, Heidi; Silverberg, Noah D; Wäljas, Minna; Turunen, Senni; Rosti-Otajärvi, Eija; Helminen, Mika; Luoto, Teemu Miikka Artturi; Julkunen, Juhani; Öhman, Juha; Iverson, Grant L

    2015-07-01

    Resilient individuals manifest adaptive behavior and are better able to recover from adversity. The association between resilience and outcome from mild traumatic brain injury (mTBI) is examined, and the reliability and validity of the Resilience Scale and its short form in mTBI research is evaluated. Patients with mTBI (n=74) and orthopedic controls (n=39) completed the Resilience Scale at one, six, and 12 months after injury. Additionally, self-reported post-concussion symptoms, fatigue, insomnia, pain, post-traumatic stress, and depression, as well as quality of life, were evaluated. The internal consistency of the Resilience Scale and the short form ranged from 0.91 to 0.93 for the mTBI group and from 0.86 to 0.95 for controls. The test-retest reliability ranged from 0.70 to 0.82. Patients with mTBI and moderate-to-high resilience reported significantly fewer post-concussion symptoms, less fatigue, insomnia, traumatic stress, and depressive symptoms, and better quality of life, than the patients with low resilience. No association between resilience and time to return to work was found. Resilience was associated with self-reported outcome from mTBI, and based on this preliminary study, can be reliably evaluated with Resilience Scale and its short form in those with mTBIs.

  20. Defense Health: Coordinating Authority Needed for Psychological Health and Traumatic Brain Injury Activities

    Science.gov (United States)

    2012-01-01

    Traumatic Brain Injury 1 Deployment Family Stress: Child Neglect and Maltreatment in U.S. Army Families 1 Deployment, PTSD Symptoms, and Comorbid...Sodium for Affective Liability and Alcohol Use Following Traumatic Brain Injury (TBI) 1 A Placebo-Controlled Augmentation Trial of Prazosin for...to Care for Traumatic Stress and PTSD 1 Motivating Treatment Seeking and Behavior Change by Untreated Military Personnel Abusing Alcohol or Drugs 1

  1. The Effect of Hyperbaric Oxygen on Symptoms after Mild Traumatic Brain Injury

    Science.gov (United States)

    2012-11-20

    Journal Article 3. DATES COVERED (From – To) Aug 2008 – Dec 2013 4. TITLE AND SUBTITLE The Effect of Hyperbaric Oxygen on Symptoms after Mild...absolute (ATA) hyperbaric oxygen (HBO2) on post-concussion symptoms in 50 military service members with at least one combat-related, mild traumatic brain...symptoms after mild TBI. 15. SUBJECT TERMS: hyperbaric oxygen, HBOT, HBO, HBO2, traumatic brain injury, TBI, mTBI, post-traumatic stress disorder, PTSD

  2. 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...

  3. Placebo-controlled trial of amantadine for severe traumatic brain injury

    DEFF Research Database (Denmark)

    Giacino, Joseph T; Whyte, John; Bagiella, Emilia

    2012-01-01

    Amantadine hydrochloride is one of the most commonly prescribed medications for patients with prolonged disorders of consciousness after traumatic brain injury. Preliminary studies have suggested that amantadine may promote functional recovery.......Amantadine hydrochloride is one of the most commonly prescribed medications for patients with prolonged disorders of consciousness after traumatic brain injury. Preliminary studies have suggested that amantadine may promote functional recovery....

  4. Hydrocephalus following severe traumatic brain injury in adults. Incidence, timing, and clinical predictors during rehabilitation

    DEFF Research Database (Denmark)

    Kammersgaard, Lars Peter; Linnemann, Mia; Tibæk, Maiken

    2013-01-01

    To investigate timing and clinical predictors that might predict hydrocephalus emerging during rehabilitation until 1 year following severe traumatic brain injury (TBI).......To investigate timing and clinical predictors that might predict hydrocephalus emerging during rehabilitation until 1 year following severe traumatic brain injury (TBI)....

  5. Gait and Glasgow Coma Scale scores can predict functional recovery in patients with traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Sevil Bilgin; Arzu Guclu-Gunduz; Hakan Oruckaptan; Nezire Kose; Bülent Celik

    2012-01-01

    Fifty-one patients with mild (n = 14), moderate (n = 10) and severe traumatic brain injury (n = 27)received early rehabilitation. Level of consciousness was evaluated using the Glasgow Coma Score. Functional level was determined using the Glasgow Outcome Score, whilst mobility was evaluated using the Mobility Scale for Acute Stroke. Activities of daily living were assessed using the Barthel Index. Following Bobath neurodevelopmental therapy, the level of consciousness was significantly improved in patients with moderate and severe traumatic brain injury, but was not greatly influenced in patients with mild traumatic brain injury. Mobility and functional level were significantly improved in patients with mild, moderate and severe traumatic brain injury. Gait recovery was more obvious in patients with mild traumatic brain injury than in patients with moderate and severe traumatic brain injury. Activities of daily living showed an improvement but this was insignificant except for patients with severe traumatic brain injury. Nevertheless, complete recovery was not acquired at discharge. Multiple regression analysis showed that gait and Glasgow Coma Scale scores can be considered predictors of functional outcomes following traumatic brain injury.

  6. Subacute posttraumatic complaints and psychological distress in trauma patients with or without mild traumatic brain injury

    NARCIS (Netherlands)

    de Koning, M. E.; Gareb, Barzi; El Moumni, M.; Scheenen, M. E.; van der Horn, H. J.; Timmerman, M. E.; Spikman, J. M.; van der Naalt, J.

    2016-01-01

    Objective: To identify the frequency, nature and profile of complaints for trauma patients with and without mild traumatic brain injury (mTBI), and to assess their relation to anxiety and depression. Methods: A prospective cohort study in a level-one trauma centre was conducted. Mild traumatic brain

  7. Glial and neuronal proteins in serum predict outcome after severe traumatic brain injury.

    NARCIS (Netherlands)

    Vos, P.E.; Lamers, K.J.B.; Hendriks, J.C.M.; Haaren, M. van; Beems, T.; Zimmerman, C.; Geel, W.J.A. van; Reus, H.P.M. de; Biert, J.; Verbeek, M.M.

    2004-01-01

    OBJECTIVE: To study the ability of glial (glial fibrillary acidic protein [GFAP] and S100b) and neuronal (neuron specific enolase [NSE]) protein levels in peripheral blood to predict outcome after severe traumatic brain injury. METHODS: Eighty-five patients with severe traumatic brain injury (admiss

  8. Severe Traumatic Brain Injury In Children: An Evidence-Based Review Of Emergency Department Management.

    Science.gov (United States)

    Morrissey, Kirsten; Fairbrother, Hilary

    2016-10-01

    More than 1.7 million traumatic brain injuries occur in adults and children each year in the United States, with approximately 30% occurring in children aged blood pressure in the emergency department to improve neurologic outcomes following pediatric severe traumatic brain injury.

  9. 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.

  10. 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.

  11. 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.

  12. 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.

  13. Traumatic brain injury: future assessment tools and treatment prospects

    Directory of Open Access Journals (Sweden)

    Steven R Flanagan

    2008-10-01

    Full Text Available Steven R Flanagan1, Joshua B Cantor2, Teresa A Ashman21New York University School of Medicine, The Rusk Institute of Rehabilitation, New York, NY, USA; 2Department of Rehabilitation Medicine, Mount Sinai School of Medicine, New York, NY, USAAbstract: Traumatic brain injury (TBI is widespread and leads to death and disability in millions of individuals around the world each year. Overall incidence and prevalence of TBI are likely to increase in absolute terms in the future. Tackling the problem of treating TBI successfully will require improvements in the understanding of normal cerebral anatomy, physiology, and function throughout the lifespan, as well as the pathological and recuperative responses that result from trauma. New treatment approaches and combinations will need to be targeted to the heterogeneous needs of TBI populations. This article explores and evaluates the research evidence in areas that will likely lead to a reduction in TBI-related morbidity and improved outcomes. These include emerging assessment instruments and techniques in areas of structural/chemical and functional neuroimaging and neuropsychology, advances in the realms of cell-based therapies and genetics, promising cognitive rehabilitation techniques including cognitive remediation and the use of electronic technologies including assistive devices and virtual reality, and the emerging field of complementary and alternative medicine.Keywords: traumatic brain injury, assessments, treatments

  14. 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.

  15. 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.

  16. The Evolution of Post-Traumatic Stress Disorder following Moderate-to-Severe Traumatic Brain Injury.

    Science.gov (United States)

    Alway, Yvette; Gould, Kate Rachel; McKay, Adam; Johnston, Lisa; Ponsford, Jennie

    2016-05-01

    Increasing evidence indicates that post-traumatic stress disorder (PTSD) may develop following traumatic brain injury (TBI), despite most patients having no conscious memory of their accident. This prospective study examined the frequency, timing of onset, symptom profile, and trajectory of PTSD and its psychiatric comorbidities during the first 4 years following moderate-to-severe TBI. Participants were 85 individuals (78.8% male) with moderate or severe TBI recruited following admission to acute rehabilitation between 2005 and 2010. Using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Disorders (SCID-I), participants were evaluated for pre- and post-injury PTSD soon after injury and reassessed at 6 months, 12 months, 2 years, 3 years, and 4 years post-injury. Over the first 4 years post-injury, 17.6% developed injury-related PTSD, none of whom had PTSD prior to injury. PTSD onset peaked between 6 and 12 months post-injury. The majority of PTSD cases (66.7%) had a delayed-onset, which for a third was preceded by subsyndromal symptoms in the first 6 months post-injury. PTSD frequency increased over the first year post-injury, remained stable during the second year, and gradually declined thereafter. The majority of subjects with PTSD experienced a chronic symptom course and all developed one or more than one comorbid psychiatric disorder, with mood, other anxiety, and substance-use disorders being the most common. Despite event-related amnesia, post-traumatic stress symptoms, including vivid re-experiencing phenomena, may develop following moderate-to-severe TBI. Onset is typically delayed and symptoms may persist for several years post-injury.

  17. Hyperbaric oxygen therapy for the treatment of traumatic brain injury: a meta-analysis.

    Science.gov (United States)

    Wang, Fei; Wang, Yong; Sun, Tao; Yu, Hua-Lin

    2016-05-01

    Compelling evidence suggests the advantage of hyperbaric oxygen therapy (HBOT) in traumatic brain injury. The present meta-analysis evaluated the outcomes of HBOT in patients with traumatic brain injury (TBI). Prospective studies comparing hyperbaric oxygen therapy vs. control in patients with mild (GCS 13-15) to severe (GCS 3-8) TBI were hand-searched from medical databases using the terms "hyperbaric oxygen therapy, traumatic brain injury, and post-concussion syndrome". Glasgow coma scale (GCS) was the primary outcome, while Glasgow outcome score (GOS), overall mortality, and changes in post-traumatic stress disorder (PTSD) score, constituted the secondary outcomes. The results of eight studies (average age of patients, 23-41 years) reveal a higher post-treatment GCS score in the HBOT group (pooled difference in means = 3.13, 95 % CI 2.34-3.92, P traumatic brain injury.

  18. Genetic vulnerability following traumatic brain injury: the role of apolipoprotein E

    OpenAIRE

    Nathoo, N; Chetty, R; van Dellen, J R; Barnett, G H

    2003-01-01

    Apolipoprotein E (APOE) is thought to be responsible for the transportation of lipids within the brain, maintaining structural integrity of the microtubule within the neurone, and assisting with neural transmission. Possession of the APOE ɛ4 allele has also been shown to influence neuropathological findings in patients who die from traumatic brain injury, including the accumulation of amyloid β protein. Previous clinical studies reporting varying outcome severities of traumatic brain injury, ...

  19. A brief report on MRI investigation of experimental traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Timothy Q.Duong; Lora T.Watts

    2016-01-01

    Traumatic brain injury is a major cause of death and disability. This is a brief report based on a symposium presentation to the2014 Chinese Neurotrauma Association Meeting in San Francisco, USA. It covers the work from our laboratory in applying multimodal MRI to study experimental traumatic brain injury in rats with comparisons made to behavioral tests and histology. MRI protocols include structural, perfusion, manganese-enhanced, diffusion-tensor MRI, and MRI of blood-brain barrier integrity and cerebrovascular reactivity.

  20. Outcome of 2 284 cases with acute traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To analyze the prognosis of 2 284 cases with acute traumatic brain injury and discuss possible methods to improve the outcome of head injuries.   Methods: The relationship between trauma cause, trauma severity and management and patients outcome was retrospectively analyzed.   Results: Good recovery was achieved in 60.20%, moderate disability was 13.22%, severe disability 15.24%, vegetative status 0.31% and mortality 11.03%. The mortality was 1.07% in cases with GCS 15-13, 2.47% in cases with GCS 12-9, 13.29% in cases with GCS 8-6, and 57.4% in cases with GCS 5-3.   Conclusions: To prevent hypoxia, remove intracranial hematoma as soon as possible, use standard large traumatic craniotomy and apply mild hypothermia may be useful means for improving the outcome of severely head injured patients.

  1. Neurosensory Symptom Complexes after Acute Mild Traumatic Brain Injury.

    Directory of Open Access Journals (Sweden)

    Michael E Hoffer

    Full Text Available Mild Traumatic Brain Injury (mTBI is a prominent public health issue. To date, subjective symptom complaints primarily dictate diagnostic and treatment approaches. As such, the description and qualification of these symptoms in the mTBI patient population is of great value. This manuscript describes the symptoms of mTBI patients as compared to controls in a larger study designed to examine the use of vestibular testing to diagnose mTBI. Five symptom clusters were identified: Post-Traumatic Headache/Migraine, Nausea, Emotional/Affective, Fatigue/Malaise, and Dizziness/Mild Cognitive Impairment. Our analysis indicates that individuals with mTBI have headache, dizziness, and cognitive dysfunction far out of proportion to those without mTBI. In addition, sleep disorders and emotional issues were significantly more common amongst mTBI patients than non-injured individuals. A simple set of questions inquiring about dizziness, headache, and cognitive issues may provide diagnostic accuracy. The consideration of other symptoms may be critical for providing prognostic value and treatment for best short-term outcomes or prevention of long-term complications.

  2. Hypothalamic-Pituitary Autoimmunity and Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Federica Guaraldi

    2015-05-01

    Full Text Available Background: Traumatic brain injury (TBI is a leading cause of secondary hypopituitarism in children and adults, and is responsible for impaired quality of life, disabilities and compromised development. Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Although the exact pathophysiology is unknown, several mechanisms have been hypothesized, including hypothalamic-pituitary autoimmunity (HP-A. The aim of this study was to systematically review literature on the association between HP-A and TBI-induced hypopituitarism. Major pitfalls related to the HP-A investigation were also discussed. Methods: The PubMed database was searched with a string developed for this purpose, without temporal or language limits, for original articles assessing the association of HP-A and TBI-induced hypopituitarism. Results: Three articles from the same group met the inclusion criteria. Anti-pituitary and anti-hypothalamic antibodies were detected using indirect immunofluorescence in a significant number of patients with acute and chronic TBI. Elevated antibody titer was associated with an increased risk of persistent hypopituitarism, especially somatotroph and gonadotroph deficiency, while no correlations were found with clinical parameters. Conclusion: HPA seems to contribute to TBI-induced pituitary damage, although major methodological issues need to be overcome and larger studies are warranted to confirm these preliminary data.

  3. [Hypopituitarism following traumatic brain injury: diagnostic and therapeutic issues].

    Science.gov (United States)

    Lecoq, A-L; Chanson, P

    2015-10-01

    Traumatic Brain Injury (TBI) is a well-known public health problem worldwide and is a leading cause of death and disability, particularly in young adults. Besides neurological and psychiatric issues, pituitary dysfunction can also occur after TBI, in the acute or chronic phase. The exact prevalence of post-traumatic hypopituitarism is difficult to assess due to the wide heterogeneity of published studies and bias in interpretation of hormonal test results in this specific population. Predictive factors for hypopituitarism have been proposed and are helpful for the screening. The pathophysiology of pituitary dysfunction after TBI is not well understood but the vascular hypothesis is privileged. Activation of pituitary stem/progenitor cells is probably involved in the recovery of pituitary functions. Those cells also play a role in the induction of pituitary tumors, highlighting their crucial place in pituitary conditions. This review updates the current data related to anterior pituitary dysfunction after TBI and discusses the bias and difficulties encountered in its diagnosis.

  4. Standard large trauma craniotomy for severe traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    L(U) Li-quan 吕立权; JIANG Ji-yao 江基尧; YU Ming-kun 于明琨; HOU Li-jun 侯立军; CHEN Zhi-gang 陈志刚; ZHANG Guang-ji 张光霁; ZHU Cheng 朱诚

    2003-01-01

    Objective: To study the effect of standard large trauma craniotomy(SLTC) on outcomes of patients with severe traumatic brain injury (TBI) (GCS≤8).Methods: 230 patients with severe TBI were randomly divided into two groups.115 patients underwent SLTC (10 cm×12 cm) as an SLTC group, and other 115 patients underwent temporo-parietal or fronto-temporal craniotomy (6 cm×8 cm) according to the position of hematomas as a routine craniotomy (RC) group.Other treatments were identical in two groups.According to Glasgow outcome scale (GOS), the prognosis of the patients was evaluated and the complications were compared between two groups.Results: 27 patients got good outcome and moderate disability (23.5%), 40 severe disability and vegetative survival (34.8%), and 48 died (41.7%) in SLTC group.21 patients got good outcome and moderate disability (18.3%), 28 severe disability and vegetative survival (24.3%), and 66 died (57.4%) in RC group.The incidence of incision hernia was lower in SLTC group than in RC group.However, the incidence of operative encephalocele, traumatic epilepsy and intracranial infection were not different in two groups.Conclusions: Standard large trauma craniotomy significantly reduces the mortality of patients with severe TBI without serious complications, but does not improve the life quality of the patients.

  5. Overview of Traumatic Brain Injury: An Immunological Context

    Science.gov (United States)

    Nizamutdinov, Damir; Shapiro, Lee A.

    2017-01-01

    Traumatic brain injury (TBI) afflicts people of all ages and genders, and the severity of injury ranges from concussion/mild TBI to severe TBI. Across all spectrums, TBI has wide-ranging, and variable symptomology and outcomes. Treatment options are lacking for the early neuropathology associated with TBIs and for the chronic neuropathological and neurobehavioral deficits. Inflammation and neuroinflammation appear to be major mediators of TBI outcomes. These systems are being intensively studies using animal models and human translational studies, in the hopes of understanding the mechanisms of TBI, and developing therapeutic strategies to improve the outcomes of the millions of people impacted by TBIs each year. This manuscript provides an overview of the epidemiology and outcomes of TBI, and presents data obtained from animal and human studies focusing on an inflammatory and immunological context. Such a context is timely, as recent studies blur the traditional understanding of an “immune-privileged” central nervous system. In presenting the evidence for specific, adaptive immune response after TBI, it is hoped that future studies will be interpreted using a broader perspective that includes the contributions of the peripheral immune system, to central nervous system disorders, notably TBI and post-traumatic syndromes. PMID:28124982

  6. 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.

  7. 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.

  8. 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.

  9. Application of minimally invasive surgery in traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Liu Baiyun

    2014-12-01

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

  10. Neuropsychology of Neuroendocrine Dysregulation after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Josef Zihl

    2015-05-01

    Full Text Available Endocrine dysfunction is a common effect of traumatic brain injury (TBI. In addition to affecting the regulation of important body functions, the disruption of endocrine physiology can significantly impair mental functions, such as attention, memory, executive function, and mood. This mini-review focuses on alterations in mental functioning that are associated with neuroendocrine disturbances in adults who suffered TBI. It summarizes the contribution of hormones to the regulation of mental functions, the consequences of TBI on mental health and neuroendocrine homeostasis, and the effects of hormone substitution on mental dysfunction caused by TBI. The available empirical evidence suggests that comprehensive assessment of mental functions should be standard in TBI subjects presenting with hormone deficiency and that hormone replacement therapy should be accompanied by pre- and post-assessments.

  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. Vergence in mild traumatic brain injury: A pilot study

    Directory of Open Access Journals (Sweden)

    Dora Szymanowicz, OD, MS

    2012-10-01

    Full Text Available Vergence dysfunction in individuals with mild traumatic brain injury (mTBI may have a negative effect on quality of life, functional abilities, and rehabilitative progress. In this study, we used a range of dynamic and static objective and subjective measures of vergence to assess 21 adult patients with mTBI and nearwork symptoms. The results were compared with 10 control adult subjects. With respect to dynamic parameters, responses in those with mTBI were slowed, variable, and delayed. With respect to static parameters, reduced near point of convergence and restricted near vergence ranges were found in those with mTBI. The present results provide evidence for the substantial adverse effect of mTBI on vergence function.

  13. Persistent vertigo and dizziness after mild traumatic brain injury.

    Science.gov (United States)

    Fife, Terry D; Kalra, Deepak

    2015-04-01

    Vertigo, dizziness, and disequilibrium are common symptoms following concussion or mild traumatic brain injury (mTBI). Dizziness and vertigo may be the result of trauma to the peripheral vestibular system or the central nervous system, or, in some cases, may be due to anxiety, depression, or posttraumatic stress disorder; these mechanisms are not mutually exclusive. While most peripheral vestibular disorders can be identified by testing and examination, those without inner-ear causes that have persisting complaints of dizziness and motion sickness are more difficult to understand and to manage. Some of these patients exhibit features compatible with vestibular migraine and may be treated successfully with migraine-preventative medications. This paper reviews the nonotogenic causes of persisting dizziness, the possible mechanisms, and the pathophysiology, as a framework for patient management and for future research.

  14. 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.

  15. Astrocyte Hypertrophy Contributes to Aberrant Neurogenesis after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Clark Robinson

    2016-01-01

    Full Text Available Traumatic brain injury (TBI is a widespread epidemic with severe cognitive, affective, and behavioral consequences. TBIs typically result in a relatively rapid inflammatory and neuroinflammatory response. A major component of the neuroinflammatory response is astrocytes, a type of glial cell in the brain. Astrocytes are important in maintaining the integrity of neuronal functioning, and it is possible that astrocyte hypertrophy after TBIs might contribute to pathogenesis. The hippocampus is a unique brain region, because neurogenesis persists in adults. Accumulating evidence supports the functional importance of these newborn neurons and their associated astrocytes. Alterations to either of these cell types can influence neuronal functioning. To determine if hypertrophied astrocytes might negatively influence immature neurons in the dentate gyrus, astrocyte and newborn neurons were analyzed at 30 days following a TBI in mice. The results demonstrate a loss of radial glial-like processes extending through the granule cell layer after TBI, as well as ectopic growth and migration of immature dentate neurons. The results further show newborn neurons in close association with hypertrophied astrocytes, suggesting a role for the astrocytes in aberrant neurogenesis. Future studies are needed to determine the functional significance of these alterations to the astrocyte/immature neurons after TBI.

  16. 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

  17. 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.

  18. Traumatic Brain Injury Severity Affects Neurogenesis in Adult Mouse Hippocampus.

    Science.gov (United States)

    Wang, Xiaoting; Gao, Xiang; Michalski, Stephanie; Zhao, Shu; Chen, Jinhui

    2016-04-15

    Traumatic brain injury (TBI) has been proven to enhance neural stem cell (NSC) proliferation in the hippocampal dentate gyrus. However, various groups have reported contradictory results on whether TBI increases neurogenesis, partially due to a wide range in the severities of injuries seen with different TBI models. To address whether the severity of TBI affects neurogenesis in the injured brain, we assessed neurogenesis in mouse brains receiving different severities of controlled cortical impact (CCI) with the same injury device. The mice were subjected to mild, moderate, or severe TBI by a CCI device. The effects of TBI severity on neurogenesis were evaluated at three stages: NSC proliferation, immature neurons, and newly-generated mature neurons. The results showed that mild TBI did not affect neurogenesis at any of the three stages. Moderate TBI promoted NSC proliferation without increasing neurogenesis. Severe TBI increased neurogenesis at all three stages. Our data suggest that the severity of injury affects adult neurogenesis in the hippocampus, and thus it may partially explain the inconsistent results of different groups regarding neurogenesis following TBI. Further understanding the mechanism of TBI-induced neurogenesis may provide a potential approach for using endogenous NSCs to protect against neuronal loss after trauma.

  19. 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.

  20. 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.

  1. Glycolysis and the significance of lactate in traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Keri Linda Carpenter

    2015-04-01

    Full Text Available In traumatic brain injury (TBI patients, elevation of the brain extracellular lactate concentration and the lactate/pyruvate ratio are well recognised, and are associated statistically with unfavourable clinical outcome. Brain extracellular lactate was conventionally regarded as a waste product of glucose, when glucose is metabolised via glycolysis (Embden-Meyerhof-Parnas pathway to pyruvate, followed by conversion to lactate by the action of lactate dehydrogenase, and export of lactate into the extracellular fluid. In TBI, glycolytic lactate is ascribed to hypoxia or mitochondrial dysfunction, although the precise nature of the latter is incompletely understood. Seemingly in contrast to lactate’s association with unfavourable outcome is a growing body of evidence that lactate can be beneficial. The idea that the brain can utilise lactate by feeding into the tricarboxylic acid (TCA cycle of neurons, first published two decades ago, has become known as the astrocyte-neuron lactate shuttle hypothesis. Direct evidence of brain utilisation of lactate was first obtained 5 years ago in a cerebral microdialysis study in TBI patients, where administration of 13C-labelled lactate via the microdialysis catheter and simultaneous collection of the emerging microdialysates, with 13C NMR analysis, revealed 13C labelling in glutamine consistent with lactate utilisation via the TCA cycle. This suggests that where neurons are too damaged to utilise the lactate produced from glucose by astrocytes, i.e. uncoupling of neuronal and glial metabolism, high extracellular levels of lactate would accumulate, explaining association between high lactate and poor outcome. An intravenous exogenous lactate supplementation study in TBI patients showed evidence for a beneficial effect judged by surrogate endpoints. Here we review current knowledge about glycolysis and lactate in TBI, how it can be measured in patients, and whether it can be modulated to achieve better

  2. Dietary fructose aggravates the pathobiology of traumatic brain injury by influencing energy homeostasis and plasticity.

    Science.gov (United States)

    Agrawal, Rahul; Noble, Emily; Vergnes, Laurent; Ying, Zhe; Reue, Karen; Gomez-Pinilla, Fernando

    2016-05-01

    Fructose consumption has been on the rise for the last two decades and is starting to be recognized as being responsible for metabolic diseases. Metabolic disorders pose a particular threat for brain conditions characterized by energy dysfunction, such as traumatic brain injury. Traumatic brain injury patients experience sudden abnormalities in the control of brain metabolism and cognitive function, which may worsen the prospect of brain plasticity and function. The mechanisms involved are poorly understood. Here we report that fructose consumption disrupts hippocampal energy homeostasis as evidenced by a decline in functional mitochondria bioenergetics (oxygen consumption rate and cytochrome C oxidase activity) and an aggravation of the effects of traumatic brain injury on molecular systems engaged in cell energy homeostasis (sirtuin 1, peroxisome proliferator-activated receptor gamma coactivator-1alpha) and synaptic plasticity (brain-derived neurotrophic factor, tropomyosin receptor kinase B, cyclic adenosine monophosphate response element binding, synaptophysin signaling). Fructose also worsened the effects of traumatic brain injury on spatial memory, which disruption was associated with a decrease in hippocampal insulin receptor signaling. Additionally, fructose consumption and traumatic brain injury promoted plasma membrane lipid peroxidation, measured by elevated protein and phenotypic expression of 4-hydroxynonenal. These data imply that high fructose consumption exacerbates the pathology of brain trauma by further disrupting energy metabolism and brain plasticity, highlighting the impact of diet on the resilience to neurological disorders.

  3. Development of in Vivo Biomarkers for Progressive Tau Pathology after Traumatic Brain Injury

    Science.gov (United States)

    2016-02-01

    Bailes J, et al. Chronic traumatic encephalopathy in an Iraqi war veteran with posttraumatic stress disorder who committed suicide . Neurosurgical focus... post - mortem 1, 3, 6, 18-20. Tau pathology has also been observed after single more severe traumatic brain injuries 21-23. Currently, there are no...AD_________________ Award Number: W81XWH-13-2-0016 TITLE: Development of in Vivo Biomarkers for Progressive Tau Pathology after Traumatic

  4. Endocannabinoids: A Promising Impact for Traumatic Brain Injury

    Science.gov (United States)

    Schurman, Lesley D.; Lichtman, Aron H.

    2017-01-01

    The endogenous cannabinoid (endocannabinoid) system regulates a diverse array of physiological processes and unsurprisingly possesses considerable potential targets for the potential treatment of numerous disease states, including two receptors (i.e., CB1 and CB2 receptors) and enzymes regulating their endogenous ligands N-arachidonoylethanolamine (anandamide) and 2-arachidonyl glycerol (2-AG). Increases in brain levels of endocannabinoids to pathogenic events suggest this system plays a role in compensatory repair mechanisms. Traumatic brain injury (TBI) pathology remains mostly refractory to currently available drugs, perhaps due to its heterogeneous nature in etiology, clinical presentation, and severity. Here, we review pre-clinical studies assessing the therapeutic potential of cannabinoids and manipulations of the endocannabinoid system to ameliorate TBI pathology. Specifically, manipulations of endocannabinoid degradative enzymes (e.g., fatty acid amide hydrolase, monoacylglycerol lipase, and α/β-hydrolase domain-6), CB1 and CB2 receptors, and their endogenous ligands have shown promise in modulating cellular and molecular hallmarks of TBI pathology such as; cell death, excitotoxicity, neuroinflammation, cerebrovascular breakdown, and cell structure and remodeling. TBI-induced behavioral deficits, such as learning and memory, neurological motor impairments, post-traumatic convulsions or seizures, and anxiety also respond to manipulations of the endocannabinoid system. As such, the endocannabinoid system possesses potential drugable receptor and enzyme targets for the treatment of diverse TBI pathology. Yet, full characterization of TBI-induced changes in endocannabinoid ligands, enzymes, and receptor populations will be important to understand that role this system plays in TBI pathology. Promising classes of compounds, such as the plant-derived phytocannabinoids, synthetic cannabinoids, and endocannabinoids, as well as their non-cannabinoid receptor

  5. 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.

  6. Predictors of Hypopituitarism in Patients with Traumatic Brain Injury.

    Science.gov (United States)

    Silva, Paula P B; Bhatnagar, Saurabha; Herman, Seth D; Zafonte, Ross; Klibanski, Anne; Miller, Karen K; Tritos, Nicholas A

    2015-11-15

    Hypopituitarism may often occur in association with traumatic brain injury (TBI). Identification of reliable predictors of pituitary dysfunction is of importance in order to establish a rational testing approach. We searched the records of patients with TBI, who underwent neuroendocrine evaluation in our institution between 2007 and 2013. One hundred sixty-six adults (70% men) with TBI (median age: 41.6 years; range: 18-76) were evaluated at a median interval of 40.4 months (0.2-430.4).Of these, 31% had ≥1 pituitary deficiency, including 29% of patients with mild TBI and 35% with moderate/severe TBI. Growth hormone deficiency was the most common deficiency (21%); when body mass index (BMI)-dependent cutpoints were used, this was reduced to 15%. Central hypoadrenalism occurred in10%, who were more likely to have suffered a motor vehicle accident (MVA, p = 0.04), experienced post-traumatic seizures (p = 0.04), demonstrated any intracranial hemorrhage (p = 0.05), petechial brain hemorrhages (p = 0.017), or focal cortical parenchymal contusions (p = 0.02). Central hypothyroidism occurred in 8% and central hypogonadism in 12%; the latter subgroup had higher BMI (p = 0.03), were less likely to be working after TBI (p = 0.002), and had lower Global Assessment of Functioning (GAF) scores (p = 0.03). Central diabetes insipidus (DI) occurred in 6%, who were more likely to have experienced MVA (p hypopituitarism.

  7. Traumatic Brain Injury Hospitalizations of U.S. Army Soldiers Deployed to Afghanistan and Iraq

    Science.gov (United States)

    2010-01-01

    Traumatic brain injury ( TBI ) is a life-altering... TBI , traumatic brain injury anuary 2010Helmet-use data from the DCIPS fıle specifıed whether helmet was worn, not worn, or unknown during the...78.3 9.5) 12.2 78.0 9.6) 12.4 ation nd Tcessing System; TBI , traumatic brain injury www.ajpm-online.net p s d E r o r r g p m p s m p T a b c C

  8. Amelioration of Acute Sequelae of Blast Induced Mild Traumatic Brain Injury by N-Acetyl Cysteine: A Double-Blind, Placebo Controlled Study

    Science.gov (United States)

    2013-01-23

    Janos, BA and Jeannine B. Mielke, PhD for assistance with choice of the cognitive tests used. The authors would like to thank and acknowledge the...Olive MF, Gass JT, et al. (2009) N- Acetylcysteine reverses cocaine-induced metaplasticity. Nature Neuroscience 12: 182–189. 17. Schubert MC, Tusa RJ...Agrawal Y, Carey JP, Hoffman HJ, Sklare DA, Schubert MC (2011) The modified Romberg Balance Test: normative data in U.S. adults. Otol Neurotol 32: 309–311

  9. 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

  10. Protective effects of decay-accelerating factor on blast-induced neurotrauma in rats

    OpenAIRE

    Li, Yansong; Chavko, Mikulas; Slack, Jessica L.; Liu, Bin; McCarron, Richard M.; Ross, James D. (Dalhousie University); Dalle Lucca, Jurandir J

    2013-01-01

    Background Blast-induced neurotrauma (BINT) is the signature life threatening injury of current military casualties. Neuroinflammation is a key pathological occurrence of secondary injury contributing to brain damage after blast injury. We have recently demonstrated that blast-triggered complement activation and cytokine release are associated with BINT. Here, we evaluated if administration of the complement inhibitor recombinant human decay-accelerating factor (rhDAF) is beneficial on neuroi...

  11. 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.

  12. 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.

  13. 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.

  14. Riding out the storm: sympathetic storming after traumatic brain injury.

    Science.gov (United States)

    Lemke, Denise M

    2004-02-01

    Following acute multiple trauma, hypothalamic stimulation of the sympathetic nervous system and adrenal glands causes an increase in circulating corticoids and catecholamines, or a stress response. In individuals with severe traumatic brain injury or a Glasgow Coma Scale score of 3-8, this response can be exaggerated and episodic. A term commonly used by nurses caring for these individuals to describe this phenomenon is storming. Symptoms can include alterations in level of consciousness, increased posturing, dystonia, hypertension, hyperthermia, tachycardia, tachypnea, diaphoresis, and agitation. These individuals generally are at a low level of neurological activity with minimal alertness, minimal awareness, and reflexive motor response to stimulation, and the storming can take a seemingly peaceful individual into a state of chaos. Diagnosis is commonly made solely on clinical assessment, and treatment is aimed at controlling the duration and severity of the symptoms and preventing additional brain injury. Storming can pose a challenge for the nurse, from providing daily care for the individual in the height of the storming episode and treating the symptoms, to educating the family. Careful assessment of the individual leads the nurse to the diagnosis and places the nurse in the role of moderator of the storming episode, including providing treatment and evaluating outcomes.

  15. Complications induced by decompressive craniectomies after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    杨学军; 洪国良; 苏少波; 杨树源

    2003-01-01

    Objective: To find out the optimal approach to decompress externally the severe injured brain and to avoid possible complications caused by external decompression.Methods: 68 patients who underwent external decompression after traumatic brain injury were admitted into Tianjin Medical University General Hospital for cranioplasty from 1995 to 2001. Complications were retrospectively investigated and analyzed in all patients. The findings were compared between the patients who accepted the decompressive craniectomy in our hospital and in local hospitals. Χ2-test was employed for statistical analysis and complication evaluation. Results: Large craniectomy definitely caused some side effects to patients. Among various complications, several of them showed significantly high incidence (P0.05) between the two groups including dilation or/and migration of lateral ventricle underlying the cranial defect, skin flap concavity, encephalomalacia of the decompressive area, seizure and infection.Conclusions: To reduce the incidence of iatrogenic side effects, surgical craniectomy should be performed according to the strict indication and standard and any abuse should be avoided.

  16. Raven's progressive matrices performance in adults with traumatic brain injury.

    Science.gov (United States)

    Hiscock, Merrill; Inch, Roxanne; Gleason, Angela

    2002-01-01

    Raven's Progressive Matrices (RPM), a widely used test of reasoning, is sensitive to aging, but it has not proven to be helpful in the assessment of acquired focal or lateralized brain damage. Clinical experience suggests that the test is insensitive to traumatic brain injury (TBI), but the data are difficult to interpret because of rapid inflation of norms over time (the Flynn effect). In examining data from 64 adult patients with TBI who were administered the Standard RPM between 1981 and 1989, we used previous and subsequent norms conjointly to adjust for the Flynn effect. Anterograde and retrograde adjustment of norms led to highly convergent results. After adjustment for the Flynn effect, RPM performance was comparable to Wechsler IQ, significantly below estimated premorbid IQ, and nearly 2 SD above performance on 2 TBI-sensitive neuropsychological tests. We conclude that RPM performance is neither more nor less sensitive than Wechsler IQ to the consequences of TBI in the adult, but erroneous conclusions are likely to be reached if the Flynn effect is not taken into account.

  17. 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.

  18. 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.

  19. Gabapentin in the management of dysautonomia following severe traumatic brain injury: a case series

    DEFF Research Database (Denmark)

    Baguley, Ian J; Heriseanu, Roxana E; Gurka, Joseph A;

    2007-01-01

    The pharmacological management of dysautonomia, otherwise known as autonomic storms, following acute neurological insults, is problematic and remains poorly researched. This paper presents six subjects with dysautonomia following extremely severe traumatic brain injury where gabapentin controlled...

  20. Selective CDK inhibitors:promising candidates for future clinical traumatic brain injury trials

    Institute of Scientific and Technical Information of China (English)

    Shruti V.Kabadi; Alan I.Faden

    2014-01-01

    Traumatic brain injury induces secondary injury that contributes to neuroinlfammation, neuronal loss, and neurological dysfunction. One important injury mechanism is cell cycle activation which causes neuronal apoptosis and glial activation. The neuroprotective effects of both non-selective (Flavopiridol) and selective (Roscovitine and CR-8) cyclin-dependent kinase inhibitors have been shown across multiple experimental traumatic brain injury models and species. Cyclin-depen-dent kinaseinhibitors, administered as a single systemic dose up to 24 hours after traumatic brain injury, provide strong neuroprotection-reducing neuronal cell death, neuroinflammation and neurological dysfunction. Given their effectiveness and long therapeutic window, cyclin-depen-dent kinase inhibitors appear to be promising candidates for clinical traumatic brain injury trials.

  1. Neuropsychiatric disturbances and hypopituitarism after traumatic brain injury in an elderly man.

    Science.gov (United States)

    Chang, Yi-Cheng; Tsai, Jui-Chang; Tseng, Fen-Yu

    2006-02-01

    Neuropsychiatric or cognitive disturbances are common complications after traumatic brain injury. They are commonly regarded as irreversible sequelae of organic brain injuries. We report a case of hypopituitarism in a 77-year-old man who presented with long-term neuropsychiatric disturbances, including cognitive impairment, disturbed sleep patterns, personality change, loss of affect, and visual and auditory hallucinations after a traumatic subdural hemorrhage. The treatment response to hormone replacement therapy was nearly complete. Hypopituitarism is rarely considered in patients who sustain traumatic brain injury and the neuropsychiatric manifestations of posttraumatic hypopituitarism have rarely been reported. This case highlights the importance of hypopituitarism as a potential reversible cause of neuropsychiatric disturbances after traumatic brain injury.

  2. 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

  3. Attention and driving in traumatic brain injury : A question of coping with time-pressure

    NARCIS (Netherlands)

    Brouwer, WH; Withaar, FK; Tant, MLM; van Zomeren, AH

    2002-01-01

    Background: Diffuse and focal traumatic brain injury (TBI) can result in perceptual, cognitive, and motor dysfunction possibly leading to activity limitations in driving. Characteristic dysfunctions for severe diffuse TBI are confronted with function requirements derived from the hierarchical task a

  4. 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

  5. Acute, regional inflammatory response after traumatic brain injury: Implications for cellular therapy

    OpenAIRE

    Harting, Matthew T.; jimenez, fernando; Adams, Sasha D.; Mercer, David W.; Cox, Charles S.

    2008-01-01

    While cellular therapy has shown promise in the management of traumatic brain injury (TBI), microenvironment interactions between the intracerebral milieu and therapeutic stem cells are poorly understood. We sought to characterize the acute, regional inflammatory response after TBI.

  6. 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

  7. Too Hard to Control: Compromised Pain Anticipation and Modulation in Mild Traumatic Brain Injury

    Science.gov (United States)

    2014-01-07

    instrumental for both facilitation and inhibition of ascending nociceptive input.52,53 In previous studies of acute pain stimulations, the anticipatory...OPEN ORIGINAL ARTICLE Too hard to control: compromised pain anticipation and modulation in mild traumatic brain injury IA Strigo1,2,3, AD Spadoni1,2...J Lohr1,2 and AN Simmons1,2 Mild traumatic brain injury (MTBI) is a vulnerability factor for the development of pain -related conditions above and

  8. Erythropoietin in traumatic brain injury: study protocol for a randomised controlled trial.

    LENUS (Irish Health Repository)

    Nichol, Alistair

    2015-02-08

    Traumatic brain injury is a leading cause of death and disability worldwide. Laboratory and clinical studies demonstrate a possible beneficial effect of erythropoietin in improving outcomes in the traumatic brain injury cohort. However, there are concerns regarding the association of erythropoietin and thrombosis in the critically ill. A large-scale, multi-centre, blinded, parallel-group, placebo-controlled, randomised trial is currently underway to address this hypothesis.

  9. Telephone-Delivered Cognitive Behavioral Therapy for Chronic Pain Following Traumatic Brain Injury

    Science.gov (United States)

    2015-10-01

    AWARD NUMBER: W81XWH-12-2-0109 TITLE: Telephone-Delivered Cognitive Behavioral Therapy for Chronic Pain Following Traumatic Brain Injury...2014-29 Sept 2015 4. TITLE AND SUBTITLE Telephone-Delivered Cognitive Behavioral Therapy for Chronic Pain 5a. CONTRACT NUMBER W81XWH-12-2-0109...study is to evaluate the efficacy of a telephone-delivered cognitive behavioral treatment (T-CBT) in Veterans with a history of traumatic brain injury

  10. Traumatic Brain Injury Due to Bull Assault in a Girl: a Case Report

    Science.gov (United States)

    ALVIS-MIRANDA, Hernando Raphael; CASTELLAR-LEONES, Sandra Milena; VELÁSQUEZ-LOPERENA, Dufays Danith; VILLA-DELGADO, Rosmery; ALCALA-CERRA, Gabriel; MOSCOTE-SALAZAR, Luis Rafael

    2013-01-01

    ABSTRACT Traumatic brain injury is a common condition in the emergency services, affecting the pediatric and adult population significantly. Patterns of head injury as well as management principles in children are important differences compared to adults. Traumatic brain injury by bull rush is usually seen in adults but has not been described in children-report a pediatric cranial trauma present bull rush, which to our knowledge is the first report in the literature of this nature. PMID:24790672

  11. Occurrence and severity of agitated behavior after severe traumatic brain injury

    DEFF Research Database (Denmark)

    Moth Wolffbrandt, Mia; Poulsen, Ingrid; Engberg, Aase W;

    2013-01-01

    To investigate the occurrence and severity of agitation in patients after severe traumatic brain injury (TBI), to identify predictors of agitation and to study interrater reliability for a translated version of the Agitated Behavior Scale (ABS).......To investigate the occurrence and severity of agitation in patients after severe traumatic brain injury (TBI), to identify predictors of agitation and to study interrater reliability for a translated version of the Agitated Behavior Scale (ABS)....

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

    OpenAIRE

    2015-01-01

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

  13. 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.

  14. Blast Exposure Induces Post-Traumatic Stress Disorder-Related Traits in a Rat Model of Mild Traumatic Brain Injury

    OpenAIRE

    Elder, Gregory A; Dorr, Nathan P.; De Gasperi, Rita; Gama Sosa, Miguel A.; Shaughness, Michael C.; Maudlin-Jeronimo, Eric; Hall, Aaron A; McCarron, Richard M.; Ahlers, Stephen T

    2012-01-01

    Blast related traumatic brain injury (TBI) has been a major cause of injury in the wars in Iraq and Afghanistan. A striking feature of the mild TBI (mTBI) cases has been the prominent association with post-traumatic stress disorder (PTSD). However, because of the overlapping symptoms, distinction between the two disorders has been difficult. We studied a rat model of mTBI in which adult male rats were exposed to repetitive blast injury while under anesthesia. Blast exposure induced a variety ...

  15. 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.

  16. Systems Biology, Neuroimaging, Neuropsychology, Neuroconnectivity and Traumatic Brain Injury.

    Science.gov (United States)

    Bigler, Erin D

    2016-01-01

    The patient who sustains a traumatic brain injury (TBI) typically undergoes neuroimaging studies, usually in the form of computed tomography (CT) and magnetic resonance imaging (MRI). In most cases the neuroimaging findings are clinically assessed with descriptive statements that provide qualitative information about the presence/absence of visually identifiable abnormalities; though little if any of the potential information in a scan is analyzed in any quantitative manner, except in research settings. Fortunately, major advances have been made, especially during the last decade, in regards to image quantification techniques, especially those that involve automated image analysis methods. This review argues that a systems biology approach to understanding quantitative neuroimaging findings in TBI provides an appropriate framework for better utilizing the information derived from quantitative neuroimaging and its relation with neuropsychological outcome. Different image analysis methods are reviewed in an attempt to integrate quantitative neuroimaging methods with neuropsychological outcome measures and to illustrate how different neuroimaging techniques tap different aspects of TBI-related neuropathology. Likewise, how different neuropathologies may relate to neuropsychological outcome is explored by examining how damage influences brain connectivity and neural networks. Emphasis is placed on the dynamic changes that occur following TBI and how best to capture those pathologies via different neuroimaging methods. However, traditional clinical neuropsychological techniques are not well suited for interpretation based on contemporary and advanced neuroimaging methods and network analyses. Significant improvements need to be made in the cognitive and behavioral assessment of the brain injured individual to better interface with advances in neuroimaging-based network analyses. By viewing both neuroimaging and neuropsychological processes within a systems biology

  17. The Effect of Hemoglobin Levels on Mortality in Pediatric Patients with Severe Traumatic Brain Injury

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    Kevin F. Yee

    2016-01-01

    Full Text Available Objective. There is increasing evidence of adverse outcomes associated with blood transfusions for adult traumatic brain injury patients. However, current evidence suggests that pediatric traumatic brain injury patients may respond to blood transfusions differently on a vascular level. This study examined the influence of blood transfusions and anemia on the outcome of pediatric traumatic brain injury patients. Design. A retrospective cohort analysis of severe pediatric traumatic brain injury (TBI patients was undertaken to investigate the association between blood transfusions and anemia on patient outcomes. Measurements and Main Results. One hundred and twenty patients with severe traumatic brain injury were identified and included in the analysis. The median Glasgow Coma Scale (GCS was 6 and the mean hemoglobin (Hgb on admission was 115.8 g/L. Forty-three percent of patients (43% received at least one blood transfusion and the mean hemoglobin before transfusion was 80.1 g/L. Multivariable regression analysis revealed that anemia and the administration of packed red blood cells were not associated with adverse outcomes. Factors that were significantly associated with mortality were presence of abusive head trauma, increasing PRISM score, and low GCS after admission. Conclusion. In this single centre retrospective cohort study, there was no association found between anemia, blood transfusions, and hospital mortality in a pediatric traumatic brain injury patient population.

  18. Brain structure in post-traumatic stress disorder A voxel-based morphometry analysis**

    Institute of Scientific and Technical Information of China (English)

    Liwen Tan; Li Zhang; Rongfeng Qi; Guangming Lu; Lingjiang Li; Jun Liu; Weihui Li

    2013-01-01

    This study compared the difference in brain structure in 12 mine disaster survivors with chronic post-traumatic stress disorder, 7 cases of improved post-traumatic stress disorder symptoms, and 14 controls who experienced the same mine disaster but did not suffer post-traumatic stress disorder, us-ing the voxel-based morphometry method. The correlation between differences in brain structure and post-traumatic stress disorder symptoms was also investigated. Results showed that the gray matter volume was the highest in the trauma control group, fol owed by the symptoms-improved group, and the lowest in the chronic post-traumatic stress disorder group. Compared with the symptoms-improved group, the gray matter volume in the lingual gyrus of the right occipital lobe was reduced in the chronic post-traumatic stress disorder group. Compared with the trauma control group, the gray matter volume in the right middle occipital gyrus and left middle frontal gyrus was reduced in the symptoms-improved group. Compared with the trauma control group, the gray matter volume in the left superior parietal lobule and right superior frontal gyrus was reduced in the chronic post-traumatic stress disorder group. The gray matter volume in the left superior parietal lobule was significantly positively correlated with the State-Trait Anxiety Inventory subscale score in the symptoms-improved group and chronic post-traumatic stress disorder group (r = 0.477, P = 0.039). Our findings indicate that (1) chronic post-traumatic stress disorder patients have gray matter structural damage in the prefrontal lobe, occip-ital lobe, and parietal lobe, (2) after post-traumatic stress, the disorder symptoms are improved and gray matter structural damage is reduced, but cannot recover to the trauma-control level, and (3) the superior parietal lobule is possibly associated with chronic post-traumatic stress disorder. Post-traumatic stress disorder patients exhibit gray matter abnormalities.

  19. Brain structure in post-traumatic stress disorder: A voxel-based morphometry analysis.

    Science.gov (United States)

    Tan, Liwen; Zhang, Li; Qi, Rongfeng; Lu, Guangming; Li, Lingjiang; Liu, Jun; Li, Weihui

    2013-09-15

    This study compared the difference in brain structure in 12 mine disaster survivors with chronic post-traumatic stress disorder, 7 cases of improved post-traumatic stress disorder symptoms, and 14 controls who experienced the same mine disaster but did not suffer post-traumatic stress disorder, using the voxel-based morphometry method. The correlation between differences in brain structure and post-traumatic stress disorder symptoms was also investigated. Results showed that the gray matter volume was the highest in the trauma control group, followed by the symptoms-improved group, and the lowest in the chronic post-traumatic stress disorder group. Compared with the symptoms-improved group, the gray matter volume in the lingual gyrus of the right occipital lobe was reduced in the chronic post-traumatic stress disorder group. Compared with the trauma control group, the gray matter volume in the right middle occipital gyrus and left middle frontal gyrus was reduced in the symptoms-improved group. Compared with the trauma control group, the gray matter volume in the left superior parietal lobule and right superior frontal gyrus was reduced in the chronic post-traumatic stress disorder group. The gray matter volume in the left superior parietal lobule was significantly positively correlated with the State-Trait Anxiety Inventory subscale score in the symptoms-improved group and chronic post-traumatic stress disorder group (r = 0.477, P = 0.039). Our findings indicate that (1) chronic post-traumatic stress disorder patients have gray matter structural damage in the prefrontal lobe, occipital lobe, and parietal lobe, (2) after post-traumatic stress, the disorder symptoms are improved and gray matter structural damage is reduced, but cannot recover to the trauma-control level, and (3) the superior parietal lobule is possibly associated with chronic post-traumatic stress disorder. Post-traumatic stress disorder patients exhibit gray matter abnormalities.

  20. 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

  1. Non-invasive brain stimulation for the treatment of symptoms following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Simarjot K Dhaliwal

    2015-08-01

    Full Text Available Background: Traumatic brain injury (TBI is a common cause of physical, psychological, and cognitive impairment, but many current treatments for TBI are ineffective or produce adverse side effects. Non-invasive methods of brain stimulation could help ameliorate some common trauma-induced symptoms.Objective: This review summarizes instances in which repetitive Transcranial Magnetic Stimulation (rTMS and transcranial Direct Current Stimulation (tDCS have been used to treat symptoms following a traumatic brain injury. A subsequent discussion attempts to determine the value of these methods in light of their potential risks.Methods: The research databases of PubMed/MEDLINE and PsycINFO were electronically searched using terms relevant to the use of rTMS and tDCS as a tool to decrease symptoms in the context of rehabilitation post-TBI.Results: Eight case-studies and four multi-subject reports using rTMS and six multi-subject studies using tDCS were found. Two instances of seizure are discussed. Conclusions: There is evidence that rTMS can be an effective treatment option for some post-TBI symptoms such as depression, tinnitus, and neglect. Although the safety of this method remains uncertain, the use of rTMS in cases of mild-TBI without obvious structural damage may be justified. Evidence on the effectiveness of tDCS is mixed, highlighting the need for additional

  2. 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.

  3. Movement preparation and execution: differential functional activation patterns after traumatic brain injury.

    Science.gov (United States)

    Gooijers, Jolien; Beets, Iseult A M; Albouy, Genevieve; Beeckmans, Kurt; Michiels, Karla; Sunaert, Stefan; Swinnen, Stephan P

    2016-09-01

    Years following the insult, patients with traumatic brain injury often experience persistent motor control problems, including bimanual coordination deficits. Previous studies revealed that such deficits are related to brain structural white and grey matter abnormalities. Here, we assessed, for the first time, cerebral functional activation patterns during bimanual movement preparation and performance in patients with traumatic brain injury, using functional magnetic resonance imaging. Eighteen patients with moderate-to-severe traumatic brain injury (10 females; aged 26.3 years, standard deviation = 5.2; age range: 18.4-34.6 years) and 26 healthy young adults (15 females; aged 23.6 years, standard deviation = 3.8; age range: 19.5-33 years) performed a complex bimanual tracking task, divided into a preparation (2 s) and execution (9 s) phase, and executed either in the presence or absence of augmented visual feedback. Performance on the bimanual tracking task, expressed as the average target error, was impaired for patients as compared to controls (P traumatic brain injury patients showed enhanced activations compared with controls in frontal (left dorsolateral prefrontal cortex, left lateral anterior prefrontal cortex, and left orbitofrontal cortex), parietal (bilateral inferior parietal lobe, bilateral superior parietal lobe, right precuneus, right primary somatosensory cortex), occipital (right striate and extrastriate visual cortices), and subcortical (left cerebellum crus II) areas (P's traumatic brain injury (i.e. decreased neural differentiation). In sum, our findings point towards poorer predictive control in traumatic brain injury patients in comparison to controls. Moreover, irrespective of the feedback condition, overactivations were observed in traumatically brain injured patients during movement execution, pointing to more controlled processing of motor task performance.

  4. Common biochemical defects linkage between post-traumatic stress disorders, mild traumatic brain injury (TBI) and penetrating TBI.

    Science.gov (United States)

    Prasad, Kedar N; Bondy, Stephen C

    2015-03-02

    Post-traumatic stress disorder (PTSD) is a complex mental disorder with psychological and emotional components, caused by exposure to single or repeated extreme traumatic events found in war, terrorist attacks, natural or man-caused disasters, and by violent personal assaults and accidents. Mild traumatic brain injury (TBI) occurs when the brain is violently rocked back and forth within the skull following a blow to the head or neck as in contact sports, or when in close proximity to a blast pressure wave following detonation of explosives in the battlefield. Penetrating TBI occurs when an object penetrates the skull and damages the brain, and is caused by vehicle crashes, gunshot wound to the head, and exposure to solid fragments in the proximity of explosions, and other combat-related head injuries. Despite clinical studies and improved understanding of the mechanisms of cellular damage, prevention and treatment strategies for patients with PTSD and TBI remain unsatisfactory. To develop an improved plan for treating and impeding progression of PTSD and TBI, it is important to identify underlying biochemical changes that may play key role in the initiation and progression of these disorders. This review identifies three common biochemical events, namely oxidative stress, chronic inflammation and excitotoxicity that participate in the initiation and progression of these conditions. While these features are separately discussed, in many instances, they overlap. This review also addresses the goal of developing novel treatments and drug regimens, aimed at combating this triad of events common to, and underlying, injury to the brain.

  5. 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

  6. Developing a Cognition Endpoint for Traumatic Brain Injury Clinical Trials.

    Science.gov (United States)

    Silverberg, Noah D; Crane, Paul K; Dams-O'Connor, Kristen; Holdnack, James; Ivins, Brian J; Lange, Rael T; Manley, Geoffrey T; McCrea, Michael; Iverson, Grant L

    2017-01-15

    Cognitive impairment is a core clinical feature of traumatic brain injury (TBI). After TBI, cognition is a key determinant of post-injury productivity, outcome, and quality of life. As a final common pathway of diverse molecular and microstructural TBI mechanisms, cognition is an ideal endpoint in clinical trials involving many candidate drugs and nonpharmacological interventions. Cognition can be reliably measured with performance-based neuropsychological tests that have greater granularity than crude rating scales, such as the Glasgow Outcome Scale-Extended, which remain the standard for clinical trials. Remarkably, however, there is no well-defined, widely accepted, and validated cognition endpoint for TBI clinical trials. A single cognition endpoint that has excellent measurement precision across a wide functional range and is sensitive to the detection of small improvements (and declines) in cognitive functioning would enhance the power and precision of TBI clinical trials and accelerate drug development research. We outline methodologies for deriving a cognition composite score and a research program for validation. Finally, we discuss regulatory issues and the limitations of a cognition endpoint.

  7. Theory of mind in children with traumatic brain injury.

    Science.gov (United States)

    Dennis, Maureen; Simic, Nevena; Gerry Taylor, H; Bigler, Erin D; Rubin, Kenneth; Vannatta, Kathryn; Gerhardt, Cynthia A; Stancin, Terry; Roncadin, Caroline; Yeates, Keith Owen

    2012-09-01

    Theory of mind (ToM) involves thinking about mental states and intentions to understand what other people know and to predict how they will act. We studied ToM in children with traumatic brain injury (TBI) and age- and gender-matched children with orthopedic injuries (OI), using a new three-frame Jack and Jill cartoon task that measures intentional thinking separate from contingent task demands. In the key ToM trials, which required intentional thinking, Jack switched a black ball from one hat to another of a different color, but Jill did not witness the switch; in the otherwise identical non-ToM trials, the switch was witnessed. Overall accuracy was higher in children with OI than in those with TBI. Children with severe TBI showed a larger decline in accuracy on ToM trials, suggesting a specific deficit in ToM among children with severe TBI. Accuracy was significantly higher on trials following errors than on trials following correct responses, suggesting that all groups monitored performance and responded to errors with increased vigilance. TBI is associated with poorer intentional processing in school-age children and adolescents relative to peers with OI; furthermore, children with TBI are challenged specifically by intentional demands, especially when their injury is severe. (JINS, 2012, 19, 1-9).

  8. Cognitive impairment and rehabilitation strategies after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Apurba Barman

    2016-01-01

    Full Text Available Traumatic brain injury (TBI is among the significant causes of morbidity and mortality in the present world. Around 1.6 million persons sustain TBI, whereas 200,000 die annually in India, thus highlighting the rising need for appropriate cognitive rehabilitation strategies. This literature review assesses the current knowledge of various cognitive rehabilitation training strategies. The entire spectrum of TBI severity; mild to severe, is associated with cognitive deficits of varying degree. Cognitive insufficiency is more prevalent and longer lasting in TBI persons than in the general population. A multidisciplinary approach with neuropsychiatric evaluation is warranted. Attention process training and tasks for attention deficits, compensatory strategies and errorless learning training for memory deficits, pragmatic language skills and social behavior guidance for cognitive-communication disorder, meta-cognitive strategy, and problem-solving training for executive disorder are the mainstay of therapy for cognitive deficits in persons with TBI. Cognitive impairments following TBI are common and vary widely. Different cognitive rehabilitation techniques and combinations in addition to pharmacotherapy are helpful in addressing various cognitive deficits.

  9. Electrophysiological Correlates of Word Retrieval in Traumatic Brain Injury

    Science.gov (United States)

    DeLaRosa, Bambi L.; Didehbani, Nyaz; Hart, John; Kraut, Michael A

    2017-01-01

    Abstract Persons who have had a traumatic brain injury (TBI) often have word retrieval deficits; however, the underlying neural mechanisms of such deficits are yet to be clarified. Previous studies in normal subjects have shown that during a word retrieval task, there is a 750 msec event-related potential (ERP) divergence detected at the left fronto-temporal region when subjects evaluate word pairs that facilitate retrieval compared with responses elicited by word pairs that do not facilitate retrieval. In this study, we investigated the neurophysiological correlates of word retrieval networks in 19 retired professional athletes with TBI and 19 healthy control (HC) subjects. We recorded electroencephalography (EEG) in the participants during a semantic object retrieval task. In this task, participants indicated whether presented word pairs did (retrieval) or did not (non-retrieval) facilitate the retrieval of an object name. There were no significant differences in accuracy or reaction time between the two groups. The EEG showed a significant group by condition interaction over the left fronto-temporal region. The HC group mean amplitudes were significantly different between conditions, but the TBI group data did not show this difference, suggesting neurophysiological effects of injury. These findings provide evidence that ERP amplitudes may be used as a marker of disrupted semantic retrieval circuits in persons with TBI even when those persons perform normally. PMID:27596052

  10. Exploring Vocational Evaluation Practices following Traumatic Brain Injury

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    Christina Dillahunt-Aspillaga

    2015-01-01

    Full Text Available Background. Individuals with traumatic brain injury (TBI face many challenges when attempting to return to work (RTW. Vocational evaluation (VE is a systematic process that involves assessment and appraisal of an individual’s current work-related characteristics and abilities. Objective. The aims of this study are to (1 examine demographic and employment characteristics of vocational rehabilitation providers (VRPs, (2 identify the specific evaluation methods that are used in the VE of individuals with TBI, and (3 examine the differences in assessment method practices based upon evaluator assessment preferences. Methods. This exploratory case study used a forty-six-item online survey which was distributed to VRPs. Results. One hundred and nine VRPs accessed the survey. Of these, 74 completed the survey. A majority of respondents were female (79.7%, Caucasian (71.6%, and holding a master’s degree (74.3%, and more than half (56.8% were employed as state vocational rehabilitation counselors (VRCs. In addition, over two-thirds (67.6% were certified rehabilitation counselors (CRCs. Respondents reported using several specific tools and assessments during the VE process. Conclusions. Study findings reveal differences in use of and rationales for specific assessments amongst VRPs. Understanding VRP assessment practices and use of an evidence-based framework for VE following TBI may inform and improve VE practice.

  11. Understanding paroxysmal sympathetic hyperactivity after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Kimberly S Meyer

    2014-01-01

    Full Text Available Background: Paroxysmal sympathetic hyperactivity (PSH is a condition occurring in a small percentage of patients with severe traumatic brain injury (TBI. It is characterized by a constellation of symptoms associated with excessive adrenergic output, including tachycardia, hypertension, tachypnea, and diaphoresis. Diagnosis is one of exclusion and, therefore, is often delayed. Treatment is aimed at minimizing triggers and pharmacologic management of symptoms. Methods: A literature review using medline and cinahl was conducted to identify articles related to PSH. Search terms included paroxysmal sympathetic hyperactivity, autonomic storming, diencephalic seizures, and sympathetic storming. Reference lists of pertinent articles were also reviewed and these additional papers were included. Results: The literature indicates that the understanding of PSH following TBI is in its infancy. The majority of information is based on small case series. The review revealed treatments that may be useful in treating PSH. Conclusions: Nurses play a critical role in the identification of at-risk patients, symptom complexes, and in the education of family. Early detection and treatment is likely to decrease overall morbidity and facilitate recovery. Further research is needed to establish screening tools and treatment algorithms for PSH.

  12. Voltage-Gated Calcium Channel Antagonists and Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Bruce Lyeth

    2013-06-01

    Full Text Available Traumatic brain injury (TBI is a leading cause of death and disability in the United States. Despite more than 30 years of research, no pharmacological agents have been identified that improve neurological function following TBI. However, several lines of research described in this review provide support for further development of voltage gated calcium channel (VGCC antagonists as potential therapeutic agents. Following TBI, neurons and astrocytes experience a rapid and sometimes enduring increase in intracellular calcium ([Ca2+]i. These fluxes in [Ca2+]i drive not only apoptotic and necrotic cell death, but also can lead to long-term cell dysfunction in surviving cells. In a limited number of in vitro experiments, both L-type and N-type VGCC antagonists successfully reduced calcium loads as well as neuronal and astrocytic cell death following mechanical injury. In rodent models of TBI, administration of VGCC antagonists reduced cell death and improved cognitive function. It is clear that there is a critical need to find effective therapeutics and rational drug delivery strategies for the management and treatment of TBI, and we believe that further investigation of VGCC antagonists should be pursued before ruling out the possibility of successful translation to the clinic.

  13. Risk Factors Analysis on Traumatic Brain Injury Prognosis

    Institute of Scientific and Technical Information of China (English)

    Xiao-dong Qu; Resha Shrestha; Mao-de Wang

    2011-01-01

    To investigate the independent risk factors of traumatic brain injury (TBI) prognosis.Methods A retrospective analysis was performed in 885 hospitalized TEl patients from January 1,2003 to January 1, 2010 in the First Affiliated Hospital of Medical College of Xi' an Jiaotong University. Single-factor and logistic regression analysis were conducted to evaluate the association of different variables with TBI outcome.Results The single-factor analysis revealed significant association between several variables and TEl outcome, including age (P=0.044 for the age group 40-60, P<0.001 for the age group ≥60), complications (P<0.001), cerebrospinal fluid leakage (P<0.001), Glasgow Coma Scale (GCS) (P<0.001), pupillary light reflex (P<0.001), shock (P<0.001), associated extra-cranial lesions (P=0.01), subdural hematoma (P<0.001), cerebral contusion (P<0.001), diffuse axonal injury (P<0.001), and subarachnoid hemorrhage (P<0.001), suggesting the influence of those factors on the prognosis of TBI. Furthermore, logistic regression analysis identified age, GCS score, pupillary light reflex, subdural hematoma, and subarachnoid hemorrhage as independent risk factors of TEl prognosis.Conclusion Age, GCS score, papillary light reflex, subdural hematoma, and subarachnoid hemorrhage may be risk factors influencing the prognosis of TEl. Paying attention to those factors might improve the outcome of TBI in clinical treatment.

  14. Clinical application of magnetic resonance in acute traumatic brain injury

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    Morais, Dionei F.; Gaia, Felipe F.P. [Hospital de Base de Sao Jose do Rio Preto, SP (Brazil). Servico de Neurocirurgia]. E-mail: centro@cerebroecoluna.com.br; Spotti, Antonio R.; Tognola, Waldir A. [Faculdade de Medicina de Sao Jose do Rio Preto (FAMERP), SP (Brazil). Dept. de Ciencias Neurologicas; Andrade, Almir F. [Universidade de Sao Paulo (USP), SP (Brazil). Hospital das Clinicas. Dept. de Neurocirurgia da Emergencia

    2008-07-01

    Purpose: To evaluate the clinical applications of magnetic resonance imaging (MRI) in patients with acute traumatic brain injury (TBI): to identify the type, quantity, severity; and improvement clinical-radiological correlation. Method: Assessment of 55 patients who were imaged using CT and MRI, 34 (61.8%) males and 21 (38.2%) females, with acute (0 to 5 days) and closed TBI. Results: Statistical significant differences (McNemar test): occurred fractures were detected by CT in 29.1% and by MRI in 3.6% of the patients; subdural hematoma by CT in 10.9% and MRI in 36.4 %; diffuse axonal injury (DAI) by CT in 1.8% and MRI in 50.9%; cortical contusions by CT in 9.1% and MRI in 41.8%; subarachnoid hemorrhage by CT in 18.2% and MRI in 41.8%. Conclusion: MRI was superior to the CT in the identification of DAI, subarachnoid hemorrhage, cortical contusions, and acute subdural hematoma; however it was inferior in diagnosing fractures. The detection of DAI was associated with the severity of acute TBI. (author)

  15. 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.

  16. Pain Catastrophizing Correlates with Early Mild Traumatic Brain Injury Outcome

    Science.gov (United States)

    Chaput, Geneviève; Lajoie, Susanne P.; Naismith, Laura M.; Lavigne, Gilles

    2016-01-01

    Background. Identifying which patients are most likely to be at risk of chronic pain and other postconcussion symptoms following mild traumatic brain injury (MTBI) is a difficult clinical challenge. Objectives. To examine the relationship between pain catastrophizing, defined as the exaggerated negative appraisal of a pain experience, and early MTBI outcome. Methods. This cross-sectional design included 58 patients diagnosed with a MTBI. In addition to medical chart review, postconcussion symptoms were assessed by self-report at 1 month (Time 1) and 8 weeks (Time 2) after MTBI. Pain severity, psychological distress, level of functionality, and pain catastrophizing were measured by self-report at Time 2. Results. The pain catastrophizing subscales of rumination, magnification, and helplessness were significantly correlated with pain severity (r = .31 to .44), number of postconcussion symptoms reported (r = .35 to .45), psychological distress (r = .57 to .67), and level of functionality (r = −.43 to −.29). Pain catastrophizing scores were significantly higher for patients deemed to be at high risk of postconcussion syndrome (6 or more symptoms reported at both Time 1 and Time 2). Conclusions. Higher levels of pain catastrophizing were related to adverse early MTBI outcomes. The early detection of pain catastrophizing may facilitate goal-oriented interventions to prevent or minimize the development of chronic pain and other postconcussion symptoms. PMID:27445604

  17. Pain Catastrophizing Correlates with Early Mild Traumatic Brain Injury Outcome

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    Geneviève Chaput

    2016-01-01

    Full Text Available Background. Identifying which patients are most likely to be at risk of chronic pain and other postconcussion symptoms following mild traumatic brain injury (MTBI is a difficult clinical challenge. Objectives. To examine the relationship between pain catastrophizing, defined as the exaggerated negative appraisal of a pain experience, and early MTBI outcome. Methods. This cross-sectional design included 58 patients diagnosed with a MTBI. In addition to medical chart review, postconcussion symptoms were assessed by self-report at 1 month (Time 1 and 8 weeks (Time 2 after MTBI. Pain severity, psychological distress, level of functionality, and pain catastrophizing were measured by self-report at Time 2. Results. The pain catastrophizing subscales of rumination, magnification, and helplessness were significantly correlated with pain severity (r=.31 to .44, number of postconcussion symptoms reported (r=.35 to .45, psychological distress (r=.57 to .67, and level of functionality (r=-.43 to -.29. Pain catastrophizing scores were significantly higher for patients deemed to be at high risk of postconcussion syndrome (6 or more symptoms reported at both Time 1 and Time 2. Conclusions. Higher levels of pain catastrophizing were related to adverse early MTBI outcomes. The early detection of pain catastrophizing may facilitate goal-oriented interventions to prevent or minimize the development of chronic pain and other postconcussion symptoms.

  18. 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.

  19. Early exposure to traumatic stressors impairs emotional brain circuitry.

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    Mayuresh S Korgaonkar

    Full Text Available Exposure to early life trauma (ELT is known to have a profound impact on mental development, leading to a higher risk for depression and anxiety. Our aim was to use multiple structural imaging methods to systematically investigate how traumatic stressors early in life impact the emotional brain circuits, typically found impaired with clinical diagnosis of depression and anxiety, across the lifespan in an otherwise healthy cohort. MRI data and self-reported histories of ELT from 352 healthy individuals screened for no psychiatric disorders were analyzed in this study. The volume and cortical thickness of the limbic and cingulate regions were assessed for all participants. A large subset of the cohort also had diffusion tensor imaging data, which was used to quantify white matter structural integrity of these regions. We found a significantly smaller amygdala volume and cortical thickness in the rostral anterior cingulate cortex associated with higher ELT exposure only for the adolescence group. White matter integrity of these regions was not affected. These findings demonstrate that exposure to early life trauma is associated with alterations in the gray matter of cingulate-limbic regions during adolescence in an otherwise healthy sample. These findings are interesting in the context that the affected regions are central neuroanatomical components in the psychopathology of depression, and adolescence is a peak period for risk and onset of the disorder.

  20. Emergent Endotracheal Intubation and Mortality in Traumatic Brain Injury

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    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

  1. The characteristics of chronic central pain after traumatic brain injury.

    Science.gov (United States)

    Ofek, Hadas; Defrin, Ruth

    2007-10-01

    Central pain following traumatic brain injury (TBI) has not been studied in depth. Our purpose was to conduct a systematic study of patients with TBI suffering from chronic central pain, and to describe the characteristics of the central pain. Groups were TBI patients with (TBIP) and without central pain (TBINP) and healthy controls. TBI patients with other pain mechanisms were excluded from the study. Participants underwent quantitative somatosensory testing in the painful and pain-free body regions. Thresholds for warmth, cold, heat-pain, touch and graphesthesia were measured and pathologically evoked pain (allodynia, hyperpathia and wind-up pain) evaluated. Chronic pain was mapped and characterized. Chronic pain developed at a relatively late onset (6.6+/-9 months) was almost exclusively unilateral and reported as pricking, throbbing and burning. Although both TBIP and TBINP exhibited a significant reduction in thermal and tactile sensations compared to controls, thermal sensations in the painful regions of TBIP were significantly more impaired than pain-free regions in the same patients (p<0.01) and in TBINP (p<0.01). Painful regions also exhibited very high rates of allodynia, hyperpathia and exaggerated wind-up. The characteristics of the chronic pain resembled those of other central pain patients although TBIP displayed several unique features. The sensory profile indicated that damage to the pain and temperature systems is a necessary but not sufficient condition for the development of chronic central pain following TBI. Neuronal hyperexcitability may be a contributing factor to the chronic pain.

  2. Mild traumatic brain injury screening, diagnosis, and treatment.

    Science.gov (United States)

    Marshall, Kathryn R; Holland, Sherray L; Meyer, Kimberly S; Martin, Elisabeth Moy; Wilmore, Michael; Grimes, Jamie B

    2012-08-01

    The majority of combat-related traumatic brain injury (TBI) within the U.S. Armed Forces is mild TBI (mTBI). This article focuses specifically on the screening, diagnosis, and treatment aspects of mTBI within the military community. Aggressive screening measures were instituted in 2006 to ensure that the mTBI population is identified and treated. Screenings occur in-theater, outside the contiguous United States, and in-garrison. We discuss specific screening procedures at each screening setting. Current diagnosis of mTBI is based upon self-report or through witnesses to the event. TBI severity is determined by specific Department of Defense criteria. Abundant clinician resources are available for mTBI in the military health care setting. Education resources for both the patient and the clinician are discussed in detail. An evidence-based clinical practice guideline for the care of mTBI was created through collaborative efforts of the DoD and the U.S. Department of Veterans Affairs. Although symptoms following mTBI generally resolve with time, active treatment is centered on symptom management, supervised rest, recovery, and patient education. Medical specialty care, ancillary services, and other therapeutic services may be required.

  3. Traumatic brain injury–Modeling neuropsychiatric symptoms in rodents

    Directory of Open Access Journals (Sweden)

    Oz eMalkesman

    2013-10-01

    Full Text Available Each year in the United States, approximately 1.5 million people sustain a traumatic brain injury (TBI. Victims of TBI can suffer from chronic post-TBI symptoms, such as sensory and motor deficits, cognitive impairments including problems with memory, learning, and attention, and neuropsychiatric symptoms such as depression, anxiety, irritability, aggression, and suicidal rumination. Although partially associated with the site and severity of injury, the biological mechanisms associated with many of these symptoms—and why some patients experience differing assortments of persistent maladies—are largely unknown. The use of animal models is a promising strategy for elucidation of the mechanisms of impairment and treatment, and learning, memory, sensory and motor tests have widespread utility in rodent models of TBI and psychopharmacology. Comparatively, behavioral tests for the evaluation of neuropsychiatric symptomatology are rarely employed in animal models of TBI and, as determined in this review, the results have been inconsistent. Animal behavioral studies contribute to the understanding of the biological mechanisms by which TBI is associated with neurobehavioral symptoms and offer a powerful means for pre-clinical treatment validation. Therefore, further exploration of the utility of animal behavioral tests for the study of injury mechanisms and therapeutic strategies for the alleviation of emotional symptoms are relevant and essential.

  4. Dynamic pituitary hormones change after traumatic brain injury

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    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.

  5. Hypopituitarism in Traumatic Brain Injury—A Critical Note

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    Marianne Klose

    2015-07-01

    Full Text Available 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 on mainly isolated deficiencies in TBI patients, and particularly isolated growth hormone (GH deficiency, raise the question of the potential impact of methodological confounding, determined by variable test-retest reproducibility, appropriateness of cut-off values, importance of BMI stratified cut-offs, assay heterogeneity, pre-test probability of hypopituitarism and lack of proper individual laboratory controls as reference population. In this review, current recommendations are discussed in light of recent available evidence.

  6. Verbal learning strategy following mild traumatic brain injury.

    Science.gov (United States)

    Geary, Elizabeth K; Kraus, Marilyn F; Rubin, Leah H; Pliskin, Neil H; Little, Deborah M

    2011-07-01

    That learning and memory deficits persist many years following mild traumatic brain injury (mTBI) is controversial due to inconsistent objective evidence supporting subjective complaints. Our prior work demonstrated significant reductions in performance on the initial trial of a verbal learning task and overall slower rate of learning in well-motivated mTBI participants relative to demographically matched controls. In our previous work, we speculated that differences in strategy use could explain the differences in rate of learning. The current study serves to test this hypothesis by examining strategy use on the California Verbal Learning Test-Second Edition. Our present findings support the primary hypothesis that mTBI participants under-utilize semantic clustering strategies during list-learning relative to control participants. Despite achieving comparable total learning scores, we posit that the persisting learning and memory difficulties reported by some mTBI patients may be related to reduced usage of efficient internally driven strategies that facilitate learning. Given that strategy training has demonstrated improvements in learning and memory in educational and occupational settings, we offer that these findings have translational value in offering an additional approach in remediation of learning and memory complaints reported by some following mTBI.

  7. Social reintegration of traumatic brain-injured: the French experience.

    Science.gov (United States)

    Truelle, J-L; Wild, K Von; Onillon, M; Montreuil, M

    2010-01-01

    Traumatic Brain Injury (TBI) may lead to specific handicap, often hidden, mainly due to cognitive and behavioural sequelae. Social re-entry is a long-term, fluctuant and precarious process. The French experience will be illustrated by 6 initiatives answering to 6 challenges to do with TBI specificities:1. bridging the gap, between initial rehabilitation and community re-entry, via transitional units dealing with assessment, retraining, social/vocational orientation and follow-up. Today, there are 30 such units based on multidisciplinary teams.2. assessing recovery by TBI-specific and validated evaluation tools: EBIS holistic document, BNI Screening of higher cerebral functions, Glasgow outcome extended, and QOLIBRI, a TBI-specific quality of life tool.3. promoting specific re-entry programmes founded on limited medication, ecological neuro-psychological rehabilitation, exchange groups and workshops, violence prevention, continuity of care, environmental structuration, and "resocialisation".4. taking into account the "head injured family"5. facilitating recovery after sports-related concussion6. facing medico-legal consequences and compensation: In that perspective, we developed guidelines for TBI-specific expert appraisal, including mandatory neuro-psychological assessment, family interview and an annual forum gathering lawyers and health professionals.

  8. Attention remediation following traumatic brain injury in childhood and adolescence.

    Science.gov (United States)

    Galbiati, Susanna; Recla, Monica; Pastore, Valentina; Liscio, Mariarosaria; Bardoni, Alessandra; Castelli, Enrico; Strazzer, Sandra

    2009-01-01

    Traumatic brain injury (TBI) frequently affects both the basic and the superordinate components of attention; deficits vary according to patient age. This study evaluated the efficacy of a specific remediation intervention for attention. Sixty-five TBI patients (aged 6?18 years) with attention deficit were assessed at baseline and at 1-year follow-up: 40 patients received attention-specific neuropsychological training for 6 months, and the control group comprised 25 patients. Cognitive assessment included a Wechsler Intelligence Scale (e.g., A. Orsini, 1993) and the Continuous Performance Test II (CPT II; C. K. Conners, 2000). The Vineland Adaptive Behavior Scales (VABS; S. Sparrow, D. Balla & D. V. Cicchetti, 1984) was administered to assess the treatment's ecological validity. At baseline, all patients presented with a mild intellectual disability and pathological scores on the CPT II. At follow-up, significant differences were found between the 2 groups on the CPT II and VABS: The clinical group improved more than the control group. Specific remediation training for attention, including a combination of a process-specific approach and metacognitive strategies, significantly improved attention performance. Improvement in attention skills also affected adaptive skills positively.

  9. Prognostic significance of age in traumatic brain injury

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    S S Dhandapani

    2012-01-01

    Full Text Available Background: Age is a strong prognostic factor following traumatic brain injury (TBI, with discrepancies defining the critical prognostic age threshold. This study was undertaken to determine the impact of various age thresholds on outcome after TBI. Materials and Methods : The ages of patients admitted with TBI were prospectively studied in relation to mode of injury, Glasgow coma score (GCS, CT category and surgical intervention. Mortality was assessed at 1 month, and neurological outcome was assessed at 6 months. Appropriate statistical analyzes (details in article were performed. Results: Of the total 244 patients enrolled, 144 patients had severe, 38 patients had moderate and 62 patients had mild TBI, respectively. Age had significant association with grade of injury, CT category and surgical intervention (P 59 years respectively (P 40 years in all subgroups, based on GCS and surgical intervention (P < 0.05. Conclusions : In patients with TBI, age demonstrates independent association with unfavorable outcome at 6 months, in stepwise manner centered on a threshold of 40 years.

  10. Assessment of impulsivity after moderate to severe traumatic brain injury.

    Science.gov (United States)

    Rochat, Lucien; Beni, Catia; Billieux, Joël; Azouvi, Philippe; Annoni, Jean-Marie; Van der Linden, Martial

    2010-10-01

    The aim of the study was to develop and validate a short questionnaire assessing four dimensions of impulsivity (urgency, lack of premeditation, lack of perseverance, sensation seeking) in patients with traumatic brain injury (TBI). To this end, 82 patients with TBI and their caregivers completed a short questionnaire adapted from the UPPS Impulsive Behavior Scale designed to assess impulsivity changes after TBI. Confirmatory factor analyses (CFAs) performed on the version of the scale completed by the relatives revealed that a hierarchical model holding that lack of premeditation and lack of perseverance are facets of a higher order construct (lack of conscientiousness), with urgency and sensation seeking as separate correlated factors, fit the data best. Urgency, lack of premeditation, and lack of perseverance increased after the TBI, whereas sensation seeking decreased. CFA failed to reveal a satisfactory model in the version of the scale completed by the patients. The psychological processes related to these impulsivity changes and the discrepancy observed between self-report and informant-report are discussed. This short questionnaire opens up interesting prospects for better comprehension and assessment of behavioural symptoms of TBI.

  11. Effect of cocaine use on outcomes in traumatic brain injury

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    Jacky T Yeung

    2013-01-01

    Full Text Available Context: Animal and molecular studies have shown that cocaine exerts a neuroprotective effect against cerebral ischemia. Aims: To determine if the presence of cocaine metabolites on admission following traumatic brain injury (TBI is associated with better outcomes. Settings and Design: Level-1 trauma center, retrospective cohort. Materials and Methods: After obtaining Institutional Review Board (IRB approval, the trauma registry was searched from 2006 to 2009 for all patients aged 15-55 years with blunt head trauma and non-head AIS <3. Exclusion criteria were pre-existing brain pathology and death within 30 min of admission. The primary outcome was in-hospital mortality; secondary outcomes were hospital length of stay (LOS, and Glasgow Outcome Score (GOS. Statistical Analysis: Logistic regression was used to determine the independent effect of cocaine on mortality. Hospital LOS was compared with multiple linear regression. Results: A total of 741 patients met criteria and had drug screens. The screened versus unscreened groups were similar. Cocaine positive patients were predominantly African-American (46% vs. 21%, P < 0.0001, older (40 years vs. 30 years, P < 0.0001, and had ethanol present more often (50.7% vs. 37.8%, P = 0.01. There were no differences in mortality (cocaine-positive 1.4% vs. cocaine-negative 2.7%, P = 0.6 on both univariate and multivariate analysis. Conclusions: Positive cocaine screening was not associated with mortality in TBI. An effect may not have been detected because of the low mortality rate. LOS is affected by many factors unrelated to the injury and may not be a good surrogate for recovery. Similarly, GOS may be too coarse a measure to identify a benefit.

  12. Traumatic brain injury upregulates phosphodiesterase expression in the hippocampus

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    Nicole M Wilson

    2016-02-01

    Full Text Available Traumatic brain injury (TBI results in significant impairments in hippocampal synaptic plasticity. A molecule critically involved in hippocampal synaptic plasticity, 3',5'-cyclic adenosine monophosphate (cAMP, is downregulated in the hippocampus after TBI, but the mechanism that underlies this decrease is unknown. To address this question, we determined whether phosphodiesterase (PDE expression in the hippocampus is altered by TBI. Young adult male Sprague Dawley rats received sham surgery or moderate parasagittal fluid-percussion brain injury. Animals were analyzed by western blotting for changes in PDE expression levels in the hippocampus. We found that PDE1A levels were significantly increased at 30 min, 1 hr and 6 hr after TBI. PDE4B2 and 4D2 were also significantly increased at 1, 6 and 24 hr after TBI. Additionally, phosphorylation of PDE4A was significantly increased at 6 and 24 hr after TBI. No significant changes were observed in levels of PDE1B, 1C, 3A, 8A or 8B between 30 min to 7 days after TBI. To determine the spatial profile of these increases, we used immunohistochemistry and flow cytometry at 24 hr after TBI. PDE1A and phospho-PDE4A localized to neuronal cell bodies. PDE4B2 was expressed in neuronal dendrites, microglia and infiltrating CD11b+ immune cells. PDE4D was predominantly found in microglia and infiltrating CD11b+ immune cells. To determine if inhibition of PDE4 would improve hippocampal synaptic plasticity deficits after TBI, we treated hippocampal slices with rolipram, a pan-PDE4 inhibitor. Rolipram partially rescued the depression in basal synaptic transmission and converted a decaying form of LTP into long-lasting LTP. Overall, these results identify several possible PDE targets for reducing hippocampal synaptic plasticity deficits and improving cognitive dysfunction acutely after TBI.

  13. 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.

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

    OpenAIRE

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

    2009-01-01

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

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

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    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.

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

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

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

  17. Top-cited articles in traumatic brain injury.

    Science.gov (United States)

    Sharma, Bhanu; Lawrence, David Wyndham

    2014-01-01

    A review of the top-cited articles in a scientific discipline can identify areas of research that are well established and those in need of further development, and may, as a result, inform and direct future research efforts. Our objective was to identify and characterize the top-cited articles in traumatic brain injury (TBI). We used publically available software to identify the 50 TBI articles with the most lifetime citations, and the 50 TBI articles with the highest annual citation rates. A total of 73 articles were included in this review, with 27 of the 50 papers with the highest annual citation rates common to the cohort of 50 articles with the most lifetime citations. All papers were categorized by their primary topic or focus, namely: predictor of outcome, pathology/natural history, treatment, guidelines and consensus statements, epidemiology, assessment measures, or experimental model of TBI. The mean year of publication of the articles with the most lifetime citations and highest annual citation rates was 1990 ± 14.9 years and 2003 ± 6.7 years, respectively. The 50 articles with the most lifetime citations typically studied predictors of outcome (34.0%, 17/50) and were specific to severe TBI (38.0%, 19/50). In contrast, the most common subject of papers with the highest annual citation rates was treatment of brain injury (22.0%, 11/50), and these papers most frequently investigated mild TBI (36.0%, 18/50). These findings suggest an intensified focus on mild TBI, which is perhaps a response to the dedicated attention these injuries are currently receiving in the context of sports and war, and because of their increasing incidence in developing nations. Our findings also indicate increased focus on treatment of TBI, possibly due to the limited efficacy of current interventions for brain injury. This review provides a cross-sectional summary of some of the most influential articles in TBI, and a bibliometric examination of the current status of

  18. Cerebral Edema in Traumatic Brain Injury: Pathophysiology and Prospective Therapeutic Targets.

    Science.gov (United States)

    Winkler, Ethan A; Minter, Daniel; Yue, John K; Manley, Geoffrey T

    2016-10-01

    Traumatic brain injury is a heterogeneous disorder resulting from an external force applied to the head. The development of cerebral edema plays a central role in the evolution of injury following brain trauma and is closely associated with neurologic outcomes. Recent advances in the understanding of the molecular and cellular pathways contributing to the posttraumatic development of cerebral edema have led to the identification of multiple prospective therapeutic targets. The authors summarize the pathogenic mechanisms underlying cerebral edema and highlight the molecular pathways that may be therapeutically targeted to mitigate cerebral edema and associated sequelae following traumatic brain injury.

  19. Investigating Metacognition, Cognition, and Behavioral Deficits of College Students with Acute Traumatic Brain Injuries

    Science.gov (United States)

    Martinez, Sarah; Davalos, Deana

    2016-01-01

    Objective: Executive dysfunction in college students who have had an acute traumatic brain injury (TBI) was investigated. The cognitive, behavioral, and metacognitive effects on college students who endorsed experiencing a brain injury were specifically explored. Participants: Participants were 121 college students who endorsed a mild TBI, and 121…

  20. PET Imaging of Mild Traumatic Brain Injury and Whiplash Associated Disorder

    NARCIS (Netherlands)

    Vállez García, David

    2015-01-01

    Traumatic brain injury is the leading cause of brain injury in our society with 235 per 100,000 inhabitants per year in the European Union and about 500 per 100,000 inhabitants per year in the United States. About 80% of all these events are accounted for as mild cases. At the same time, whiplash-as

  1. Neural and Behavioral Sequelae of Blast-Related Traumatic Brain Injury

    Science.gov (United States)

    2012-11-01

    bipolar disorder, schizophrenia ) with the exception of post-traumatic stress disorder (PTSD), penetrating gunshot wound to the brain or contraindications...matter degeneration16, increased levels of mortality, brain edema17, and downregulation of genes associated with hippocampal neurogenesis.18

  2. Functional oral intake and time to reach unrestricted dieting for patients with traumatic brain injury

    DEFF Research Database (Denmark)

    Hansen, Trine S; Engberg, Aase W; Larsen, Klaus

    2008-01-01

    OBJECTIVES: To investigate the status of functional oral intake for patients with severe traumatic brain injury (TBI) and time to return to unrestricted dieting; and to investigate whether severity of brain injury is a predictor for unrestricted dieting. DESIGN: Observational retrospective cohort...... planning rehabilitation, giving information to patients and relatives, and designing efficacy studies of facial oral tract therapy, which are highly recommended....

  3. Treatment of traumatic brain injury in rats with transplantation of human amniotic cells

    Institute of Scientific and Technical Information of China (English)

    LU Yi; HUI Guo-zhen; WU Zhi-yuan; GUO Li-he; JI Xun-he; WU Xin

    2006-01-01

    @@ Traumatic brain injury (TBI), which is an important reason of human mortality and morbidity in industrialized countries, still cannot be treated effectively. Since the self-repair capacity of brain is limited, cellular transplantation in TBI may be a therapeutic option.

  4. Brain core temperature of patients with mild traumatic brain injury as assessed by DWI-thermometry

    Energy Technology Data Exchange (ETDEWEB)

    Tazoe, Jun; Yamada, Kei; Akazawa, Kentaro [Kyoto Prefectural University of Medicine, Department of Radiology, Graduate School of Medical Science, Kyoto City, Kyoto (Japan); Sakai, Koji [Kyoto University, Department of Human Health Science, Graduate School of Medicine, Kyoto (Japan); Mineura, Katsuyoshi [Kyoto Prefectural University of Medicine, Department of Neurosurgery, Graduate School of Medical Science, Kyoto City, Kyoto (Japan)

    2014-10-15

    The aim of this study was to assess the brain core temperature of patients with mild traumatic brain injury (mTBI) using a noninvasive temperature measurement technique based on the diffusion coefficient of the cerebrospinal fluid. This retrospective study used the data collected from April 2008 to June 2011. The patient group comprised 20 patients with a Glasgow Coma Scale score of 14 or 15 who underwent magnetic resonance imaging within 30 days after head trauma. The normal control group comprised 14 subjects who volunteered for a brain checkup (known in Japan as ''brain dock''). We compared lateral ventricular (LV) temperature between patient and control groups. Follow-up studies were performed for four patients. LV temperature measurements were successfully performed for both patients and controls. Mean (±standard deviation) measured LV temperature was 36.9 ± 1.5 C in patients, 38.7 ± 1.8 C in follow-ups, and 37.9 ± 1.2 C in controls, showing a significant difference between patients and controls (P = 0.017). However, no significant difference was evident between patients and follow-ups (P = 0.595) or between follow-ups and controls (P = 0.465). A reduction in brain core temperature was observed in patients with mTBI, possibly due to a global decrease in metabolism. (orig.)

  5. The potential of endogenous neurogenesis for brain repair and regeneration following traumatic brain injur y

    Institute of Scientific and Technical Information of China (English)

    Dong Sun

    2014-01-01

    Traumatic brain injury (TBI) is the leading cause of death and disability of persons under 45 years old in the United States, affecting over 1.5 million individuals each year. It had been th ought that recovery from such injuries is severely limited due to the inability of the adult bra in to replace damaged neurons. However, recent studies indicate that the mature mammalian central nervous system (CNS) has the potential to replenish damaged neurons by proliferation and neuronal differentiation of adult neural stem/progenitor cells residing in the neurogenic regions in the brain. Furthermore, increasing evidence indicates that these endogenous stem/progenitor cells may play regenerative and reparative roles in response to CNS injuries or diseases. In support of this notion, heightened levels of cell proliferation and neurogenesis have been ob-served in response to brain trauma or insults suggesting that the brain has the inherent potential to restore populations of damaged or destroyed neurons. This review will discuss the potential functions of adult neurogenesis and recent development of strategies aiming at harnessing this neurogenic capacity in order to repopulate and repair the injured brain.

  6. Brain activity patterns uniquely supporting visual feature integration after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Anjali eRaja Beharelle

    2011-12-01

    Full Text Available Traumatic brain injury (TBI patients typically respond more slowly and with more variability than controls during tasks of attention requiring speeded reaction time. These behavioral changes are attributable, at least in part, to diffuse axonal injury (DAI, which affects integrated processing in distributed systems. Here we use a multivariate method sensitive to distributed neural activity to compare brain activity patterns of patients with chronic phase moderate-to-severe TBI to those of controls during performance on a visual feature-integration task assessing complex attentional processes that has previously shown sensitivity to TBI. The TBI patients were carefully screened to be free of large focal lesions that can affect performance and brain activation independently of DAI. The task required subjects to hold either one or three features of a target in mind while suppressing responses to distracting information. In controls, the multi-feature condition activated a distributed network including limbic, prefrontal, and medial temporal structures. TBI patients engaged this same network in the single-feature and baseline conditions. In multi-feature presentations, TBI patients alone activated additional frontal, parietal, and occipital regions. These results are consistent with neuroimaging studies using tasks assessing different cognitive domains, where increased spread of brain activity changes was associated with TBI. Our results also extend previous findings that brain activity for relatively moderate task demands in TBI patients is similar to that associated with of high task demands in controls.

  7. Marrow stromal cells administrated intracisternally to rats after traumatic brain injury migrate into the brain and improve neurological function

    Institute of Scientific and Technical Information of China (English)

    胡德志; 周良辅; 朱剑虹

    2004-01-01

    @@ Marrow stromal cells(MSCs) have been reported to transplant into injured brain via intravenous or intraarterial or direct intracerebral administration.1-3 In the present study, we observed that MSCs migrated into the brain, survived and diffeneriated into neural cells after they were injected into the cisterna magna of rats, and that the behavior of the rats after traumatic brain injury (TBI) was improved.

  8. 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.

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

    Science.gov (United States)

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

    2015-01-01

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

  10. Repetitive Traumatic Brain Injury in Patients From Kashan, Iran

    Directory of Open Access Journals (Sweden)

    Fakharian

    2016-05-01

    Full Text Available Background Traumatic brain injury (TBI is a worldwide problem, especially in countries with high incidence of road traffic accidents such as Iran. Patients with a single occurrence of TBI have been shown to be at increased risk to sustain future TBI. Objectives The aim of this study was to present the incidence and characteristics of repeated TBI (RTBI in Iranian patients. Patients and Methods During one year, all admitted TBI patients with prior TBI history were enrolled into the study. In each patient, data such as age, gender, past medical history, injury cause, anatomic site of injury, TBI severity, clinical findings and CT scan findings were collected. Results RTBI comprised 2.5% of TBI cases (41 of 1629. The incidence of RTBI per 100,000 individuals per years was 9.7. The main cause of RTBI was road traffic accident (68.3%; 9.7 % of cases had preexisting seizure/epilepsy disorder; 36.6% of patients with RTBI had pervious ICU admission due to severe TBI. Ten patients had Glasgow coma scale (GCS ≤ 13 (24.4%. Seizure was seen in seven patients (17.1%. Thirty-nine percent of patients with RTBI had associated injuries. Eleven patients had abnormal CT scan findings (26.9%. Conclusions Considering the high incidence of trauma in developing countries, RTBI may also be more common compared with that of developed countries. This mandates a newer approach to preventive strategies, particularly in those with a previous experience of head injury.

  11. Pharmacological treatment of neurobehavioural sequelae of traumatic brain injury.

    Science.gov (United States)

    Lombardi, F

    2008-01-01

    Neurobehavioural sequelae of traumatic brain injuries require an appropriate/effective pharmacological response in that they represent an important cause of disability. In this field, there is no evidence that reaches the level of a standard: there are guidelines on the use of methylphenidate, donepezil and bromocriptine for the treatment of cognitive disturbances, for the non-use of phenytoin and for the use of beta-blockers for controlling aggressiveness. Resolving a single symptom is not relevant in a rehabilitation project if it is not in the context of a more complex picture of neurobehavioural recovery, in which the positive and negative effects of every therapeutic choice are considered. For example, phenytoin could be used for the positive control of epileptic crises but is not advised since it impedes the recovery of cognitive functions in general. Analogous effects not yet identified may concern benzodiazepine, neuroleptics and other sedatives usually prescribed in cases of cranial trauma. Psychotropic drugs are considered to be able to influence the neuronal plasticity processes. Studies on animals have shown that the administration of D-amphetamine combined with sensorial-motor exercise produces the steady acceleration of motor recovery, which acts as a catalyst to the neurological recovery process. On the other hand, alpha1-NA receptor antagonist drugs produce negative effects; these include clonidine (antihypertension) and haloperidol (neuroleptic). Studies need to be carried out to evaluate the effectiveness of particular drugs. These studies need to focus not only on the disappearance of symptoms but also on the positive and negative effects on overall rehabilitation and on the neurobiological recovery of the patient.

  12. GH and Pituitary Hormone Alterations After Traumatic Brain Injury.

    Science.gov (United States)

    Karaca, Züleyha; Tanrıverdi, Fatih; Ünlühızarcı, Kürşad; Kelestimur, Fahrettin

    2016-01-01

    Traumatic brain injury (TBI) is a crucially important public health problem around the world, which gives rise to increased mortality and is the leading cause of physical and psychological disability in young adults, in particular. Pituitary dysfunction due to TBI was first described 95 years ago. However, until recently, only a few papers have been published in the literature and for this reason, TBI-induced hypopituitarism has been neglected for a long time. Recent studies have revealed that TBI is one of the leading causes of hypopituitarism. TBI which causes hypopituitarism may be characterized by a single head injury such as from a traffic accident or by chronic repetitive head trauma as seen in combative sports including boxing, kickboxing, and football. Vascular damage, hypoxic insult, direct trauma, genetic predisposition, autoimmunity, and neuroinflammatory changes may have a role in the development of hypopituitarism after TBI. Because of the exceptional structure of the hypothalamo-pituitary vasculature and the special anatomic location of anterior pituitary cells, GH is the most commonly lost hormone after TBI, and the frequency of isolated GHD is considerably high. TBI-induced pituitary dysfunction remains undiagnosed and therefore untreated in most patients because of the nonspecific and subtle clinical manifestations of hypopituitarism. Treatment of TBI-induced hypopituitarism depends on the deficient anterior pituitary hormones. GH replacement therapy has some beneficial effects on metabolic parameters and neurocognitive dysfunction. Patients with TBI without neuroendocrine changes and those with TBI-induced hypopituitarism share the same clinical manifestations, such as attention deficits, impulsion impairment, depression, sleep abnormalities, and cognitive disorders. For this reason, TBI-induced hypopituitarism may be neglected in TBI victims and it would be expected that underlying hypopituitarism would aggravate the clinical picture of TBI

  13. Epidemiology and clinical characteristics of traumatic brain injury in Lebanon

    Science.gov (United States)

    Abou-Abbass, Hussein; Bahmad, Hisham; Ghandour, Hiba; Fares, Jawad; Wazzi-Mkahal, Rayyan; Yacoub, Basel; Darwish, Hala; Mondello, Stefania; Harati, Hayat; El Sayed, Mazen J.; Tamim, Hani; Kobeissy, Firas

    2016-01-01

    Abstract Background: Traumatic brain injury (TBI) is a debilitating medical and emerging public health problem that is affecting people worldwide due to a multitude of factors including both domestic and war-related acts. The objective of this paper is to systematically review the status of TBI in Lebanon – a Middle Eastern country with a weak health system that was chartered by several wars and intermittent outbursts of violence - in order to identify the present gaps in knowledge, direct future research initiatives and to assist policy makers in planning progressive and rehabilitative policies. Methods: OVID/Medline, PubMed, Scopus databases and Google Scholar were lastly searched on April 15th, 2016 to identify all published research studies on TBI in Lebanon. Studies published in English, Arabic or French that assessed Lebanese patients afflicted by TBI in Lebanon were warranting inclusion in this review. Case reports, reviews, biographies and abstracts were excluded. Throughout the whole review process, reviewers worked independently and in duplicate during study selection, data abstraction and methodological assessment using the Downs and Black Checklist. Results: In total, 11 studies were recognized eligible as they assessed Lebanese patients afflicted by TBI on Lebanese soils. Considerable methodological variation was found among the identified studies. All studies, except for two that evaluated domestic causes such as falls, reported TBI due to war-related injuries. Age distribution of TBI victims revealed two peaks, young adults between 18 and 40 years, and older adults aged 60 years and above, where males constituted the majority. Only three studies reported rates of mild TBI. Mortality, rehabilitation and systemic injury rates were rarely reported and so were the complications involved; infections were an exception. Conclusion: Apparently, status of TBI in Lebanon suffers from several gaps which need to be bridged through implementing more basic

  14. Phenytoin toxicity in patients with traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Ananth P Abraham

    2014-01-01

    Full Text Available Background: We observed that in patients with traumatic brain injury (TBI who did not improve as expected, serum levels of phenytoin were in the toxic range and that their sensorium improved with modification of the dose. This led us to study the usage of phenytoin in patients with TBI. Aims: To determine the prevalence of phenytoin toxicity in TBI patients and to study the suitability of using ideal body weight (IBW to guide phenytoin dosing. Setting and Design: Neurotrauma unit of a tertiary care centre in India. Prospective data collection from an already established protocol of drug level monitoring. Materials and Methods: The study cohort included 100 consecutive adult patients with mild or moderate TBI who were administered phenytoin based on IBW. Trough serum phenytoin and albumin levels were measured on day 4 after administration of the loading dose and actual body weight obtained when it was possible. Statistical Analysis: Chi-square was used for comparing categorical variables, student′s t-test for continuous variables and multivariate regression analysis to obtain independent risk factors. Results: Clinical toxicity was observed in 15% of patients and biochemical toxicity in 36%, with a significant association between the two (P < 0.01. Using multivariate analysis, abdominal girth ≤75 cm (P = 0.07, neck circumference ≤34 cm (P = 0.025 and IV dose proportion ≥80% (P = 0.003 were independent risk factors for biochemical toxicity. The plot between actual weight and IBW showed that toxicity occurred when IBW was higher than actual weight. Conclusion: The prevalence of biochemical phenytoin toxicity was high, with independent risk factors being a higher proportion of IV administration and overestimation of weight by IBW. Clinical suspicion of phenytoin toxicity was a good predictor of biochemical toxicity.

  15. Spironolactone in preventing hypokalemia following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Saeid Abrishamkar; Mehdi Shafiei; Mohammad Shafiei

    2010-01-01

    Objective: Hypokalemia is a frequent complication observed after traumatic brain injury (TBI).We evaluated the effect of spironolactone on preventing hypokalemia following moderate to severe TBI.Methods: Patients with moderate to severe TBI, whose Glasgow Coma Scale (GCS) scores of 9-12 and <9,respectively, were equally randomized into intervention and control groups, matching with severity of trauma and baseline serum level of potassium. For the intervention group, we administrated spironolactone (1 mg/kg per day)on the second day of admission or the first day of gavage tolerance and continued it for seven days. No additional intervention was done for controls. Hypokalemia (mild: 3-3.5 mg/L, moderate: 2.5-3 mg/L, and severe: <2.5 mg/L serum K+) and other electrolyte abnormalities were compared between the two groups at the end of the intervention.Results: Sixty-eight patients (58 males and 10 females)were included with mean age=(33.1±11.8) years, and GCS=7.6±2.8. The two groups were similar in baseline characteristics.Patients who received spironolactone were significantly less likely to experience mild, moderate, or severe hypokalemia (8.8%, 2.9%, and 0) compared with controls (29.4%, 11.7%,and 2.9%, respectively, P<0.05). No significant difference was observed between the two groups in the occurrence of other electrolyte abnormalities, hyperglycemia or oliguria.Conclusion: Spironolactone within the first week of head injury could prevent the occurrence of late hypokalemia with no severe side effects.

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

    Institute of Scientific and Technical Information of China (English)

    Jindou Jiang; Xingyao Bu; Meng Liu; Peixun Cheng

    2012-01-01

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

  17. PHIT for Duty, a Personal Health Intervention Tool for Psychological Health and Traumatic Brain Injury

    Science.gov (United States)

    2015-04-01

    this task was performed this year. 2 2.2. Task 2: Prototype design and development 2.2.1. The Personal Health Information Tool architecture The PHIT...Award Number: W81XWH-11-2-0129 TITLE: PHIT for Duty, a Personal Health Intervention Tool for Psychological Health and Traumatic Brain Injury...TITLE AND SUBTITLE 5a. CONTRACT NUMBER W81XWH-11-2-0129 PHIT for Duty, a Personal Health Intervention Tool for Psychological Health and Traumatic

  18. Mechanism and Therapy for the Shared Susceptibility to Migraine and Epilepsy after Traumatic Brain Injury (TBI)

    Science.gov (United States)

    2013-10-01

    Implementation of post- TBI pain behavior measurements. 15. SUBJECT TERMS Traumatic brain injury, cortical spreading depression, seizure, post-traumatic...conventional recovery is complete. We test with video EEG monitoring for increased excitability, and use behavioral measures to test the pain response...months after CCI TBI (Brennan/Dudek, Months 18-36). Pending. Will be performed simultaneous with task 1.f. above. g. Perform nociception

  19. Mismatch negativity, social cognition, and functional outcomes in patients after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Hui-yan Sun

    2015-01-01

    Full Text Available Mismatch negativity is generated automatically, and is an early monitoring indicator of neuronal integrity impairment and functional abnormality in patients with brain injury, leading to decline of cognitive function. Antipsychotic medication cannot affect mismatch negativity. The present study aimed to explore the relationships of mismatch negativity with neurocognition, daily life and social functional outcomes in patients after brain injury. Twelve patients with traumatic brain injury and 12 healthy controls were recruited in this study. We examined neurocognition with the Wechsler Adult Intelligence Scale-Revised China, and daily and social functional outcomes with the Activity of Daily Living Scale and Social Disability Screening Schedule, respectively. Mismatch negativity was analyzed from electroencephalogram recording. The results showed that mismatch negativity amplitudes decreased in patients with traumatic brain injury compared with healthy controls. Mismatch negativity amplitude was negatively correlated with measurements of neurocognition and positively correlated with functional outcomes in patients after traumatic brain injury. Further, the most significant positive correlations were found between mismatch negativity in the fronto-central region and measures of functional outcomes. The most significant positive correlations were also found between mismatch negativity at the FCz electrode and daily living function. Mismatch negativity amplitudes were extremely positively associated with Social Disability Screening Schedule scores at the Fz electrode in brain injury patients. These experimental findings suggest that mismatch negativity might efficiently reflect functional outcomes in patients after traumatic brain injury.

  20. Mismatch negativity, social cognition, and functional outcomes in patients after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Hui-yan Sun; Qiang Li; Xi-ping Chen; Lu-yang Tao

    2015-01-01

    Mismatch negativity is generated automatically, and is an early monitoring indicator of neuronal integrity impairment and functional abnormality in patients with brain injury, leading to decline of cognitive function. Antipsychotic medication cannot affect mismatch negativity. The present study aimed to explore the relationships of mismatch negativity with neurocognition, daily life and social functional outcomes in patients after brain injury. Twelve patients with traumatic brain injury and 12 healthy controls were recruited in this study. We examined neurocogni-tion with the Wechsler Adult Intelligence Scale-Revised China, and daily and social functional outcomes with the Activity of Daily Living Scale and Social Disability Screening Schedule, re-spectively. Mismatch negativity was analyzed from electroencephalogram recording. The results showed that mismatch negativity amplitudes decreased in patients with traumatic brain injury compared with healthy controls. Mismatch negativity amplitude was negatively correlated with measurements of neurocognition and positively correlated with functional outcomes in patients after traumatic brain injury. Further, the most signiifcant positive correlations were found be-tween mismatch negativity in the fronto-central region and measures of functional outcomes. The most signiifcant positive correlations were also found between mismatch negativity at the FCz electrode and daily living function. Mismatch negativity amplitudes were extremely positive-ly associated with Social Disability Screening Schedule scores at the Fz electrode in brain injury patients. These experimental ifndings suggest that mismatch negativity might efifciently relfect functional outcomes in patients after traumatic brain injury.

  1. Traumatic brain injury alters methionine metabolism: implications for pathophysiology

    Directory of Open Access Journals (Sweden)

    Pramod K Dash

    2016-04-01

    Full Text Available Methionine is an essential proteinogenic amino acid that is obtained from the diet. In addition to its requirement for protein biosynthesis, methionine is metabolized to generate metabolites that play key roles in a number of cellular functions. Metabolism of methionine via the transmethylation pathway generates S-adenosylmethionine (SAM that serves as the principal methyl (-CH3 donor for DNA and histone methyltransferases to regulate epigenetic changes in gene expression. SAM is also required for methylation of other cellular proteins that serve various functions and phosphatidylcholine synthesis that participate in cellular signaling.. Under conditions of oxidative stress, homocysteine (which is derived from SAM enters the transsulfuration pathway to generate glutathione, an important cytoprotective molecule against oxidative damage. As both experimental and clinical studies have shown that traumatic brain injury (TBI alters DNA and histone methylation and causes oxidative stress, we examined if TBI alters the plasma levels of methionine and its metabolites in human patients. Blood samples were collected from healthy volunteers (n = 20 and patients with mild TBI (GCS > 12; n = 20 or severe TBI (GCS < 8; n = 20 within the first 24 hours of injury. The levels of methionine and its metabolites in the plasma samples were analyzed by either liquid chromatography-mass spectrometry or gas chromatography-mass spectrometry (LC-MS or GC-MS. Severe TBI decreased the levels of methionine, SAM, betaine and 2-methylglycine as compared to healthy volunteers, indicating a decrease in metabolism through the transmethylation cycle. In addition, precursors for the generation of glutathione, cysteine and glycine were also found to be decreased as were intermediate metabolites of the gamma-glutamyl cycle (gamma-glutamyl amino acids and 5-oxoproline. Mild TBI also decreased the levels of methionine, α-ketobutyrate, 2 hydroxybutyrate and glycine, albeit to lesser

  2. Neurotherapy for chronic headache following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    David V Nelson; Mary Lee Esty

    2015-01-01

    Background:Chronic headache following traumatic brain injury (TBI) sustained in military service, while common, is highly challenging to treat with existing pharmacologic and non-pharmacologic interventions, and it may be complicated by co-morbid posttraumatic stress. Recently, a novel form of brainwave-based intervention known as the Flexyx Neurotherapy System (FNS), which involves minute pulses of electromagnetic energy stimulation of brainwave activity, has been suggested as a means to address symptoms of TBI. This study reports on a clinical series of patients with chronic headache following service-connected TBI treated with FNS. Methods: Nine veterans of the wars in Afghanistan and Iraq with moderate to severe chronic headaches following service-connected TBI complicated by posttraumatic stress symptoms were treated in 20 individual FNS sessions at the Brain Wellness and Biofeedback Center of Washington (in Bethesda, Maryland, USA). They periodically completed measures including the Brief Pain Inventory-Headache (BPI-HA), previous week worst and average pain ratings, the Posttraumatic Stress Disorder Checklist-Military version (PCL-M), and an individual treatment session numerical rating scale (NRS) for the degree of cognitive dysfunction. Data analyses included beginning-to-end of treatmentt-test comparisons for the BPI-HA, PCL-M, and cognitive dysfunction NRS. Results: All beginning-to-end of treatmentt-test comparisons for the BPI-HA, PCL-M, and cognitive dysfunction NRS indicated statistically significant decreases. All but one participant experienced a reduction in headaches along with reductions in posttraumatic stress and perceived cognitive dysfunction, with a subset experiencing the virtual elimination of headaches. One participant obtained modest headache relief but no improvements in posttraumatic stress or cognitive dysfunction. Conclusions: FNS may be a potentially efficacious treatment for chronic posttraumatic headache sustained in military

  3. Influence of post-traumatic stress disorder on neuroinflammation and cell proliferation in a rat model of traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Sandra A Acosta

    Full Text Available Long-term consequences of traumatic brain injury (TBI are closely associated with the development of severe psychiatric disorders, such as post-traumatic stress disorder (PTSD, yet preclinical studies on pathological changes after combined TBI with PTSD are lacking. In the present in vivo study, we assessed chronic neuroinflammation, neuronal cell loss, cell proliferation and neuronal differentiation in specific brain regions of adult Sprague-Dawley male rats following controlled cortical impact model of moderate TBI with or without exposure to PTSD. Eight weeks post-TBI, stereology-based histological analyses revealed no significant differences between sham and PTSD alone treatment across all brain regions examined, whereas significant exacerbation of OX6-positive activated microglial cells in the striatum, thalamus, and cerebral peduncle, but not cerebellum, in animals that received TBI alone and combined TBI-PTSD compared with PTSD alone and sham treatment. Additional immunohistochemical results revealed a significant loss of CA3 pyramidal neurons in the hippocampus of TBI alone and TBI-PTSD compared to PTSD alone and sham treatment. Further examination of neurogenic niches revealed a significant downregulation of Ki67-positive proliferating cells, but not DCX-positive neuronally migrating cells in the neurogenic subgranular zone and subventricular zone for both TBI alone and TBI-PTSD compared to PTSD alone and sham treatment. Comparisons of levels of neuroinflammation and neurogenesis between TBI alone and TBI+PTSD revealed that PTSD did not exacerbate the neuropathological hallmarks of TBI. These results indicate a progressive deterioration of the TBI brain, which, under the conditions of the present approach, was not intensified by PTSD, at least within our time window and within the examined areas of the brain. Although the PTSD manipulation employed here did not exacerbate the pathological effects of TBI, the observed long

  4. Loss of PAFR prevents neuroinflammation and brain dysfunction after traumatic brain injury

    Science.gov (United States)

    Yin, Xiang-Jie; Chen, Zhen-Yan; Zhu, Xiao-Na; Hu, Jin-Jia

    2017-01-01

    Traumatic brain injury (TBI) is a principal cause of death and disability worldwide, which is a major public health problem. Death caused by TBI accounts for a third of all damage related illnesses, which 75% TBI occurred in low and middle income countries. With the increasing use of motor vehicles, the incidence of TBI has been at a high level. The abnormal brain functions of TBI patients often show the acute and long-term neurological dysfunction, which mainly associated with the pathological process of malignant brain edema and neuroinflammation in the brain. Owing to the neuroinflammation lasts for months or even years after TBI, which is a pivotal causative factor that give rise to neurodegenerative disease at late stage of TBI. Studies have shown that platelet activating factor (PAF) inducing inflammatory reaction after TBI could not be ignored. The morphological and behavioral abnormalities after TBI in wild type mice are rescued by general knockout of PAFR gene that neuroinflammation responses and cognitive ability are improved. Our results thus define a key inflammatory molecule PAF that participates in the neuroinflammation and helps bring about cerebral dysfunction during the TBI acute phase. PMID:28094295

  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. Myocardial function at the early phase of traumatic brain injury: a prospective controlled study

    OpenAIRE

    Cuisinier, Adrien; Maufrais, Claire; Payen, Jean-François; Nottin, Stephane; Walther, Guillaume; Bouzat, Pierre

    2016-01-01

    Background The concept of brain-heart interaction has been described in several brain injuries. Traumatic brain injury (TBI) may also lead to cardiac dysfunction but evidences are mainly based upon experimental and clinical retrospective studies. Methods We conducted a prospective case-control study in a level I trauma center. Twenty consecutive adult patients with severe TBI were matched according to age and gender with 20 control patients. The control group included adult patients undergoin...

  7. Investigation of Chronic Pain Following Traumatic Brain Injury

    Science.gov (United States)

    2014-03-01

    to those in other chronic pain states such as migraine and fibromyalgia when controlled for co-morbid insomnia, depression and PTSD. The study groups...to be compared for this work include patients with chronic migraine, fibromyalgia , post-traumatic pain post mTBI, asymptomatic individuals post mTBI...migraine, fibromyalgia , post-traumatic pain post mTBI, asymptomatic individuals post mTBI, and normal controls. The understanding of the

  8. 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.

  9. Evaluation of hyperbaric oxygen treatment of neuropsychiatric disorders following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    SHI Xiao-yan; TANG Zhong-quan; SUN Da; HE Xiao-jun

    2006-01-01

    Background Improvement of clinical symptoms following hyperbaric oxygen (HBO) treatment of neuropsychiatric disorders arising from traumatic brain injury was proved by our previous study. This study was aim to obtain the evidence of other changes.Methods Three hundred and ten patients with neuropsychiatric disorders arising from traumatic brain injury were treated twice with hyperbaric oxygen. Cerebral single photon emissions computed tomography (SPECT)images and computed tomography scans (CT) before and after hyperbaric oxygen treatment, were compared.Results Before treatment, the proportion of abnormal cerebral changes detected by SPECT was 81.3% but only 15.2% by CT. After HBO treatment, 70.3% of SPECT scans showed no abnormalities and these patients were clinically improved. Treatment improved regional cerebral blood flow.Conclusion SPECT was much more sensitive than CT in the diagnosis of neuropsychiatric disorders following hyperbaric oxygen treatment of neuropsychiatric disorders arising from traumatic brain injury.

  10. Analysis on the risk factors of intracranial infection secondary to traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Chao Lin; Xin Zhao; Haichen Sun

    2015-01-01

    Objective: To discuss the characteristics and risk factors for intracranial infection post traumatic brain injury to prevent and better the clinical care.Methods: Retrospective study of 520 patients with traumatic brain injury were included, 308 male and 212 female.The risky factors of intracranial infection were identified.Results: Thirty two cases (6.54%, 32/520) of intracranial infection were diagnosed.Intracranial infection most likely happened 4-10 days after injury.Cerebrospinal fluid leakage, drainage, multiple craniotomies were significant related to intracranial infection.Logistic regression predicted cerebrospinal fluid leakage and drainage as independent factors.Conclusion: Intracranial infection is a serious complication after traumatic brain injury.Patients with drainage or cerebrospinal fluid leakage are more risky for intracranial infection.Aggressive precaution should be taken to better outcome.

  11. Severe Traumatic Brain Injury, Frontal Lesions, and Social Aspects of Language Use: A Study of French-Speaking Adults

    Science.gov (United States)

    Dardier, Virginie; Bernicot, Josie; Delanoe, Anaig; Vanberten, Melanie; Fayada, Catherine; Chevignard, Mathilde; Delaye, Corinne; Laurent-Vannier, Anne; Dubois, Bruno

    2011-01-01

    The purpose of this study was to gain insight into the social (pragmatic) aspects of language use by French-speaking individuals with frontal lesions following a severe traumatic brain injury. Eleven participants with traumatic brain injury performed tasks in three areas of communication: production (interview situation), comprehension (direct…

  12. Traumatic Brain Injury: General Information. Fact Sheet Number 18 = Lesion Cerebral: Informacion General. Fact Sheet Number 18.

    Science.gov (United States)

    National Information Center for Children and Youth with Disabilities, Washington, DC.

    This fact sheet offers general information about traumatic brain injury. Information includes a definition, incidence, individual characteristics, and educational implications. The fact sheet notes that the designation of traumatic brain injury as a separate category of disability signals that schools should provide children and youth with access…

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

    Directory of Open Access Journals (Sweden)

    Byrnes Kimberly R

    2012-02-01

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

  14. Diagnostic confirmation of mild traumatic brain injury by diffusion tensor imaging: a case report

    Directory of Open Access Journals (Sweden)

    Krishna Ranga

    2012-02-01

    Full Text Available Abstract Introduction Traumatic brain injury is a form of acquired brain injury that results from sudden trauma to the head. Specifically, mild traumatic brain injury is a clinical diagnosis that can have significant effects on an individual's life, yet is difficult to identify through traditional imaging techniques. Case presentation This is the case of a 68-year-old previously healthy African American woman who was involved in a motor vehicle accident that resulted in significant head trauma. After the accident, she experienced symptoms indicative of mild traumatic brain injury and sought a neurological consultation when her symptoms did not subside. She was initially evaluated with a neurological examination, psychological evaluation, acute concussion evaluation and a third-party memory test using software from CNS Vital Signs for neurocognitive function. A diagnosis of post-concussion syndrome was suggested. Diffusion tensor imaging revealed decreased fractional anisotropy in the region immediately adjacent to both lateral ventricles, which was used to confirm the diagnosis. Fractional anisotropy is a scalar value between zero and one that describes the degree of anisotropy of a diffusion process. These results are indicative of post-traumatic gliosis and are undetectable by magnetic resonance imaging. Our patient was treated with cognitive therapy. Conclusion Minor traumatic brain injury is a common injury with variable clinical presentation. The system of diagnosis used in this case found a significant relationship between the clinical assessment and imaging results. This would not have been possible using traditional imaging techniques and highlights the benefits of using diffusion tensor imaging in the sub-acute assessment of minor traumatic brain injury.

  15. 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.

  16. Targeting Epigenetic Mechanisms in Pain Due to Trauma and Traumatic Brain Injury (TBI)

    Science.gov (United States)

    2015-10-01

    Pain  ( nociceptive ) sensitization was followed using the von Frey method. Those measures were continued until  the resolution of sensitization. We...AWARD NUMBER: W81XWH-14-1-0579 TITLE: Targeting Epigenetic Mechanisms in Pain due to Trauma and Traumatic Brain Injury (TBI) PRINCIPAL...SUBTITLE Targeting Epigenetic Mechanisms in Pain due to Trauma and Traumatic Brain Injury (TBI) 5a. CONTRACT NUMBER 5b. GRANT NUMBER W81XWH-14-1-0579 5c

  17. Traumatic brain injury: unmet support needs of caregivers and families in Florida.

    Science.gov (United States)

    Dillahunt-Aspillaga, Christina; Jorgensen-Smith, Tammy; Ehlke, Sarah; Sosinski, Melanie; Monroe, Douglas; Thor, Jennifer

    2013-01-01

    Sustaining a Traumatic Brain Injury results in familial strain due to the significant impact the injury has upon the role and function of individuals and their families at home and in the community. Using the Stress Process Model of Caregiving, a caregiver needs assessment survey was developed and conducted to better understand the needs of individuals with a Traumatic Brain Injury and their caregivers. Survey results indicate that caregivers experience many challenges including unmet needs in areas of relational supports such as maintaining relationships, long-term emotional and financial support for themselves and the survivor, and the need for a patient or caregiver advocate. Implications for future practice are presented.

  18. Association of Symptoms Following Mild Traumatic Brain Injury With Posttraumatic Stress Disorder vs Postconcussion Syndrome

    DEFF Research Database (Denmark)

    Lagarde, E.; Salmi, L. R.; Holm, L. W.

    2014-01-01

    IMPORTANCE A proportion of patients experience long-lasting symptoms following mild traumatic brain injury (MTBI). The postconcussion syndrome (PCS), included in the DSM-IV, has been proposed to describe this condition. Because these symptoms are subjective and common to other conditions, there i......IMPORTANCE A proportion of patients experience long-lasting symptoms following mild traumatic brain injury (MTBI). The postconcussion syndrome (PCS), included in the DSM-IV, has been proposed to describe this condition. Because these symptoms are subjective and common to other conditions...

  19. Cranial findings and iatrogenesis from craniosacral manipulation in patients with traumatic brain syndrome.

    Science.gov (United States)

    Greenman, P E; McPartland, J M

    1995-03-01

    Craniosacral findings were recorded for all patients with traumatic brain injury entering an outpatient rehabilitation program between 1978 and 1992. The average cranial rhythmic impulse was low in all 55 patients (average, 7.2 c/min). At least one cranial strain pattern was exhibited by 95%, and 87% had one or more bony motion restrictions. Sacral findings were similar to those in patients with low back pain. Although craniosacral manipulation has been found empirically useful in patients with traumatic brain injury, three cases of iatrogenesis occurred. The incidence rate is low (5%), but the practitioner must be prepared to deal with the possibility of adverse reactions.

  20. A rapid lateral fluid percussion injury rodent model of traumatic brain injury and post-traumatic epilepsy.

    Science.gov (United States)

    Hameed, Mustafa Q; Goodrich, Grant S; Dhamne, Sameer C; Amandusson, Asa; Hsieh, Tsung-Hsun; Mou, Danlei; Wang, Yingpeng; Rotenberg, Alexander

    2014-05-07

    Traumatic brain injury is a leading cause of acquired epilepsy. Initially described in 1989, lateral fluid percussion injury (LFPI) has since become the most extensively used and well-characterized rodent traumatic brain injury and post-traumatic epilepsy model. Universal findings, particularly seizures that reliably develop after an initial latent period, are evident across studies from multiple laboratories. However, the LFPI procedure is a two-stage process, requiring initial surgical attachment of a skull fluid cannula and then reanesthesia for delivery of the epidural fluid pressure wave. We now describe a modification of the original technique, termed 'rapid lateral fluid percussion injury' (rLFPI), which allows for a one-stage procedure and thus shorter operating time and reduced anesthesia exposure. Anesthetized male Long-Evans rats were subjected to rLFPI through a length of plastic tubing fitted with a pipette tip cannula with a 4-mm aperture. The cannula opening was positioned over a craniectomy of slightly smaller diameter and exposed dura such that the edges of the cannula fit tightly when pressed to the skull with a micromanipulator. Fluid percussion was then delivered immediately thereafter, in the same surgery session. rLFPI resulted in nonlethal focal cortical injury in all animals. We previously demonstrated that the rLFPI procedure resulted in post-traumatic seizures and regional gliosis, but had not examined other histopathologic elements. Now, we show apoptotic cell death confined to the perilesional cortex and chronic pathologic changes such as ipsilesional ventriculomegaly that are seen in the classic model. We conclude that the rLFPI method is a viable alternative to classic LFPI, and--being a one-stage procedure--has the advantage of shorter experiment turnaround and reduced exposure to anesthetics.

  1. Genetic vulnerability following traumatic brain injury: the role of apolipoprotein E.

    Science.gov (United States)

    Nathoo, N; Chetty, R; van Dellen, J R; Barnett, G H

    2003-06-01

    Apolipoprotein E (APOE) is thought to be responsible for the transportation of lipids within the brain, maintaining structural integrity of the microtubule within the neurone, and assisting with neural transmission. Possession of the APOE epsilon4 allele has also been shown to influence neuropathological findings in patients who die from traumatic brain injury, including the accumulation of amyloid beta protein. Previous clinical studies reporting varying outcome severities of traumatic brain injury, including cognitive and functional recovery, all support the notion that APOE epsilon4 allele possession is associated with an unfavourable outcome. Evidence from experimental and clinical brain injury studies confirms that APOE plays an important role in the response of the brain to injury.

  2. [Deep Vein Thrombosis Prophylaxis in Patients with Traumatic Brain Injury].

    Science.gov (United States)

    Silva, Vinícius Trindade Gomes da; Iglesio, Ricardo; Paiva, Wellingson Silva; Siqueira, Mario Gilberto; Teixeira, Manoel Jacobsen

    2015-01-01

    Introdução: O risco de trombose venosa profunda encontra-se aumentado em doentes vítimas de traumatismo cranioencefálico, mas a profilaxia da trombose venosa profunda se confronta com o possível risco de piora de lesões hemorrágicas relacionados ao traumatismo cranioencefálico. Neste artigo apresentamos uma revisão crítica do tema e propomos um protocolo de profilaxia para estes doentes.Material e Métodos: Foi realizada uma pesquisa na base de dados Medline/PubMed, Cochrane, e Scielo de janeiro de 1998 a janeiro de 2014 com a expressão de busca âÄúdeep venous thrombosis and prophylaxis and traumatic brain injuryâÄù. Foram encontrados 44 artigos usando os termos MeSH definidos. Destes foram selecionados 23 artigos, usando como critérios: publicação em inglês ou português, fase aguda do traumatismo cranioencefálico moderado e grave, profilaxia mecânica não invasiva ou química.Resultados: O traumatismo cranioencefálico é um fator de risco para trombose venosa profunda e tromboembolismo pulmonar. A chance de trombose venosa profunda é 2,59 vezes maior em doentes com traumatismo cranioencefálico. A prevalência de trombose venosa profunda e embolia pulmonar em doentes que sofreram traumatismo cranioencefálico é de 20%, podendo atingir 30% dos doentes em alguns estudos.Discussão e Conclusão: As diversas formas de traumatismo de forma isolada constituem fator de risco para trombose venosa profunda e tromboembolismo pulmonar. Ensaios clínicos são necessários para estabelecer a eficácia da profilaxia e o melhor momento de iniciar medicação para trombose venosa profunda em doentes com traumatismo craniencefálico.

  3. 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

  4. Preclinical care of children with traumatic brain injury (TBI

    Directory of Open Access Journals (Sweden)

    Sefrin, Peter

    2004-03-01

    Full Text Available The fact that injuries caused by accidents are the most common cause of death in children and adolescents in Germany gave rise to the study, which mainly deals with traffic accidents in this group. 200,221 records of emergency-service physicians in Bavaria which cover the period 1995-1999 were analysed with respect to the importance of traumatic brain injury (TBI in children and adolescents (n = 721 - representing 45.8% of traffic injuries in this age group. The highest incidence of TBI was in summer (34.3% and in the evening between 16.00 and 18.00 (23.7%. The time taken between accident and arrival of the emergency services was 8.8 ± 3.1 minutes. The preclinical phase lasted 19.3 ± 5.8 minutes. The probability of having an accident with TBI increases with age, the maximum being in the age-range 7 - 14 years (61.6%. Boys (63.2% were almost twice as susceptible to injury as girls. 36.8% of all cases had no noticeable neurological disorder, 71.1% resulted in a Glasgow Coma Scale (GCS score of 15. Only 6.3% had most severe neurological disorders, resulting in a GCS score of 3 - 5. Circulation parameters in the form of adapted hypotension were abnormal in only 3.4%, 21.9% of the children had a bradycardia and in 12.3% the blood oxygen saturation fell below 94%. The most frequent intervention was the laying of an i.v. line for infusions. 8.6% of the patients were intubated to allow for ventilation with oxygen. Analgesics were given in 16.7% of the cases. In 84.7% of all cases, the condition was stable and in only 3.3% was a severe deterioration to be observed. The assessments were made using both the National Advisory Committee for Aeronautics (NACA and Glasgow Coma Scales (GCS. Discrepancies occurred, as a NACA scale of I - III and a GCS score of < 9 was reported in 4.9% of cases. In contrast a NACA scale of IV - VI was reported with a GCS score of 15 in 30% of all cases. TBI symptoms in children are less obvious than in adults, which leads to an

  5. Energy Drinks, Alcohol, Sports and Traumatic Brain Injuries among Adolescents.

    Directory of Open Access Journals (Sweden)

    Gabriela Ilie

    Full Text Available The high prevalence of traumatic brain injuries (TBI among adolescents has brought much focus to this area in recent years. Sports injuries have been identified as a main mechanism. Although energy drinks, including those mixed with alcohol, are often used by young athletes and other adolescents they have not been examined in relation to TBI.We report on the prevalence of adolescent TBI and its associations with energy drinks, alcohol and energy drink mixed in with alcohol consumption.Data were derived from the Centre for Addiction and Mental Health's 2013 Ontario Student Drug Use and Health Survey (OSDUHS. This population-based cross-sectional school survey included 10,272 7th to 12th graders (ages 11-20 who completed anonymous self-administered questionnaires in classrooms.Mild to severe TBI were defined as those resulting in a loss of consciousness for at least five minutes, or being hospitalized for at least one night. Mechanism of TBI, prevalence estimates of TBI, and odds of energy drink consumption, alcohol use, and consumption of energy drinks mixed with alcohol are assessed.Among all students, 22.4% (95% CI: 20.7, 24.1 reported a history of TBI. Sports injuries remain the main mechanism of a recent (past year TBI (45.5%, 95% CI: 41.0, 50.1. Multinomial logistic regression showed that relative to adolescents who never sustained a TBI, the odds of sustaining a recent TBI were greater for those consuming alcohol, energy drinks, and energy drinks mixed in with alcohol than abstainers. Odds ratios were higher for these behaviors among students who sustained a recent TBI than those who sustained a former TBI (lifetime but not past 12 months. Relative to recent TBI due to other causes of injury, adolescents who sustained a recent TBI while playing sports had higher odds of recent energy drinks consumption than abstainers.TBI remains a disabling and common condition among adolescents and the consumption of alcohol, energy drinks, and alcohol

  6. Delirium after a traumatic brain injury: predictors and symptom patterns

    Science.gov (United States)

    Maneewong, Jutaporn; Maneeton, Benchalak; Maneeton, Narong; Vaniyapong, Tanat; Traisathit, Patrinee; Sricharoen, Natthanidnan; Srisurapanont, Manit

    2017-01-01

    Background Delirium in traumatic brain injury (TBI) is common, may be predictable, and has a multifaceted symptom complex. This study aimed to examine: 1) the sum score of Glasgow Coma Scale (GCS) and if its component scores could predict delirium in TBI patients, and 2) the prominent symptoms and their courses over the first days after TBI. Methods TBI patients were recruited from neurosurgical ward inpatients. All participants were hospitalized within 24 hours after their TBI. Apart from the sum score of GCS, which was obtained at the emergency department (ED), the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, diagnostic criteria for delirium were applied daily. The severity of delirium symptoms was assessed daily using the Delirium Rating Scale – Revised-98 (DRS-R-98). Results The participants were 54 TBI patients with a mean GCS score of 12.7 (standard deviation [SD] =2.9). A total of 25 patients (46.3%) met the diagnosis of delirium and had a mean age of 36.7 years (SD =14.8). Compared with 29 non-delirious patients, 25 delirious patients had a significantly lower mean GCS score (P=0.04), especially a significantly lower verbal component score (P=0.03). Among 18 delirious patients, four symptoms of the DRS-R-98 cognitive domain (orientation, attention, long-term memory, and visuospatial ability) were moderate symptoms (score ≥2) at the first day of admission. After follow-up, three cognitive (orientation, attention, and visuospatial ability) and two noncognitive symptoms (lability of affect and motor agitation) rapidly resolved. Conclusion Almost half of patients with mild to moderate head injuries may develop delirium in the first 4 days after TBI. Those having a low GCS score, especially the verbal component score, at the ED were likely to have delirium in this period. Most cognitive domains of delirium described in the DRS-R-98 were prominent within the first 4 days of TBI with delirium. Three cognitive and two noncognitive

  7. Connecting combat-related mild traumatic brain injury with posttraumatic stress disorder symptoms through brain imaging.

    Science.gov (United States)

    Costanzo, Michelle E; Chou, Yi-Yu; Leaman, Suzanne; Pham, Dzung L; Keyser, David; Nathan, Dominic E; Coughlin, Mary; Rapp, Paul; Roy, Michael J

    2014-08-01

    Mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD) may share common symptom and neuropsychological profiles in military service members (SMs) following deployment; while a connection between the two conditions is plausible, the relationship between them has been difficult to discern. The intent of this report is to enhance our understanding of the relationship between findings on structural and functional brain imaging and symptoms of PTSD. Within a cohort of SMs who did not meet criteria for PTSD but were willing to complete a comprehensive assessment within 2 months of their return from combat deployment, we conducted a nested case-control analysis comparing those with combat-related mTBI to age/gender-matched controls with diffusion tensor imaging, resting state functional magnetic resonance imaging and a range of psychological measures. We report degraded white matter integrity in those with a history of combat mTBI, and a positive correlation between the white matter microstructure and default mode network (DMN) connectivity. Higher clinician-administered and self-reported subthreshold PTSD symptoms were reported in those with combat mTBI. Our findings offer a potential mechanism through which mTBI may alter brain function, and in turn, contribute to PTSD symptoms.

  8. A quantitative MRI method for imaging blood-brain barrier leakage in experimental traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Wei Li

    Full Text Available Blood-brain barrier (BBB disruption is common following traumatic brain injury (TBI. Dynamic contrast enhanced (DCE MRI can longitudinally measure the transport coefficient Ktrans which reflects BBB permeability. Ktrans measurements however are not widely used in TBI research because it is generally considered to be noisy and possesses low spatial resolution. We improved spatiotemporal resolution and signal sensitivity of Ktrans MRI in rats by using a high-sensitivity surface transceiver coil. To overcome the signal drop off profile of the surface coil, a pre-scan module was used to map the flip angle (B1 field and magnetization (M0 distributions. A series of T1-weighted gradient echo images were acquired and fitted to the extended Kety model with reversible or irreversible leakage, and the best model was selected using F-statistics. We applied this method to study the rat brain one hour following controlled cortical impact (mild to moderate TBI, and observed clear depiction of the BBB damage around the impact regions, which matched that outlined by Evans Blue extravasation. Unlike the relatively uniform T2 contrast showing cerebral edema, Ktrans shows a pronounced heterogeneous spatial profile in and around the impact regions, displaying a nonlinear relationship with T2. This improved Ktrans MRI method is also compatible with the use of high-sensitivity surface coil and the high-contrast two-coil arterial spin-labeling method for cerebral blood flow measurement, enabling more comprehensive investigation of the pathophysiology in TBI.

  9. 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.

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

    Science.gov (United States)

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

    2004-06-01

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

  11. Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy.

    Science.gov (United States)

    Puvenna, Vikram; Engeler, Madeline; Banjara, Manoj; Brennan, Chanda; Schreiber, Peter; Dadas, Aaron; Bahrami, Ashkon; Solanki, Jesal; Bandyopadhyay, Anasua; Morris, Jacqueline K; Bernick, Charles; Ghosh, Chaitali; Rapp, Edward; Bazarian, Jeffrey J; Janigro, Damir

    2016-01-01

    Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (Pbrain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE.

  12. Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury

    OpenAIRE

    Thal, Serge C.; Clara Luh; Eva-Verena Schaible; Ralph Timaru-Kast; Jana Hedrich; Luhmann, Heiko J.; Kristin Engelhard; Zehendner, Christoph M.

    2012-01-01

    Disruption of the blood-brain barrier (BBB) results in cerebral edema formation, which is a major cause for high mortalityrnafter traumatic brain injury (TBI). As anesthetic care is mandatory in patients suffering from severe TBI it may be importantrnto elucidate the effect of different anesthetics on cerebral edema formation. Tight junction proteins (TJ) such as zonularnoccludens-1 (ZO-1) and claudin-5 (cl5) play a central role for BBB stability. First, the influence of the volatile anesthet...

  13. Tau and Beta-Amyloid Deposition, Microhemorrhage and Brain Function after Traumatic Brain Injury in War Veterans

    Science.gov (United States)

    2015-10-01

    AWARD NUMBER: W81XWH-14-1-0418 TITLE: Tau and Beta-Amyloid Deposition, Microhemorrhage and Brain Function after Traumatic Brain Injury in War...REPORT DOCUMENTATION PAGE Form Approved OMB No. 0704-0188 Public reporting burden for this collection of information is estimated to average 1 hour...completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information

  14. 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...

  15. GFAP-BDP as an acute diagnostic marker in traumatic brain injury: results from the prospective transforming research and clinical knowledge in traumatic brain injury study.

    Science.gov (United States)

    Okonkwo, David O; Yue, John K; Puccio, Ava M; Panczykowski, David M; Inoue, Tomoo; McMahon, Paul J; Sorani, Marco D; Yuh, Esther L; Lingsma, Hester F; Maas, Andrew I R; Valadka, Alex B; Manley, Geoffrey T

    2013-09-01

    Reliable diagnosis of traumatic brain injury (TBI) is a major public health need. Glial fibrillary acidic protein (GFAP) is expressed in the central nervous system, and breakdown products (GFAP-BDP) are released following parenchymal brain injury. Here, we evaluate the diagnostic accuracy of elevated levels of plasma GFAP-BDP in TBI. Participants were identified as part of the prospective Transforming Research And Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) Study. Acute plasma samples (<24 h post-injury) were collected from patients presenting with brain injury who had CT imaging. The ability of GFAP-BDP level to discriminate patients with demonstrable traumatic lesions on CT, and with failure to return to pre-injury baseline at 6 months, was evaluated by the area under the receiver operating characteristic curve (AUC). Of the 215 patients included for analysis, 83% had mild, 4% had moderate, and 13% had severe TBI; 54% had acute traumatic lesions on CT. The ability of GFAP-BDP level to discriminate patients with traumatic lesions on CT as evaluated by AUC was 0.88 (95% confidence interval [CI], 0.84-0.93). The optimal cutoff of 0.68 ng/mL for plasma GFAP-BDP level was associated with a 21.61 odds ratio for traumatic findings on head CT. Discriminatory ability of unfavorable 6 month outcome was lower, AUC 0.65 (95% CI, 0.55-0.74), with a 2.07 odds ratio. GFAP-BDP levels reliably distinguish the presence and severity of CT scan findings in TBI patients. Although these findings confirm and extend prior studies, a larger prospective trial is still needed to validate the use of GFAP-BDP as a routine diagnostic biomarker for patient care and clinical research. The term "mild" continues to be a misnomer for this patient population, and underscores the need for evolving classification strategies for TBI targeted therapy. (ClinicalTrials.gov number NCT01565551; NIH Grant 1RC2 NS069409).

  16. Is Goshinjo therapy effective in cognitive impairment after severe traumatic brain injury?

    Institute of Scientific and Technical Information of China (English)

    Keiji Hashimoto; Kisho Kida

    2013-01-01

    We report a case of a 21-year-old man who had severe traumatic brain injury as a result of an accident at the age of 16 years. Two years and 4 months after the trauma, at the age of 19 years, he still had severe right hemiplegia and cognitive dysfunction including aphasia and attention and memory disturbance. Conventional rehabilitation programs could not resolve all of the neuropsychological problems. He started receiving Goshinjo therapy over a period of 22 months. Following the therapy, significant improvements in verbal intelligence quotient (assessed by the Wechsler Adult Intelligence Scale-Third Edition) and attention and concentration function (using the Wechsler Memory Scale-Revised), and remission of traumatic epilepsy were observed. Goshinjo therapy is suspected to be effective in the treatment of cognitive dysfunction in the chronic stage after severe traumatic brain injury.

  17. Neuroimaging and the school-based assessment of traumatic brain injury.

    Science.gov (United States)

    Jantz, Paul B; Bigler, Erin D

    2014-01-01

    Advanced neuroimaging contributes to a greater understanding of brain pathology following a traumatic brain injury (TBI) and has the ability to guide neurorehabilitation decisions. When integrated with the school-based psychoeducational assessment of a child with a TBI, neuroimaging can provide a different perspective when interpreting educational and behavioral variables relevant to school-based neurorehabilitation. School psychologists conducting traditional psychoeducational assessments of children with TBI seldom obtain and integrate neuroimaging, despite its availability. This article presents contextual information on the medical assessment of TBI, major types of neuroimaging, and networks of the brain. A case study illustrates the value of incorporating neuroimaging into the standard school-based psychoeducational evaluations of children with traumatic brain injury.

  18. Melatonin reduces traumatic brain injur y-induced oxidative stress in the cerebral cortex and blood of rats

    Institute of Scientific and Technical Information of China (English)

    Nilgnenol; Mustafa Nazrolu

    2014-01-01

    Free radicals induced by traumatic brain injury have deleterious effects on the function and antioxidant vitamin levels of several organ systems including the brain. Melatonin possesses antioxidant effect on the brain by maintaining antioxidant enzyme and vitamin levels. We in-vestigated the effects of melatonin on antioxidant ability in the cerebral cortex and blood of traumatic brain injury rats. Results showed that the cerebral cortex β-carotene, vitamin C, vita-min E, reduced glutathione, and erythrocyte reduced glutathione levels, and plasma vitamin C level were decreased by traumatic brain injury whereas they were increased following melatonin treatment. In conclusion, melatonin seems to have protective effects on traumatic brain inju-ry-induced cerebral cortex and blood toxicity by inhibiting free radical formation and supporting antioxidant vitamin redox system.

  19. Analysis of the cerebral transcriptome in mice subjected to traumatic brain injury: importance of IL-6

    DEFF Research Database (Denmark)

    Quintana, Albert; Giralt, Mercedes; Molinero, Amalia

    2007-01-01

    Traumatic brain injury is one of the leading causes of incapacity and death among young people. Injury to the brain elicits a potent inflammatory response, comprising recruitment of inflammatory cells, reactive astrogliosis and activation of brain macrophages. Under the influence of presumably...... such as microarrays. The combination of these modern techniques with the comparison of normal and genetically modified mice boosts the significance of the results obtained. With this approach, we have demonstrated that a cytokine such as interleukin-6 is one of the key players in the response of the brain to injury....

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

    Directory of Open Access Journals (Sweden)

    Albert-Weißenberger Christiane

    2012-02-01

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

  1. The Effects of Traumatic Brain Injury during Adolescence on Career Plans and Outcomes

    Science.gov (United States)

    Balaban, Tammy; Hyde, Nellemarie; Colantonio, Angela

    2009-01-01

    Traumatic brain injury (TBI) often occurs during the years when individuals are aiming for vocational goals and acquiring skills needed to achieve vocational success. This exploratory study aimed to describe the perceived long-term impact on career outcomes for individuals who were hospitalized with a TBI during adolescence. This study used a…

  2. Posttraumatic Stress Disorder, Traumatic Brain Injury, and Suicide Attempt History among Veterans Receiving Mental Health Services

    Science.gov (United States)

    Brenner, Lisa A.; Betthauser, Lisa M.; Homaifar, Beeta Y.; Villarreal, Edgar; Harwood, Jeri E. F.; Staves, Pamela J.; Huggins, Joseph A.

    2011-01-01

    History of posttraumatic stress disorder (PTSD) or traumatic brain injury (TBI) has been found to increase risk of suicidal behavior. The association between suicide attempt history among veterans with PTSD and/or TBI was explored. Cases (N = 81) and 2:1 matched controls (N = 160) were randomly selected from a Veterans Affairs Medical Center…

  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. The Brown University Traumatic Brain Injury Research Consortium and the Norman Prince Neurosciences Institute.

    Science.gov (United States)

    Rogg, Jeffrey; Spader, Heather; Wilcox, Bethany J; Ellermeier, Anna; Correira, Steven; Chodobski, Adam; Szmydynger-Chodobska, Joanna; Raukar, Neha; Machan, Jason T; Crisco, Joseph J; LaFrance, W Curt

    2014-05-01

    This article provides an overview of the Brown University Traumatic Brain Injury Research Consortium (TBIRC) and summarizes the multidisciplinary basic and clinical neuroscience work being conducted by investigators at Brown University and the affiliate hospitals in association with the Norman Prince Neurosciences Institute (NPNI).

  5. Research progress in mechanism of traumatic brain injury affecting speed of fracture healing

    Institute of Scientific and Technical Information of China (English)

    ZHAO Xiao-gang; ZHAO Guang-feng; MA Yue-feng; JIANG Guan-yu

    2007-01-01

    @@ In patients who have sustained traumatic brain injury with associated extremity fracture, there is often a clinical perception that the rate of new bone formation around the fracture site increases. 1 An overgrowth of callus is observed and ectopic ossification even occurs in the muscle,2 but the mechanism remains unclear.

  6. Cognitive complaints after mild traumatic brain injury: things are not always what they seem.

    NARCIS (Netherlands)

    Stulemeijer, M.; Vos, P.E.; Bleijenberg, G.; Werf, S.P. van der

    2007-01-01

    OBJECTIVE: To compare nonreferred, emergency department (ED)-admitted mild traumatic brain injury (MTBI) patients with and without self-reported cognitive complaints on (1) demographic variables and injury characteristics; (2) neuropsychological test performance; (3) 12-day self-monitoring of percei

  7. Strategic Learning in Youth with Traumatic Brain Injury: Evidence for Stall in Higher-Order Cognition

    Science.gov (United States)

    Gamino, Jacquelyn F.; Chapman, Sandra B.; Cook, Lori G.

    2009-01-01

    Little is known about strategic learning ability in preteens and adolescents with traumatic brain injury (TBI). Strategic learning is the ability to combine and synthesize details to form abstracted gist-based meanings, a higher-order cognitive skill associated with frontal lobe functions and higher classroom performance. Summarization tasks were…

  8. Hospital-School Collaboration to Serve the Needs of Children with Traumatic Brain Injury

    Science.gov (United States)

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

    2011-01-01

    Traumatic brain injuries are the leading cause of death and disability for children and adolescents each year in the United States. Children who survive these injuries often suffer from a range of impairments including intellectual, academic, behavioral, affective, and social problems, but they often become mired in a slow-moving process while…

  9. Traumatic Brain Injury: Exploring the Role of Cooperative Extension in Kansas Communities

    Science.gov (United States)

    Sellers, Debra M.; Garcia, Jane Mertz

    2012-01-01

    TBI"options" helps survivors of traumatic brain injury and their families identify, locate, and contact helpful organizations in their local communities to promote successful living. This article discusses the role of county agents in the program and the support offered by community partners. Results of pre- and post-surveys for both…

  10. Using Choice to Increase On-Task Behavior in Individuals with Traumatic Brain Injury

    Science.gov (United States)

    Tasky, Kim K.; Rudrud, Eric H.; Schulze, Kimberly A.; Rapp, John T.

    2008-01-01

    An ABA'B design was used to evaluate the effects of choice on task engagement for 3 adults who had been diagnosed with traumatic brain injury. A yoked-control condition, in which tasks that were selected by each participant were assigned subsequently to that participant by a trainer, was implemented to help distinguish between the effects of task…

  11. Traumatic Brain Injury and Grief: Considerations and Practical Strategies for School Psychologists

    Science.gov (United States)

    Jantz, Paul B.; Comerchero, Victoria A.; Canto, Angela I.; Pierson, Eric

    2015-01-01

    Traumatic brain injury (TBI) can result in a range of social, emotional, neurological, cognitive, and behavioral outcomes. If these outcomes are significant, family members and the individual who has sustained the TBI may struggle with accepting the effects of these deficits. They may grieve over disrupted family relationships, roles, and routines…

  12. Effects of a Self-Monitoring Intervention on Children with Traumatic Brain Injury

    Science.gov (United States)

    Davies, Susan C.; Jones, Kevin M.; Rafoth, Mary A.

    2010-01-01

    The purpose of this study was to examine the effects of a self-monitoring intervention on teachers' direct behavior ratings of 3 students with traumatic brain injury. The authors used a multiple-baseline-across-participants design to evaluate the effect of the strategy on each child's classwork and classroom behavior. The self-monitoring strategy…

  13. Traumatic Brain Injury: The Efficacy of a Half-Day Training for School Psychologists

    Science.gov (United States)

    Davies, Susan C.; Ray, Ashlyn M.

    2014-01-01

    The incidence rates of traumatic brain injuries (TBI) are increasing, yet educators continue to be inadequately trained in assessing and serving students with TBIs. This study examined the efficacy of a half-day TBI training program for school psychologists designed to improve their knowledge and skills. Results of quantitative and qualitative…

  14. Barriers to Meeting the Needs of Students with Traumatic Brain Injury

    Science.gov (United States)

    Canto, Angela I.; Chesire, David J.; Buckley, Valerie A.; Andrews, Terrie W.; Roehrig, Alysia D.

    2014-01-01

    Many students with traumatic brain injury (TBI) are identified by the medical community each year and many more experience head injuries that are not examined by medical personnel. School psychologists and allied consultants have important liaison roles to identify and assist these students post-injury. In this study, 75 school psychologists (the…

  15. Multimodal Approach to Testing the Acute Effects of Mild Traumatic Brain Injury (mTBI)

    Science.gov (United States)

    2015-03-01

    2013). Decreased connectivity in resting-state MEG may persist for years after mTBI ( Castellanos et al., 2011), but the abnormally reduced...of rehabilitation medicine, 36(0), 28-60. [4]   Castellanos , N.P. (2011). Principles of recovery from traumatic brain injury: Reorganization of

  16. Gas chromatography-mass spectrometric assay for propofol in cerebrospinal fluid of traumatic brain patients

    NARCIS (Netherlands)

    Peeters, Mariska Y. M.; Kuiper, Hiltjo; Greijdanus, Ben; van der Naalt, Joukje; Knibbe, Catherijne A. J.; Uges, Donald R. A.

    2007-01-01

    A sensitive gas chromatography-mass spectrometry method for measuring propofol in cerebrospinal fluid is described, validated and applied to four patients after traumatic brain injury. The limit of quantitation was 2 mu g/L using a volume of 0.5 mL. The inter- and intra-assay coefficients of variati

  17. Older age, traumatic brain injury, and cognitive slowing: Some convergent and divergent findings.

    NARCIS (Netherlands)

    Bashore, T.R.; Ridderinkhof, K.R.

    2002-01-01

    Reaction time (RT) meta-analyses of cognitive slowing indicate that all stages of processing slow equivalently and task independently among both older adults (J. Cerella & S. Hale, 1994) and adults who have suffered a traumatic brain injury (TBI; F. R. Ferraro, 1996). However, meta-analyses using bo

  18. Endocannabinoids as a Target for the Treatment of Traumatic Brain Injury

    Science.gov (United States)

    2016-01-01

    57 58 59 60 42 Running /Table of Contents title: Inhibition of EC Degradation Improves mTBI Outcomes Key Words: 2-AG, MAGL, TBI, neuroinflammation...sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms. Lab Invest. 74(2):315-42. 15. Prow NA, Irani DN

  19. Humor, Rapport, and Uncomfortable Moments in Interactions with Adults with Traumatic Brain Injury

    Science.gov (United States)

    Kovarsky, Dana; Schiemer, Christine; Murray, Allison

    2011-01-01

    We examined uncomfortable moments that damaged rapport during group interactions between college students in training to become speech-language pathologists and adults with traumatic brain injury. The students worked as staff in a community-based program affiliated with a university training program that functioned as a recreational gathering…

  20. Systematic review of the risk of Parkinson's disease after mild traumatic brain injury

    DEFF Research Database (Denmark)

    Marras, Connie; Hincapié, Cesar A; Kristman, Vicki L;

    2014-01-01

    OBJECTIVE: To synthesize the best available evidence on the risk of Parkinson's disease (PD) after mild traumatic brain injury (MTBI). DATA SOURCES: MEDLINE and other databases were searched (1990-2012) with terms including "craniocerebral trauma" and "parkinsonian disorders." Reference lists of ...

  1. Systematic review of the prognosis after mild traumatic brain injury in adults

    DEFF Research Database (Denmark)

    Carroll, Linda J; Cassidy, John David; Cancelliere, Carol;

    2014-01-01

    OBJECTIVE: To synthesize the best available evidence on objective outcomes after adult mild traumatic brain injury (MTBI). DATA SOURCES: MEDLINE and other databases were searched (2001-2012) for studies related to MTBI. Inclusion criteria included published, peer-reviewed articles in English and ...

  2. Systematic review of self-reported prognosis in adults after mild traumatic brain injury

    DEFF Research Database (Denmark)

    Cassidy, John David; Cancelliere, Carol; Carroll, Linda J;

    2014-01-01

    OBJECTIVE: To update the mild traumatic brain injury (MTBI) prognosis review published by the World Health Organization Task Force in 2004. DATA SOURCES: MEDLINE, PsycINFO, Embase, CINAHL, and SPORTDiscus were searched from 2001 to 2012. We included published, peer-reviewed studies with more than...

  3. COMT Val 158 Met polymorphism is associated with nonverbal cognition following mild traumatic brain injury

    NARCIS (Netherlands)

    E.A. Winkler (Ethan A.); J.K. Yue (John); T.W. McAllister (Thomas W.); N.R. Temkin (Nancy); S.S. Oh (Sam S.); E.G. Burchard (Esteban); D. Hu (Donglei); A.R. Ferguson (Adam); H.F. Lingsma (Hester); J.F. Burke (John F.); M.D. Sorani (Marco); J. Rosand (Jonathan); E.L. Yuh (Esther); J. Barber (Jason); P.E. Tarapore (Phiroz E.); R.C. Gardner (Raquel C.); S. Sharma (Sourabh); G.G. Satris (Gabriela G.); C. Eng (Celeste); A.M. Puccio (Ava); K.K.W. Wang (Kevin K. W.); P. Mukherjee (Pratik); A.B. Valadka (Alex); D. Okonkwo (David); R. Diaz-Arrastia (Ramon); G. Manley (Geoffrey)

    2016-01-01

    textabstractMild traumatic brain injury (mTBI) results in variable clinical outcomes, which may be influenced by genetic variation. A single-nucleotide polymorphism in catechol-o-methyltransferase (COMT), an enzyme which degrades catecholamine neurotransmitters, may influence cognitive deficits foll

  4. The Relation of Mild Traumatic Brain Injury to Chronic Lapses of Attention

    Science.gov (United States)

    Pontifex, Matthew B.; Broglio, Steven P.; Drollette, Eric S.; Scudder, Mark R.; Johnson, Chris R.; O'Connor, Phillip M.; Hillman, Charles H.

    2012-01-01

    We assessed the extent to which failures in sustained attention were associated with chronic mild traumatic brain injury (mTBI) deficits in cognitive control among college-age young adults with and without a history of sport-related concussion. Participants completed the ImPACT computer-based assessment and a modified flanker task. Results…

  5. Introduction to the findings of the International Collaboration on Mild Traumatic Brain Injury Prognosis

    DEFF Research Database (Denmark)

    Salmi, L Rachid; Cassidy, John David; Holm, Lena;

    2014-01-01

    Prognostic studies of mild traumatic brain injury (MTBI) can serve many purposes. First, they are used to describe paths and outcomes of patients with MTBI. Second, they provide information on which characteristics are associated with the occurrence of outcomes. Third, they provide insight...

  6. 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

  7. Postconcussive Complaints, Anxiety, and Depression Related to Vocational Outcome in Minor to Severe Traumatic Brain Injury

    NARCIS (Netherlands)

    van der Horn, Harm J.; Spikman, Jacoba M.; Jacobs, Bram; van der Naalt, Joukje

    2013-01-01

    Objectives: To investigate the relation of postconcussive complaints, anxiety, and depression with vocational outcome in patients with traumatic brain injury (TBI) of various severities and to assess sex differences. Design: A prospective cross-sectional cohort study. Setting: Level I trauma center.

  8. Time Perception in Severe Traumatic Brain Injury Patients: A Study Comparing Different Methodologies

    Science.gov (United States)

    Mioni, G.; Mattalia, G.; Stablum, F.

    2013-01-01

    In this study, we investigated time perception in patients with traumatic brain injury (TBI). Fifteen TBI patients and 15 matched healthy controls participated in the study. Participants were tested with durations above and below 1s on three different temporal tasks that involved time reproduction, production, and discrimination tasks. Data…

  9. Return to Work and Social Communication Ability Following Severe Traumatic Brain Injury

    Science.gov (United States)

    Douglas, Jacinta M.; Bracy, Christine A.; Snow, Pamela C.

    2016-01-01

    Purpose: Return to competitive employment presents a major challenge to adults who survive traumatic brain injury (TBI). This study was undertaken to better understand factors that shape employment outcome by comparing the communication profiles and self-awareness of communication deficits of adults who return to and maintain employment with those…

  10. Reliability, Sensitivity, and Specificity of the VA Traumatic Brain Injury Screening Tool

    NARCIS (Netherlands)

    Donnelly, K.T.; Donnelly, J.P.; Dunnam, M.; Warner, G.C.; Kittleson, C.J.; Constance, J.E.; Bradshaw, C.B.; Alt, M.

    2011-01-01

    OBJECTIVE:: To provide item analyses, estimates of temporal reliability and internal consistency, and examination of the sensitivity and specificity of a traumatic brain injury-screening tool. PARTICIPANTS:: Five hundred veterans of the wars in Iraq and Afghanistan enrolled in the study, approximate

  11. Emotion Recognition following Pediatric Traumatic Brain Injury: Longitudinal Analysis of Emotional Prosody and Facial Emotion Recognition

    Science.gov (United States)

    Schmidt, Adam T.; Hanten, Gerri R.; Li, Xiaoqi; Orsten, Kimberley D.; Levin, Harvey S.

    2010-01-01

    Children with closed head injuries often experience significant and persistent disruptions in their social and behavioral functioning. Studies with adults sustaining a traumatic brain injury (TBI) indicate deficits in emotion recognition and suggest that these difficulties may underlie some of the social deficits. The goal of the current study was…

  12. Liberal Bias Mediates Emotion Recognition Deficits in Frontal Traumatic Brain Injury

    Science.gov (United States)

    Callahan, Brandy L.; Ueda, Keita; Sakata, Daisuke; Plamondon, Andre; Murai, Toshiya

    2011-01-01

    It is well-known that patients having sustained frontal-lobe traumatic brain injury (TBI) are severely impaired on tests of emotion recognition. Indeed, these patients have significant difficulty recognizing facial expressions of emotion, and such deficits are often associated with decreased social functioning and poor quality of life. As of yet,…

  13. Traumatic brain injury in children in Denmark: a national 15-year study

    DEFF Research Database (Denmark)

    Engberg, A; Teasdale, T W

    1998-01-01

    Demographic trends are reported concerning three types of traumatic brain injury (concussions, cranial fractures, and intracranial contusions/haemorrhages) among children in Denmark of ages up to and including 14 years, for a fifteen year period from 1979 through 1993. The data were derived from ...

  14. Topic Repetitiveness after Traumatic Brain Injury: An Emergent, Jointly Managed Behaviour

    Science.gov (United States)

    Body, Richard; Parker, Mark

    2005-01-01

    Topic repetitiveness is a common component of pragmatic impairment and a powerful contributor to social exclusion. Despite this, description, characterization and intervention remain underdeveloped. This article explores the nature of repetitiveness in traumatic brain injury (TBI). A case study of one individual after TBI provides the basis for a…

  15. Classroom Strategies to Use with Students Following Traumatic Brain Injuries: Reading, Math, Writing, and Behavior

    Science.gov (United States)

    Spear, Andi

    2005-01-01

    A Traumatic Brain Injury (TBI) changes cognition and behavior in students. Their learning needs are different from students with other exceptionalities. General and special education teachers can use specific strategies based on learning style, along with certain resources, with students who have experienced a TBI to promote learning in reading,…

  16. Dysarthria Associated with Traumatic Brain Injury: Speaking Rate and Emphatic Stress

    Science.gov (United States)

    Wang, Y.T.; Kent, R.D.; Duffy, J.R.; Thomas, J.E.

    2005-01-01

    Prosodic abnormality is common in the dysarthria associated with traumatic brain injury (TBI), and adjustments of speaking rate and emphatic stress are often used as steps in treating the speech disorder in patients with TBI-induced dysarthria. However, studies to date do not present a clear and detailed picture of how speaking rate and emphatic…

  17. Academic and Language Outcomes in Children after Traumatic Brain Injury: A Meta-Analysis

    Science.gov (United States)

    Vu, Jennifer A.; Babikian, Talin; Asarnow, Robert F .

    2011-01-01

    Expanding on Babikian and Asarnow's (2009) meta-analytic study examining neurocognitive domains, this current meta-analysis examined academic and language outcomes at different time points post-traumatic brain injury (TBI) in children and adolescents. Although children with mild TBI exhibited no significant deficits, studies indicate that children…

  18. Acute Alcohol Intoxication in Patients with Mild Traumatic Brain Injury: Characteristics, Recovery and Outcome

    NARCIS (Netherlands)

    Scheenen, Myrthe; de Koning, Myrthe; van der Horn, Harm; van der Naalt, Joukje; Spikman, Jacoba

    2015-01-01

    Objectives. To investigate the incidence of acute alcohol intoxication (AAI) at the time of sustaining mild traumatic brain injury (mTBI), describe the characteristics of this intoxicated subgroup, and evaluate recovery and outcome in comparison to sober mTBI patients. Methods. Multicenter cohort st

  19. Outcome prediction in moderate and severe traumatic brain injury: a focus on computed tomography variables

    NARCIS (Netherlands)

    Jacobs, B.; Beems, T.; Vliet, T.M. van der; Vugt, A.B. van; Hoedemaekers, C.W.; Horn, J.; Franschman, G.; Haitsma, I.; Naalt, J. van der; Andriessen, T.M.J.C.; Borm, G.F.; Vos, P.E.

    2013-01-01

    BACKGROUND: With this study we aimed to design validated outcome prediction models in moderate and severe traumatic brain injury (TBI) using demographic, clinical, and radiological parameters. METHODS: Seven hundred consecutive moderate or severe TBI patients were included in this observational pros

  20. Outcome Prediction in Moderate and Severe Traumatic Brain Injury : A Focus on Computed Tomography Variables

    NARCIS (Netherlands)

    Jacobs, Bram; Beems, Tjemme; van der Vliet, Ton M.; van Vugt, Arie B.; Hoedemaekers, Cornelia; Horn, Janneke; Franschman, Gaby; Haitsma, Ian; van der Naalt, Joukje; Andriessen, Teuntje M. J. C.; Borm, George F.; Vos, Pieter E.

    2013-01-01

    With this study we aimed to design validated outcome prediction models in moderate and severe traumatic brain injury (TBI) using demographic, clinical, and radiological parameters. Seven hundred consecutive moderate or severe TBI patients were included in this observational prospective cohort study.

  1. Explaining Pragmatic Performance in Traumatic Brain Injury: A Process Perspective on Communicative Errors

    Science.gov (United States)

    Bosco, Francesca M.; Angeleri, Romina; Sacco, Katiuscia; Bara, Bruno G.

    2015-01-01

    Background: The purpose of this study is to investigate the pragmatic abilities of individuals with traumatic brain injury (TBI). Several studies in the literature have previously reported communicative deficits in individuals with TBI, however such research has focused principally on communicative deficits in general, without providing an…

  2. 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.

  3. Traumatic Brain Injury in K-12 Students: Where Have All the Children Gone?

    Science.gov (United States)

    Schutz, Larry E.; Rivers, Kenyatta O.; McNamara, Elizabeth; Schutz, Judith A.; Lobato, Emilio J.

    2010-01-01

    When children who are permanently disabled by traumatic brain injury (TBI) return to school, most are placed in mainstream classrooms and incorrectly presumed capable of resuming their education. Only one to two percent are classified as students with TBI, qualifying them for the services they need for their education. The failure to properly…

  4. Pathophysiological Concepts in Mild Traumatic Brain Injury : Diffusion Tensor Imaging Related to Acute Perfusion CT Imaging

    NARCIS (Netherlands)

    Metting, Zwany; Cerliani, Leonardo; Rodiger, Lars A.; van der Naalt, Joukje

    2013-01-01

    Background: A subgroup of patients with mild traumatic brain injury (TBI) experiences residual symptoms interfering with their return to work. The pathophysiological substrate of the suboptimal outcome in these patients is a source of debate. Objective: To provide greater insight into the pathophysi

  5. Script-event representation in patients with severe traumatic brain injury

    NARCIS (Netherlands)

    Allain, P.; Fasotti, L.; Roy, A.; Chauvire, V.; Etcharry-Bouyx, F.; Gall, D. le

    2012-01-01

    The aim of the present study was to examine the syntactic and semantic dimensions of script representation in patients with structural damage within the cerebral cortex following a severe traumatic brain injury (TBI). Forty TBI patients and 38 healthy control subjects (HC) were asked to sort cards d

  6. Cerebral perfusion and neuropsychological follow up in mild traumatic brain injury : Acute versus chronic disturbances?

    NARCIS (Netherlands)

    Metting, Zwany; Spikman, Jacoba M.; Rodiger, Lars A.; van der Naalt, Joukje

    2014-01-01

    In a subgroup of patients with mild traumatic brain injury (TBI) residual symptoms, interfering with outcome and return to work, are found. With neuropsychological assessment cognitive deficits can be demonstrated although the pathological underpinnings of these cognitive deficits are not fully unde

  7. Cognitive and Behavioral Impairment in Traumatic Brain Injury Related to Outcome and Return to Work

    NARCIS (Netherlands)

    Benedictus, Marieke R.; Spikman, Jacoba M.; van der Naalt, Joukje

    2010-01-01

    Benedictus MR, Spikman JM, van der Naalt J. Cognitive and behavioral impairment in traumatic brain injury related to outcome and return to work. Arch Phys Med Rehabil 2010;91:1436-41. Objective: To evaluate the cognitive and behavioral disturbances related to return to work (RTW) in patients with tr

  8. Neural correlates of motor dysfunction in children with traumatic brain injury: exploration of compensatory recruitment patterns.

    NARCIS (Netherlands)

    Caeyenberghs, K.; Wenderoth, N.; Smits-Engelsman, B.C.M.; Sunaert, S.; Swinnen, S.P.

    2009-01-01

    Traumatic brain injury (TBI) is a common form of disability in children. Persistent deficits in motor control have been documented following TBI but there has been less emphasis on changes in functional cerebral activity. In the present study, children with moderate to severe TBI (n = 9) and control

  9. 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.

  10. Platelet activation and dysfunction in a large-animal model of traumatic brain injury and hemorrhage

    DEFF Research Database (Denmark)

    Sillesen, Martin; Johansson, Pär I; Rasmussen, Lars S

    2013-01-01

    Traumatic brain injury (TBI) and hemorrhage are the leading causes of trauma-related mortality. Both TBI and hemorrhage are associated with coagulation disturbances, including platelet dysfunction. We hypothesized that platelet dysfunction could be detected early after injury, and that this dysfu...

  11. Long-Term Attention Problems in Children with Traumatic Brain Injury

    Science.gov (United States)

    Yeates, Keith Owen; Armstrong, Kira; Janusz, Jennifer; Taylor, H. Gerry; Wade, Shari; Stancin, Terry; Drotar, Dennis

    2005-01-01

    Objective: To examine long-term attention problems and their cognitive correlates after childhood traumatic brain injury (TBI). Method: Data were drawn from a prospective, longitudinal study conducted between 1992 and 2002. Participants included 41 children with severe TBI, 41 with moderate TBI, and 50 with orthopedic injury (OI), who were all…

  12. Neuroimaging Correlates of Novel Psychiatric Disorders after Pediatric Traumatic Brain Injury

    Science.gov (United States)

    Max, Jeffrey E.; Wilde, Elisabeth A.; Bigler, Erin D.; Thompson, Wesley K.; MacLeod, Marianne; Vasquez, Ana C.; Merkley, Tricia L.; Hunter, Jill V.; Chu, Zili D.; Yallampalli, Ragini; Hotz, Gillian; Chapman, Sandra B.; Yang, Tony T.; Levin, Harvey S.

    2012-01-01

    Objective: To study magnetic resonance imaging (MRI) correlates of novel (new-onset) psychiatric disorders (NPD) after traumatic brain injury (TBI) and orthopedic injury (OI). Method: Participants were 7 to 17 years of age at the time of hospitalization for either TBI or OI. The study used a prospective, longitudinal, controlled design with…

  13. Mood after moderate and severe traumatic brain injury: A prospective cohort study

    NARCIS (Netherlands)

    L. Valk-Kleibeuker (Linda); M.H. Heijenbrok-Kal (Majanka); G.M. Ribbers (Gerard)

    2014-01-01

    textabstractObjective: To evaluate the course of mood and identify its determinants up to 3 years after moderate to severe traumatic brain injury (TBI). Design: Prospective cohort study. Patients: Patients hospitalised with moderate to severe TBI, who survived until hospital discharge. Methods: At 3

  14. TBI-ROC Part Seven: Traumatic Brain Injury--Technologies to Support Memory and Cognition

    Science.gov (United States)

    Scherer, Marcia; Elias, Eileen; Weider, Katie

    2010-01-01

    This article is the seventh of a multi-part series on traumatic brain injury (TBI). The six earlier articles in this series have discussed the individualized nature of TBI and its consequences, the rehabilitation continuum, and interventions at various points along the continuum. As noted throughout the articles, many individuals with TBI…

  15. Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury.

    NARCIS (Netherlands)

    Andriessen, T.M.J.C.; Jacobs, B.; Vos, P.E.

    2010-01-01

    Traumatic brain injury (TBI) is a frequent and clinically highly heterogeneous neurological disorder with large socioeconomic consequences. TBI severity classification, based on the hospital admission Glasgow Coma Scale (GCS) score, ranges from mild (GCS 13-15) and moderate (GCS 9-12) to severe (GCS

  16. Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury

    NARCIS (Netherlands)

    Andriessen, Teuntje M J C; Jacobs, Bram; Vos, Pieter E

    2010-01-01

    Traumatic brain injury (TBI) is a frequent and clinically highly heterogeneous neurological disorder with large socioeconomic consequences. TBI severity classification, based on the hospital admission Glasgow Coma Scale (GCS) score, ranges from mild (GCS 13-15) and moderate (GCS 9-12) to severe (GCS

  17. TBI-ROC Part One: Understanding Traumatic Brain Injury--An Introduction

    Science.gov (United States)

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

    2011-01-01

    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,…

  18. Impaired Visual Integration in Children with Traumatic Brain Injury: An Observational Study

    NARCIS (Netherlands)

    M. Königs (Marsh); W.D. Weeda (Wouter D.); L.W.E. Van Heurn (L.W. Ernest); R.J. Vermeulen (R. Jeroen); J.C. Goslings (Carel); J.S.K. Luitse (Jan S.K.); B.T. Poll-Thé (Bwee Tien); A. Beelen (Anita); M. Van Der Wees (Marleen); R.J.J.K. Kemps (Rachèl J.J.K.); C.E. Catsman-Berrevoets (Coriene); J. Oosterlaan (Jaap)

    2015-01-01

    textabstractBackground Axonal injury after traumatic brain injury (TBI) may cause impaired sensory integration. We aim to determine the effects of childhood TBI on visual integration in relation to general neurocognitive functioning. Methods We compared children aged 6-13 diagnosed with TBI (n = 103

  19. Mirror Asymmetry of Category and Letter Fluency in Traumatic Brain Injury and Alzheimer's Patients

    Science.gov (United States)

    Capitani, Erminio; Rosci, Chiara; Saetti, Maria Cristina; Laiacona, Marcella

    2009-01-01

    In this study we contrasted the Category fluency and Letter fluency performance of 198 normal subjects, 57 Alzheimer's patients and 57 patients affected by traumatic brain injury (TBI). The aim was to check whether, besides the prevalence of Category fluency deficit often reported among Alzheimer's patients, the TBI group presented the opposite…

  20. Systematic review of the clinical course, natural history, and prognosis for pediatric mild traumatic brain injury

    DEFF Research Database (Denmark)

    Hung, Ryan; Carroll, Linda J; Cancelliere, Carol;

    2014-01-01

    OBJECTIVE: To synthesize the best available evidence on prognosis after pediatric mild traumatic brain injury (MTBI). DATA SOURCES: We searched MEDLINE, Embase, PsycINFO, CINAHL, and SPORTDiscus (2001-2012), as well as reference lists of eligible articles, and relevant systematic reviews and meta...

  1. GFAP and S100B are biomarkers of traumatic brain injury : an observational cohort study

    NARCIS (Netherlands)

    Vos, P E; Jacobs, B; Andriessen, T M J C; Lamers, K J B; Borm, G F; Beems, T; Edwards, M; Rosmalen, C F; Vissers, J L M

    2010-01-01

    BACKGROUND: Biomarker levels in blood after traumatic brain injury (TBI) may offer diagnostic and prognostic tools in addition to clinical indices. This study aims to validate glial fibrillary acidic protein (GFAP) and S100B concentrations in blood as outcome predictors of TBI using cutoff levels of

  2. Brain activation during a social attribution task in adolescents with moderate to severe traumatic brain injury.

    Science.gov (United States)

    Scheibel, Randall S; Newsome, Mary R; Wilde, Elisabeth A; McClelland, Michelle M; Hanten, Gerri; Krawczyk, Daniel C; Cook, Lori G; Chu, Zili D; Vásquez, Ana C; Yallampalli, Ragini; Lin, Xiaodi; Hunter, Jill V; Levin, Harvey S

    2011-01-01

    The ability to make accurate judgments about the mental states of others, sometimes referred to as theory of mind (ToM), is often impaired following traumatic brain injury (TBI), and this deficit may contribute to problems with interpersonal relationships. The present study used an animated social attribution task (SAT) with functional magnetic resonance imaging (fMRI) to examine structures mediating ToM in adolescents with moderate to severe TBI. The study design also included a comparison group of matched, typically developing (TD) adolescents. The TD group exhibited activation within a number of areas that are thought to be relevant to ToM, including the medial prefrontal and anterior cingulate cortex, fusiform gyrus, and posterior temporal and parietal areas. The TBI subjects had significant activation within many of these same areas, but their activation was generally more intense and excluded the medial prefrontal cortex. Exploratory regression analyses indicated a negative relation between ToM-related activation and measures of white matter integrity derived from diffusion tensor imaging, while there was also a positive relation between activation and lesion volume. These findings are consistent with alterations in the level and pattern of brain activation that may be due to the combined influence of diffuse axonal injury and focal lesions.

  3. The emerging neuroprotective role of mitochondrial uncoupling protein-2 in traumatic brain injury

    OpenAIRE

    2015-01-01

    Traumatic brain injury (TBI) is a multifaceted disease with intrinsically complex heterogeneity and remains a significant clinical challenge to manage. TBI model systems have demonstrated many mechanisms that contribute to brain parenchymal cell death, including glutamate and calcium toxicity, oxidative stress, inflammation, and mitochondrial dysfunction. Mitochondria are critically regulated by uncoupling proteins (UCP), which allow protons to leak back into the matrix and thus r...

  4. Myocardial Dysfunction in Acute Traumatic Brain Injury Relieved by Surgical Decompression

    OpenAIRE

    Vijay Krishnamoorthy; Deepak Sharma; Sumidtra Prathep; Vavilala, Monica S.

    2013-01-01

    Traumatic brain injury (TBI) is a major public health issue and is a leading cause of death in North America. After a primary TBI, secondary brain insults can predispose patients to a worse outcome. One of the earliest secondary insults encountered during the perioperative period is hypotension, which has been directly linked to both mortality and poor disposition after TBI. Despite this, it has been shown that hypotension commonly occurs during surgery for TBI. We present a case of intraoper...

  5. Perspectives on Molecular Biomarkers of Oxidative Stress and Antioxidant Strategies in Traumatic Brain Injury

    OpenAIRE

    André Mendes Arent; Luiz Felipe de Souza; Roger Walz; Alcir Luiz Dafre

    2014-01-01

    Traumatic brain injury (TBI) is frequently associated with abnormal blood-brain barrier function, resulting in the release of factors that can be used as molecular biomarkers of TBI, among them GFAP, UCH-L1, S100B, and NSE. Although many experimental studies have been conducted, clinical consolidation of these biomarkers is still needed to increase the predictive power and reduce the poor outcome of TBI. Interestingly, several of these TBI biomarkers are oxidatively modified to carbonyl group...

  6. A new way of thinking: hydrocortisone in traumatic brain-injured patients

    OpenAIRE

    Roquilly, Antoine; Vourc'h, Mickael; Cinotti, Raphael; Asehnoune, Karim

    2013-01-01

    Data suggest that treatment of critical illness-related corticosteroid insufficiency after traumatic brain injury (TBI) with a stress dose of hydrocortisone may improve the neurological outcome and the mortality rate. The mineralocorticoid properties of hydrocortisone may reduce the rate of hyponatremia and of brain swelling. The exaggerated inflammatory response may cause critical illness-related corticosteroid insufficiency by altering the function of the hypothalamic–pituitary–adrenal axis...

  7. THE INCIDENCE OF NOSOCOMIAL INFECTIONS IN PATIENTS WITH ISOLATED SEVERE TRAUMATIC BRAIN INJURY

    Directory of Open Access Journals (Sweden)

    Valenčić Lara

    2015-12-01

    Full Text Available Introduction: Traumatic brain injury is the leading cause of death in children and adults in developed countries. Severe traumatic brain injury is classified with Glasgow Coma Scale score 8 and less. About 50% of patients with severe traumatic brain injury developes at least one infection as a complication of primary condition during hospitalization in the Intensive Care Unit, resulting with fatal outcome in 28% of patients. Ventilator associated pneumonia is the leading infection that affects patients with severe traumatic brain injury, with an incidence between 41% and 74%. Following are sepsis and urinary tract infections. The aim: To analyze the number of patients with nosocomial infection and isolated severe traumatic brain injury hospitalized in the Intensive Care Unit of the Clinical Hospital Centre Rijeka, Croatia, from 31st  January 2013 to 31st December 2014. Patients and methods: A two year retrospective study included 46 patients with isolated severe traumatic brain injury and nosocomial infection hospitalized in the Intensive Care Unit of the Clinical Hospital Centre Rijeka,Croatia, in the period from 31st January 2013 to 31st December 2014. All medical data was collected from the Division of Intensive Care Unit, Clinical Hospital Centre Rijeka, Croatia. Results: From 67 patients with isolated severe traumatic brain injury, 46 (68,65% of them developed nosocomial infection. There was statistically significant more male patients than female (p<0.05. The average age of infected patients was 57,8 years. The leading were the infections of the respiratory system. Gram negative bacteria Proteus mirabilis and Pseudomonas aerugnonsa were the leading pathogens. The average duration of the infection was 5,77 days. For 16 (34,78% of 46 patients the treatment outcome was lethal. Conclusion: Nosocomial infections are becoming a major public health problem. The emphasis must be set on the prevention which includes maintaining the hygiene and

  8. Early platelet dysfunction in a rodent model of blunt traumatic brain injury reflects the acute traumatic coagulopathy found in humans.

    Science.gov (United States)

    Donahue, Deborah L; Beck, Julia; Fritz, Braxton; Davis, Patrick; Sandoval-Cooper, Mayra J; Thomas, Scott G; Yount, Robert A; Walsh, Mark; Ploplis, Victoria A; Castellino, Francis J

    2014-02-15

    Acute coagulopathy is a serious complication of traumatic brain injury (TBI) and is of uncertain etiology because of the complex nature of TBI. However, recent work has shown a correlation between mortality and abnormal hemostasis resulting from early platelet dysfunction. The aim of the current study was to develop and characterize a rodent model of TBI that mimics the human coagulopathic condition so that mechanisms of the early acute coagulopathy in TBI can be more readily assessed. Studies utilizing a highly reproducible constrained blunt-force brain injury in rats demonstrate a strong correlation with important postinjury pathological changes that are observed in human TBI patients, namely, diminished platelet responses to agonists, especially adenosine diphosphate (ADP), and subarachnoid bleeding. Additionally, administration of a direct thrombin inhibitor, preinjury, recovers platelet functionality to ADP stimulation, indicating a direct role for excess thrombin production in TBI-induced early platelet dysfunction.

  9. 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.

  10. 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

  11. Inhibitory Effect of Progesterone on Inflammatory Factors After Experimental Traumatic Brain Injury

    Institute of Scientific and Technical Information of China (English)

    2007-01-01

    Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality in young people. Inflammatory cytokines play an important part in the pathophysiology of TBI. Recent studies demonstrate that progesterone significantly reduces cerebral edema and enhances functional recovery from TBI and stroke in several animal models. This study was designed to investigate the inhibitory effect of progesterone on inflammatory response after traumatic brain injury. Methods Progesterone was injected intraperitoneally using rats as a model of traumatic brain injury,and Western blot technique was applied to detect the expression of three inflammation-related factors:nuclear factor kappa B p65 (NFk B p65),glial fibrillary acidic protein (GFAP),and tumor necrosis factor-α (TNF-α). The water content of injured brain was also examined. A neurological severity score was recorded to evaluate the effect of progesterone on neurodeficit recovery. Results NFk B p65,GFAP,and TNF-α were increased in all injured animals. In rats treated with progesterone,the expression level of NFkB p65 and TNF-α were reduced significantly in comparison with vehicle-treated rats. However,progesterone did not alter the expression of GFAP in the injured rats. Progesterone also reduced the water content of injured brain and the lesion volume. In addition,progesterone-treated injured rats showed significant improvements in the Neurological Severity Score test,compared with vehicle-treated ones.Conclusions Progesterone inhibits the inflammatory response after experimental traumatic brain injury and mitigates the severity of brain damage.

  12. Posttraumatic Stress Disorder in patients with traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Schmidt Roger

    2004-03-01

    Full Text Available Abstract Background Severe traumatic stressors such as war, rape, or life-threatening accidents can result in a debilitating psychopathological development conceptualised as Posttraumatic Stress Disorder (PTSD. Pathological memory formation during an alarm response may set the precondition for PTSD to occur. If true, a lack of memory formation by extended unconsciousness in the course of the traumatic experience should preclude PTSD. Methods 46 patients from a neurological rehabilitation clinic were examined by means of questionnaires and structured clinical interviews. All patients had suffered a TBI due to an accident, but varied with respect to falling unconscious during the traumatic event. Results 27% of the sub-sample who were not unconscious for an extended period but only 3% (1 of 31 patients who were unconscious for more than 12 hours as a result of the accident were diagnosed as having current PTSD (P Conclusion TBI and PTSD are not mutually exclusive. However, victims of accidents are unlikely to develop a PTSD if the impact to the head had resulted in an extended period of unconsciousness.

  13. Combat posttraumatic stress disorder, substance use disorders, and traumatic brain injury.

    Science.gov (United States)

    Brady, Kathleen T; Tuerk, Peter; Back, Sudie E; Saladin, Michael E; Waldrop, Angela E; Myrick, Hugh

    2009-12-01

    Among both civilian and veteran populations, substance use disorders (SUDs) and anxiety disorders frequently co-occur. One of the most common comorbid anxiety disorder is posttraumatic stress disorder (PTSD), a condition which may develop after exposure to traumatic events, such as military combat. In comparison with the general population, rates of both SUDs and PTSD are elevated among veterans. Recent data show that soldiers returning from Iraq and Afghanistan demonstrate high rates of co-occurring SUDs, PTSD, and traumatic brain injury. Careful assessment of these conditions is critical and may be complicated by symptom overlap. More research targeting integrated interventions for these conditions is needed to establish optimal treatments.

  14. [The consequences of closed traumatic brain injury and piracetam efficacy in their treatment in adolescents].

    Science.gov (United States)

    Zavadenko, N N; Guzilova, L S

    2008-01-01

    The efficacy of piracetam in the treatment of the consequences of moderate and severe closed traumatic brain injury was assessed in 42 patients, aged 12-18 years, who suffered traumatic disorders 1,5-5 years before this study. Adolescents from the main group (20 patients) received piracetam in dosage of 40-50 mg/kg (or 1600-2400 mg daily) during one month. 22 patients of the second group were examined as controls. The positive therapeutic effects of piracetam on cognitive (memory, attention, executive functions) and motor (coordination) functions as well as the speed of cognitive and motor performance were demonstrated in this study.

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

    Institute of Scientific and Technical Information of China (English)

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

    2015-01-01

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

  16. Isolated cystic lesion of the callosal genu after traumatic brain injury.

    Science.gov (United States)

    Kato, Toru; Okumura, Akihisa; Tsuji, Takeshi; Emi, Misugi; Natsume, Jun

    2012-06-01

    We report the case of a 17-month-old infant who developed an isolated cystic lesion of the callosal genu as a unique lesion of traumatic axonal injury (TAI). Although one of the most common sites of TAI is the corpus callosum, there have been no reports describing the lesion seen in our patient. Brain computed tomography findings were normal on the day of the traffic accident. After 3 months, brain magnetic resonance imaging showed an isolated cystic lesion of the callosal genu that had the appearance of a cystic cavity. This lesion decreased in size 16 months later. The neuroimaging findings of this patient suggest that an isolated cystic lesion of the callosal genu could appear as a unique form of TAI in infants after traumatic brain injury (TBI), but it is nevertheless important to attend to such lesions in children with TBI.

  17. Circulating endothelial progenitor cells in traumatic brain injury: an emerging therapeutic target?

    Institute of Scientific and Technical Information of China (English)

    WEI Hui-jie; JIANG Rong-cai; LIU Li; ZHANG Jian-ning

    2010-01-01

    Traumatic brain injury (TBI) is a major cause ofmortality and morbidity in the world. Recent clinical investigations and basic researches suggest that strategies to improve angiogenesis following TBI may provide promising opportunities to improve clinical outcomes and brain functional recovery. More and more evidences show that circulating endothelial progenitor cells (EPCs), which have been identified in the peripheral blood, may play an important role in the pathologic and physiological angiogenesis in adults. Moreover, impressive data demonstrate that EPCs are mobilized from bone marrow to blood circulation in response to traumatic or inflammatory stimulations.In this review, we discussed the role of EPCs in the repair of brain injury and the possible therapeutic implication for functional recovery of TBl in the future.

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

    Science.gov (United States)

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

    2015-01-14

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

  19. 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.

  20. Hyperbaric oxygen therapy as a potential treatment for post-traumatic stress disorder associated with traumatic brain injury

    Science.gov (United States)

    Eve, David J; Steele, Martin R; Sanberg, Paul R; Borlongan, Cesar V

    2016-01-01

    Traumatic brain injury (TBI) describes the presence of physical damage to the brain as a consequence of an insult and frequently possesses psychological and neurological symptoms depending on the severity of the injury. The recent increased military presence of US troops in Iraq and Afghanistan has coincided with greater use of improvised exploding devices, resulting in many returning soldiers suffering from some degree of TBI. A biphasic response is observed which is first directly injury-related, and second due to hypoxia, increased oxidative stress, and inflammation. A proportion of the returning soldiers also suffer from post-traumatic stress disorder (PTSD), and in some cases, this may be a consequence of TBI. Effective treatments are still being identified, and a possible therapeutic candidate is hyperbaric oxygen therapy (HBOT). Some clinical trials have been performed which suggest benefits with regard to survival and disease severity of TBI and/or PTSD, while several other studies do not see any improvement compared to a possibly poorly controlled sham. HBOT has been shown to reduce apoptosis, upregulate growth factors, promote antioxidant levels, and inhibit inflammatory cytokines in animal models, and hence, it is likely that HBOT could be advantageous in treating at least the secondary phase of TBI and PTSD. There is some evidence of a putative prophylactic or preconditioning benefit of HBOT exposure in animal models of brain injury, and the optimal time frame for treatment is yet to be determined. HBOT has potential side effects such as acute cerebral toxicity and more reactive oxygen species with long-term use, and therefore, optimizing exposure duration to maximize the reward and decrease the detrimental effects of HBOT is necessary. This review provides a summary of the current understanding of HBOT as well as suggests future directions including prophylactic use and chronic treatment. PMID:27799776