Hypopituitarism after acute brain injury.

Science.gov (United States)

Urban, Randall J

2006-07-01

Acute brain injury has many causes, but the most common is trauma. There are 1.5-2.0 million traumatic brain injuries (TBI) in the United States yearly, with an associated cost exceeding 10 billion dollars. TBI is the most common cause of death and disability in young adults less than 35 years of age. The consequences of TBI can be severe, including disability in motor function, speech, cognition, and psychosocial and emotional skills. Recently, clinical studies have documented the occurrence of pituitary dysfunction after TBI and another cause of acute brain injury, subarachnoid hemorrhage (SAH). These studies have consistently demonstrated a 30-40% occurrence of pituitary dysfunction involving at least one anterior pituitary hormone following a moderate to severe TBI or SAH. Growth hormone (GH) deficiency is the most common pituitary hormone disorder, occurring in approximately 20% of patients when multiple tests of GH deficiency are used. Within 7-21 days of acute brain injury, adrenal insufficiency is the primary concern. Pituitary function can fluctuate over the first year after TBI, but it is well established by 1 year. Studies are ongoing to assess the effects of hormone replacement on motor function and cognition in TBI patients. Any subject with a moderate to severe acute brain injury should be screened for pituitary dysfunction.

Mechanical injury induces brain endothelial-derived microvesicle release: Implications for cerebral vascular injury during traumatic brain injury

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Allison M. Andrews

2016-02-01

Full Text Available It is well established that the endothelium responds to mechanical forces induced by changes in shear stress and mechanotransduction. However, our understanding of vascular remodeling following traumatic brain injury (TBI remains incomplete. Recently published studies have revealed that lung and umbilical endothelial cells produce extracellular microvesicles (eMVs, such as microparticles, in response to changes in mechanical forces (blood flow and mechanical injury. Yet, to date, no studies have shown whether brain endothelial cells produce eMVs following TBI. The brain endothelium is highly specialized and forms the blood-brain barrier (BBB, which regulates diffusion and transport of solutes into the brain. This specialization is largely due to the presence of tight junction proteins (TJPs between neighboring endothelial cells. Following TBI, a breakdown in tight junction complexes at the BBB leads to increased permeability, which greatly contributes to the secondary phase of injury. We have therefore tested the hypothesis that brain endothelium responds to mechanical injury, by producing eMVs that contain brain endothelial proteins, specifically TJPs. In our study, primary human adult brain microvascular endothelial cells (BMVEC were subjected to rapid mechanical injury to simulate the abrupt endothelial disruption that can occur in the primary injury phase of TBI. eMVs were isolated from the media following injury at 2, 6, 24 and 48 hrs. Western blot analysis of eMVs demonstrated a time-dependent increase in TJP occludin, PECAM-1 and ICAM-1 following mechanical injury. In addition, activation of ARF6, a small GTPase linked to extracellular vesicle production, was increased after injury. To confirm these results in vivo, mice were subjected to sham surgery or TBI and blood plasma was collected 24 hrs post-injury. Isolation and analysis of eMVs from blood plasma using cryo-EM and flow cytometry revealed elevated levels of vesicles containing

Mechanical Injury Induces Brain Endothelial-Derived Microvesicle Release: Implications for Cerebral Vascular Injury during Traumatic Brain Injury.

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Andrews, Allison M; Lutton, Evan M; Merkel, Steven F; Razmpour, Roshanak; Ramirez, Servio H

2016-01-01

It is well established that the endothelium responds to mechanical forces induced by changes in shear stress and strain. However, our understanding of vascular remodeling following traumatic brain injury (TBI) remains incomplete. Recently published studies have revealed that lung and umbilical endothelial cells produce extracellular microvesicles (eMVs), such as microparticles, in response to changes in mechanical forces (blood flow and mechanical injury). Yet, to date, no studies have shown whether brain endothelial cells produce eMVs following TBI. The brain endothelium is highly specialized and forms the blood-brain barrier (BBB), which regulates diffusion and transport of solutes into the brain. This specialization is largely due to the presence of tight junction proteins (TJPs) between neighboring endothelial cells. Following TBI, a breakdown in tight junction complexes at the BBB leads to increased permeability, which greatly contributes to the secondary phase of injury. We have therefore tested the hypothesis that brain endothelium responds to mechanical injury, by producing eMVs that contain brain endothelial proteins, specifically TJPs. In our study, primary human adult brain microvascular endothelial cells (BMVEC) were subjected to rapid mechanical injury to simulate the abrupt endothelial disruption that can occur in the primary injury phase of TBI. eMVs were isolated from the media following injury at 2, 6, 24, and 48 h. Western blot analysis of eMVs demonstrated a time-dependent increase in TJP occludin, PECAM-1 and ICAM-1 following mechanical injury. In addition, activation of ARF6, a small GTPase linked to extracellular vesicle production, was increased after injury. To confirm these results in vivo, mice were subjected to sham surgery or TBI and blood plasma was collected 24 h post-injury. Isolation and analysis of eMVs from blood plasma using cryo-EM and flow cytometry revealed elevated levels of vesicles containing occludin following brain trauma

Clinical Utility and Psychometric Properties of the Traumatic Brain Injury Quality of Life Scale (TBI-QOL) in US Military Service Members.

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Lange, Rael T; Brickell, Tracey A; Bailie, Jason M; Tulsky, David S; French, Louis M

2016-01-01

To examine the clinical utility and psychometric properties of the Traumatic Brain Injury Quality of Life (TBI-QOL) scale in a US military population. One hundred fifty-two US military service members (age: M = 34.3, SD = 9.4; 89.5% men) prospectively enrolled from the Walter Reed National Military Medical Center and other nationwide community outreach initiatives. Participants included 99 service members who had sustained a mild traumatic brain injury (TBI) and 53 injured or noninjured controls without TBI (n = 29 and n = 24, respectively). Participants completed the TBI-QOL scale and 5 other behavioral measures, on average, 33.8 months postinjury (SD = 37.9). Fourteen TBI-QOL subscales; Neurobehavioral Symptom Inventory; Posttraumatic Stress Disorder Checklist-Civilian version; Alcohol Use Disorders Identification Test; Combat Exposure Scale. The internal consistency reliability of the TBI-QOL scales ranged from α = .91 to α = .98. The convergent and discriminant validity of the 14 TBI-QOL subscales was high. The mild TBI group had significantly worse scores on 10 of the 14 TBI-QOL subscales than the control group (range, P quality of life in a mild TBI military sample. Additional research is recommended to further evaluate the clinical utility of the TBI-QOL scale in both military and civilian settings.

Patterns of post-acute health care utilization after a severe traumatic brain injury: Results from the PariS-TBI cohort.

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Jourdan, Claire; Bayen, Eleonore; Darnoux, Emmanuelle; Ghout, Idir; Azerad, Sylvie; Ruet, Alexis; Vallat-Azouvi, Claire; Pradat-Diehl, Pascale; Aegerter, Philippe; Weiss, Jean-Jacques; Azouvi, Philippe

2015-01-01

To assess brain injury services utilization and their determinants using Andersen's model. Prospective follow-up of the PariS-TBI inception cohort. Out of 504 adults with severe traumatic brain injury (TBI), 245 survived and 147 received a 4-year outcome assessment (mean age 33 years, 80% men). Provision rates of medical, rehabilitation, social and re-entry services and their relations to patients' characteristics were assessed. Following acute care discharge, 78% of patients received physiotherapy, 61% speech/cognitive therapy, 50% occupational therapy, 41% psychological assistance, 63% specialized medical follow-up, 21% community re-entry assistance. Health-related need factors, in terms of TBI severity, were the main predictors of services. Provision of each therapy was significantly associated with corresponding speech, motor and psychological impairments. However, care provision did not depend on cognitive impairments and cognitive therapy was related to pre-disposing and geographical factors. Community re-entry assistance was provided to younger and more independent patients. These quantitative findings illustrate strengths and weaknesses of late brain injury care provision in urban France and highlight the need to improve treatment of cognitive impairments.

Ubiquinol treatment for TBI in male rats: Effects on mitochondrial integrity, injury severity, and neurometabolism.

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Pierce, Janet D; Gupte, Raeesa; Thimmesch, Amanda; Shen, Qiuhua; Hiebert, John B; Brooks, William M; Clancy, Richard L; Diaz, Francisco J; Harris, Janna L

2018-06-01

Following traumatic brain injury (TBI), there is significant secondary damage to cerebral tissue from increased free radicals and impaired mitochondrial function. This imbalance between reactive oxygen species (ROS) production and the effectiveness of cellular antioxidant defenses is termed oxidative stress. Often there are insufficient antioxidants to scavenge ROS, leading to alterations in cerebral structure and function. Attenuating oxidative stress following a TBI by administering an antioxidant may decrease secondary brain injury, and currently many drugs and supplements are being investigated. We explored an over-the-counter supplement called ubiquinol (reduced form of coenzyme Q10), a potent antioxidant naturally produced in brain mitochondria. We administered intra-arterial ubiquinol to rats to determine if it would reduce mitochondrial damage, apoptosis, and severity of a contusive TBI. Adult male F344 rats were randomly assigned to one of three groups: (1) Saline-TBI, (2) ubiquinol 30 minutes before TBI (UB-PreTBI), or (3) ubiquinol 30 minutes after TBI (UB-PostTBI). We found when ubiquinol was administered before or after TBI, rats had an acute reduction in brain mitochondrial damage, apoptosis, and two serum biomarkers of TBI severity, glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1). However, in vivo neurometabolic assessment with proton magnetic resonance spectroscopy did not show attenuated injury-induced changes. These findings are the first to show that ubiquinol preserves mitochondria and reduces cellular injury severity after TBI, and support further study of ubiquinol as a promising adjunct therapy for TBI. © 2018 Wiley Periodicals, Inc.

Brain injuries from blast.

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Bass, Cameron R; Panzer, Matthew B; Rafaels, Karen A; Wood, Garrett; Shridharani, Jay; Capehart, Bruce

2012-01-01

Traumatic brain injury (TBI) from blast produces a number of conundrums. This review focuses on five fundamental questions including: (1) What are the physical correlates for blast TBI in humans? (2) Why is there limited evidence of traditional pulmonary injury from blast in current military field epidemiology? (3) What are the primary blast brain injury mechanisms in humans? (4) If TBI can present with clinical symptoms similar to those of Post-Traumatic Stress Disorder (PTSD), how do we clinically differentiate blast TBI from PTSD and other psychiatric conditions? (5) How do we scale experimental animal models to human response? The preponderance of the evidence from a combination of clinical practice and experimental models suggests that blast TBI from direct blast exposure occurs on the modern battlefield. Progress has been made in establishing injury risk functions in terms of blast overpressure time histories, and there is strong experimental evidence in animal models that mild brain injuries occur at blast intensities that are similar to the pulmonary injury threshold. Enhanced thoracic protection from ballistic protective body armor likely plays a role in the occurrence of blast TBI by preventing lung injuries at blast intensities that could cause TBI. Principal areas of uncertainty include the need for a more comprehensive injury assessment for mild blast injuries in humans, an improved understanding of blast TBI pathophysiology of blast TBI in animal models and humans, the relationship between clinical manifestations of PTSD and mild TBI from blunt or blast trauma including possible synergistic effects, and scaling between animals models and human exposure to blasts in wartime and terrorist attacks. Experimental methodologies, including location of the animal model relative to the shock or blast source, should be carefully designed to provide a realistic blast experiment with conditions comparable to blasts on humans. If traditional blast scaling is

The Impact of Traumatic Brain Injury on the Aging Brain.

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Young, Jacob S; Hobbs, Jonathan G; Bailes, Julian E

2016-09-01

Traumatic brain injury (TBI) has come to the forefront of both the scientific and popular culture. Specifically, sports-related concussions or mild TBI (mTBI) has become the center of scientific scrutiny with a large amount of research focusing on the long-term sequela of this type of injury. As the populace continues to age, the impact of TBI on the aging brain will become clearer. Currently, reports have come to light that link TBI to neurodegenerative disorders such as Alzheimer's and Parkinson's diseases, as well as certain psychiatric diseases. Whether these associations are causations, however, is yet to be determined. Other long-term sequelae, such as chronic traumatic encephalopathy (CTE), appear to be associated with repetitive injuries. Going forward, as we gain better understanding of the pathophysiological process involved in TBI and subclinical head traumas, and individual traits that influence susceptibility to neurocognitive diseases, a clearer, more comprehensive understanding of the connection between brain injury and resultant disease processes in the aging brain will become evident.

When Injury Clouds Understanding of Others: Theory of Mind after Mild TBI in Preschool Children.

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Bellerose, Jenny; Bernier, Annie; Beaudoin, Cindy; Gravel, Jocelyn; Beauchamp, Miriam H

2015-08-01

There is evidence to suggest that social skills, such as the ability to understand the perspective of others (theory of mind), may be affected by childhood traumatic brain injuries; however, studies to date have only considered moderate and severe traumatic brain injury (TBI). This study aimed to assess theory of mind after early, mild TBI (mTBI). Fifty-one children who sustained mTBI between 18 and 60 months were evaluated 6 months post-injury on emotion and desires reasoning and false-belief understanding tasks. Their results were compared to that of 50 typically developing children. The two groups did not differ on baseline characteristics, except for pre- and post-injury externalizing behavior. The mTBI group obtained poorer scores relative to controls on both the emotion and desires task and the false-belief understanding task, even after controlling for pre-injury externalizing behavior. No correlations were found between TBI injury characteristics and theory of mind. This is the first evidence that mTBI in preschool children is associated with theory of mind difficulties. Reduced perspective taking abilities could be linked with the social impairments that have been shown to arise following TBI.

Mechanistic Links Between PARP, NAD, and Brain Inflammation After TBI

Science.gov (United States)

2015-10-01

1 AWARD NUMBER: W81XWH-13-2-0091 TITLE: Mechanistic Links Between PARP, NAD , and Brain Inflammation After TBI PRINCIPAL INVESTIGATOR...COVERED 25 Sep 2014 - 24 Sep 2015 4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER Mechanistic Links Between PARP, NAD , and Brain Inflammation After TBI 5b. GRANT...efficacy of veliparib and NAD as agents for suppressing inflammation and improving outcomes after traumatic brain injury. The animal models include

Predictive factors for 1-year outcome of a cohort of patients with severe traumatic brain injury (TBI): results from the PariS-TBI study.

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Jourdan, C; Bosserelle, V; Azerad, S; Ghout, I; Bayen, E; Aegerter, P; Weiss, J J; Mateo, J; Lescot, T; Vigué, B; Tazarourte, K; Pradat-Diehl, P; Azouvi, P

2013-01-01

To assess outcome and predicting factors 1 year after a severe traumatic brain injury (TBI). Multi-centre prospective inception cohort study of patients aged 15 or older with a severe TBI in the Parisian area, France. Data were collected prospectively starting the day of injury. One-year evaluation included the relatives-rating of the Dysexecutive Questionnaire (DEX-R), the Glasgow Outcome Scale-Extended (GOSE) and employment. Univariate and multivariate tests were computed. Among 257 survivors, 134 were included (mean age 36 years, 84% men). Good recovery concerned 19%, moderate disability 43% and severe disability 38%. Among patients employed pre-injury, 42% were working, 28% with no job change. DEX-R score was significantly associated with length of education only. Among initial severity measures, only the IMPACT prognostic score was significantly related to GOSE in univariate analyses, while measures relating to early evolution were more significant predictors. In multivariate analyses, independent predictors of GOSE were length of stay in intensive care (LOS), age and education. Independent predictors of employment were LOS and age. Age, education and injury severity are independent predictors of global disability and return to work 1 year after a severe TBI.

Diffusion tensor imaging (DTI) findings in adult civilian, military, and sport-related mild traumatic brain injury (mTBI): a systematic critical review.

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Asken, Breton Michael; DeKosky, Steven T; Clugston, James R; Jaffee, Michael S; Bauer, Russell M

2018-04-01

This review seeks to summarize diffusion tensor imaging (DTI) studies that have evaluated structural changes attributed to the mechanisms of mild traumatic brain injury (mTBI) in adult civilian, military, and athlete populations. Articles from 2002 to 2016 were retrieved from PubMed/MEDLINE, EBSCOhost, and Google Scholar, using a Boolean search string containing the following terms: "diffusion tensor imaging", "diffusion imaging", "DTI", "white matter", "concussion", "mild traumatic brain injury", "mTBI", "traumatic brain injury", and "TBI". We added studies not identified by this method that were found via manually-searched reference lists. We identified 86 eligible studies from English-language journals using, adult, human samples. Studies were evaluated based on duration between injury and DTI assessment, categorized as acute, subacute/chronic, remote mTBI, and repetitive brain trauma considerations. Since changes in brain structure after mTBI can also be affected by other co-occurring medical and demographic factors, we also briefly review DTI studies that have addressed socioeconomic status factors (SES), major depressive disorder (MDD), and attention-deficit hyperactivity disorder (ADHD). The review describes population-specific risks and the complications of clinical versus pathophysiological outcomes of mTBI. We had anticipated that the distinct population groups (civilian, military, and athlete) would require separate consideration, and various aspects of the study characteristics supported this. In general, study results suggested widespread but inconsistent differences in white matter diffusion metrics (primarily fractional anisotropy [FA], mean diffusivity [MD], radial diffusivity [RD], and axial diffusivity [AD]) following mTBI/concussion. Inspection of study designs and results revealed potential explanations for discrepant DTI findings, such as control group variability, analytic techniques, the manner in which regional differences were reported, and

Influence of Mild Traumatic Brain Injury (TBI) and Posttraumatic Stress Disorder (PTSD) on Pain Intensity Levels in OEF/OIF/OND Veterans.

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Stojanovic, Milan P; Fonda, Jennifer; Fortier, Catherine Brawn; Higgins, Diana M; Rudolph, James L; Milberg, William P; McGlinchey, Regina E

2016-11-01

Mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD) are common among US veterans of Operation Enduring Freedom/Operation Iraqi Freedom/Operation New Dawn (OEF/OIF/OND). We postulated that these injuries may modulate pain processing in these individuals and affect their subjective pain levels. Cross-sectional. 310 deployed service members of OEF/OIF/OND without a lifetime history of moderate or severe TBI were included in this study. All participants completed a comprehensive evaluation for Blast Exposure, mTBI, PTSD, and Pain Levels. The Boston Assessment of TBI-Lifetime Version (BAT-L) was used to assess blast exposure and potential brain injury during military service. The Clinician-Administered PTSD Scale (CAPS) characterized presence and severity of PTSD. The Visual Analog Scale (VAS) was used to assess pain intensity over the previous month before the interview, with higher scores indicative of worse pain. Statistical analysis was performed by ANOVA and results were adjusted for co-morbidities, clinical characteristics and demographic data. In comparison to control participants (veterans without mTBI or current PTSD), veterans with both current PTSD and mTBI reported the highest pain intensity levels, followed by veterans with PTSD only (P Pain levels in veterans with mTBI only were comparable to control participants. Comorbid PTSD and mTBI is associated with increased self-reported pain intensity. mTBI alone was not associated with increased pain. Published by Oxford University Press on behalf of the American Academy of Pain Medicine 2016. This work is written by US Government employees and is in the public domain in the US.

Targeting Epigenetic Mechanisms in Pain due to Trauma and Traumatic Brain Injury(TBI)

Science.gov (United States)

2016-10-01

after incision and TBI, and the relationship of those changes to CXCR2 expression ST4.1 Establish spinal cord sites and cell types displaying...we plan to use oral preparations of these drugs and establish dose-response relationships as these will be pharmacologically useful and make the...Anesthesiology Annual Awards Dinner . Palo Alto, CA, June, 2016. 4. Epigenetic Regulation of Chronic Pain after Traumatic Brain Injury. De-Yong

Psychological and marital adjustment in couples following a traumatic brain injury (TBI): a critical review.

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Blais, Marie Claude; Boisvert, Jean-Marie

2005-12-20

The first part of this paper examines current data describing the psychological and marital adjustment of couples following a traumatic brain injury (TBI). Although these findings reveal some discrepancies, they highlight that adjustment following a TBI represents a genuine challenge for those involved in the process. The second part moves toward the examination of factors associated with psychological and marital adjustment in both couple partners. Here again, there exists a large diversity in empirical data and theoretical models informing this emerging area of interest. Nevertheless, cognitive variables such as coping skills are commonly seen as critical variables to explain the adjustment level in people with TBI and their spouse/caregivers. Concurrently with the discussion of the methodological issues and pitfalls encountered in this area of research, the conclusion provides suggestions of further steps to undertake in this endeavour toward a better understanding of the adjustment process following TBI.

Autobiographical memory and structural brain changes in chronic phase TBI.

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Esopenko, Carrie; Levine, Brian

2017-04-01

Traumatic brain injury (TBI) is associated with a range of neuropsychological deficits, including attention, memory, and executive functioning attributable to diffuse axonal injury (DAI) with accompanying focal frontal and temporal damage. Although the memory deficit of TBI has been well characterized with laboratory tests, comparatively little research has examined retrograde autobiographical memory (AM) at the chronic phase of TBI, with no prior studies of unselected patients drawn directly from hospital admissions for trauma. Moreover, little is known about the effects of TBI on canonical episodic and non-episodic (e.g., semantic) AM processes. In the present study, we assessed the effects of chronic-phase TBI on AM in patients with focal and DAI spanning the range of TBI severity. Patients and socioeconomic- and age-matched controls were administered the Autobiographical Interview (AI) (Levine, Svoboda, Hay, Winocur, & Moscovitch, 2002) a widely used method for dissociating episodic and semantic elements of AM, along with tests of neuropsychological and functional outcome. Measures of episodic and non-episodic AM were compared with regional brain volumes derived from high-resolution structural magnetic resonance imaging (MRI). Severe TBI (but not mild or moderate TBI) was associated with reduced recall of episodic autobiographical details and increased recall of non-episodic details relative to healthy comparison participants. There were no significant associations between AM performance and neuropsychological or functional outcome measures. Within the full TBI sample, autobiographical episodic memory was associated with reduced volume distributed across temporal, parietal, and prefrontal regions considered to be part of the brain's AM network. These results suggest that TBI-related distributed volume loss affects episodic autobiographical recollection. Copyright © 2017 Elsevier Ltd. All rights reserved.

Traumatic brain injury (TBI) outcomes in an LMIC tertiary care centre and performance of trauma scores.

Science.gov (United States)

Samanamalee, Samitha; Sigera, Ponsuge Chathurani; De Silva, Ambepitiyawaduge Pubudu; Thilakasiri, Kaushila; Rashan, Aasiyah; Wadanambi, Saman; Jayasinghe, Kosala Saroj Amarasiri; Dondorp, Arjen M; Haniffa, Rashan

2018-01-08

This study evaluates post-ICU outcomes of patients admitted with moderate and severe Traumatic Brain Injury (TBI) in a tertiary neurocritical care unit in an low middle income country and the performance of trauma scores: A Severity Characterization of Trauma, Trauma and Injury Severity Score, Injury Severity Score and Revised Trauma Score in this setting. Adult patients directly admitted to the neurosurgical intensive care units of the National Hospital of Sri Lanka between 21st July 2014 and 1st October 2014 with moderate or severe TBI were recruited. A telephone administered questionnaire based on the Glasgow Outcome Scale Extended (GOSE) was used to assess functional outcome of patients at 3 and 6 months after injury. The economic impact of the injury was assessed before injury, and at 3 and 6 months after injury. One hundred and one patients were included in the study. Survival at ICU discharge, 3 and 6 months after injury was 68.3%, 49.5% and 45.5% respectively. Of the survivors at 3 months after injury, 43 (86%) were living at home. Only 19 (38%) patients had a good recovery (as defined by GOSE 7 and 8). Three months and six months after injury, respectively 25 (50%) and 14 (30.4%) patients had become "economically dependent". Selected trauma scores had poor discriminatory ability in predicting mortality. This observational study of patients sustaining moderate or severe TBI in Sri Lanka (a LMIC) reveals only 46% of patients were alive at 6 months after ICU discharge and only 20% overall attained a good (GOSE 7 or 8) recovery. The social and economic consequences of TBI were long lasting in this setting. Injury Severity Score, Revised Trauma Score, A Severity Characterization of Trauma and Trauma and Injury Severity Score, all performed poorly in predicting mortality in this setting and illustrate the need for setting adapted tools.

Multi-scale mechanics of traumatic brain injury

NARCIS (Netherlands)

Cloots, R.J.H.

2011-01-01

Traumatic brain injury (TBI) can be caused by road traffic, sports-related or other types of accidents and often leads to permanent health issues or even death. For a good prevention or diagnosis of TBI, brain injury criteria are used to assess the probability of brain injury as a result of a

Severe Traumatic Brain Injury

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... TBI Online Concussion Training Press Room Guide to Writing about TBI in News and Social Media Living with TBI HEADS UP to Brain Injury Awareness Get Email Updates To receive email updates about this topic, ...

Agmatine Attenuates Brain Edema and Apoptotic Cell Death after Traumatic Brain Injury.

Science.gov (United States)

Kim, Jae Young; Lee, Yong Woo; Kim, Jae Hwan; Lee, Won Taek; Park, Kyung Ah; Lee, Jong Eun

2015-07-01

Traumatic brain injury (TBI) is associated with poor neurological outcome, including necrosis and brain edema. In this study, we investigated whether agmatine treatment reduces edema and apoptotic cell death after TBI. TBI was produced by cold injury to the cerebral primary motor cortex of rats. Agmatine was administered 30 min after injury and once daily until the end of the experiment. Animals were sacrificed for analysis at 1, 2, or 7 days after the injury. Various neurological analyses were performed to investigate disruption of the blood-brain barrier (BBB) and neurological dysfunction after TBI. To examine the extent of brain edema after TBI, the expression of aquaporins (AQPs), phosphorylation of mitogen-activated protein kinases (MAPKs), and nuclear translocation of nuclear factor-κB (NF-κB) were investigated. Our findings demonstrated that agmatine treatment significantly reduces brain edema after TBI by suppressing the expression of AQP1, 4, and 9. In addition, agmatine treatment significantly reduced apoptotic cell death by suppressing the phosphorylation of MAPKs and by increasing the nuclear translocation of NF-κB after TBI. These results suggest that agmatine treatment may have therapeutic potential for brain edema and neural cell death in various central nervous system diseases.

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…

Project Career: Perceived benefits of iPad apps among college students with Traumatic Brain Injury (TBI).

Science.gov (United States)

Jacobs, K; Leopold, A; Hendricks, D J; Sampson, E; Nardone, A; Lopez, K B; Rumrill, P; Stauffer, C; Elias, E; Scherer, M; Dembe, J

2017-09-14

Project Career is an interprofessional five-year development project designed to improve academic and employment success of undergraduate students with a traumatic brain injury (TBI) at two- and four-year colleges and universities. Students receive technology in the form of iPad applications ("apps") to support them in and out of the classroom. To assess participants' perspectives on technology at baseline and perceived benefit of apps after 6 and 12 months of use. This article address a component of a larger study. Participants included 50 college-aged students with traumatic brain injuries. Statistical analysis included data from two Matching Person and Technology (MPT) assessment forms, including the Survey of Technology Use at baseline and the Assistive Technology Use Follow-Up Survey: Apps Currently Using, administered at 6- and 12-months re-evaluation. Analyses included frequencies and descriptives. Average scores at baseline indicated positive perspectives on technology. At 6 months, quality of life (67%) and academics (76%) improved moderately or more from the use of iPad apps. At 12 months, quality of life (65%) and academics (82%) improved moderately or more from the use of iPad apps. Students with a TBI have positive perspectives on technology use. The results on perceived benefit of apps indicated that students with a TBI (including civilians and veterans) report that the apps help them perform in daily life and academic settings.

Variation in structure and process of care in traumatic brain injury: Provider profiles of European Neurotrauma Centers participating in the CENTER-TBI study

NARCIS (Netherlands)

M.C. Cnossen (Maryse); S. Polinder (Suzanne); Lingsma, H.F. (Hester F.); A.I.R. Maas (Andrew); D.K. Menon (David ); E.W. Steyerberg (Ewout); Adams, H. (Hadie); Alessandro, M. (Masala); J.E. Allanson (Judith); Amrein, K. (Krisztina); Andaluz, N. (Norberto); N. Andelic (Nada); Andrea, N. (Nanni); L. Andreassen (Lasse); Anke, A. (Audny); Antoni, A. (Anna); Ardon, H. (Hilko); G. Audibert (Gérard); Auslands, K. (Kaspars); Azouvi, P. (Philippe); Baciu, C. (Camelia); Bacon, A. (Andrew); Badenes, R. (Rafael); Baglin, T. (Trevor); Bartels, R. (Ronald); Barzó, P. (Pál); Bauerfeind, U. (Ursula); R. Beer (Ronny); Belda, F.J. (Francisco Javier); B.-M. Bellander (Bo-Michael); A. Belli (Antonio); Bellier, R. (Rémy); H. Benali (Habib); Benard, T. (Thierry); M. Berardino (Maurizio); Beretta, L. (Luigi); Beynon, C. (Christopher); Bilotta, F. (Federico); H. Binder (Harald); Biqiri, E. (Erta); Blaabjerg, M. (Morten); Borgen, L.S. (Lund Stine); Bouzat, P. (Pierre); Bragge, P. (Peter); A. Brazinova (Alexandra); F. Brehar (Felix); Brorsson, C. (Camilla); Buki, A. (Andras); M. Bullinger (Monika); Bučková, V. (Veronika); Calappi, E. (Emiliana); P. Cameron (Peter); Carbayo, L.G. (Lozano Guillermo); Carise, E. (Elsa); Carpenter, C.; Castaño-León, A.M. (Ana M.); Causin, F. (Francesco); Chevallard, G. (Giorgio); A. Chieregato (Arturo); G. Citerio (Giuseppe); M. Coburn (Mark); J.P. Coles (Jonathan P.); Cooper, J.D. (Jamie D.); Correia, M. (Marta); A. Covic (Amra); N. Curry (Nicola); E. Czeiter (Endre); M. Czosnyka (Marek); Dahyot-Fizelier, C. (Claire); F. Damas (François); P. Damas (Pierre); H. Dawes (Helen); De Keyser, V. (Véronique); F. Della Corte (Francesco); B. Depreitere (Bart); Ding, S. (Shenghao); D.W.J. Dippel (Diederik); K. Dizdarevic (Kemal); Dulière, G.-L. (Guy-Loup); Dzeko, A. (Adelaida); G. Eapen (George); Engemann, H. (Heiko); A. Ercole (Ari); P. Esser (Patrick); Ezer, E. (Erzsébet); M. Fabricius (Martin); V.L. Feigin (V.); Feng, J. (Junfeng); Foks, K. (Kelly); F. Fossi (Francesca); Francony, G. (Gilles); J. Frantzén (Janek); Freo, U. (Ulderico); S.K. Frisvold (Shirin Kordasti); Furmanov, A. (Alex); P. Gagliardo (Pablo); D. Galanaud (Damien); G. Gao (Guoyi); K. Geleijns (Karin); A. Ghuysen (Alexandre); Giraud, B. (Benoit); Glocker, B. (Ben); Gomez, P.A. (Pedro A.); Grossi, F. (Francesca); R.L. Gruen (Russell); Gupta, D. (Deepak); J.A. Haagsma (Juanita); E. Hadzic (Ermin); I. Haitsma (Iain); J.A. Hartings (Jed); R. Helbok (Raimund); E. Helseth (Eirik); Hertle, D. (Daniel); S. Hill (Sean); Hoedemaekers, A. (Astrid); S. Hoefer (Stefan); P.J. Hutchinson (Peter J.); Håberg, A.K. (Asta Kristine); B.C. Jacobs (Bart); Janciak, I. (Ivan); K. Janssens (Koen); J.-Y. Jiang (Ji-Yao); Jones, K. (Kelly); Kalala, J.-P. (Jean-Pierre); Kamnitsas, K. (Konstantinos); Karan, M. (Mladen); Karau, J. (Jana); A. Katila (Ari); M. Kaukonen (Maija); Keeling, D. (David); Kerforne, T. (Thomas); N. Ketharanathan (Naomi); J. Kettunen (Johannes); Kivisaari, R. (Riku); A.G. Kolias (Angelos G.); Kolumbán, B. (Bálint); E.J.O. Kompanje (Erwin); D. Kondziella (Daniel); L.-O. Koskinen (Lars-Owe); Kovács, N. (Noémi); F. Kalovits (Ferenc); A. Lagares (Alfonso); L. Lanyon (Linda); S. Laureys (Steven); Lauritzen, M. (Martin); F.E. Lecky (Fiona); C. Ledig (Christian); R. Lefering; V. Legrand (Valerie); Lei, J. (Jin); L. Levi (Leon); R. Lightfoot (Roger); H.F. Lingsma (Hester); D. Loeckx (Dirk); Lozano, A. (Angels); Luddington, R. (Roger); Luijten-Arts, C. (Chantal); A.I.R. Maas (Andrew I.R.); MacDonald, S. (Stephen); MacFayden, C. (Charles); M. Maegele (Marc); M. Majdan (Marek); Major, S. (Sebastian); A. Manara (Alex); Manhes, P. (Pauline); G. Manley (Geoffrey); Martin, D. (Didier); C. Martino (Costanza); Maruenda, A. (Armando); H. Maréchal (Hugues); Mastelova, D. (Dagmara); Mattern, J. (Julia); C. McMahon (Catherine); Melegh, B. (Béla); T. Menovsky (Tomas); C. Morganti-Kossmann (Cristina); Mulazzi, D. (Davide); Mutschler, M. (Manuel); H. Mühlan (Holger); Negru, A. (Ancuta); D. Nelson (David); E. Neugebauer (Eddy); V.F. Newcombe (Virginia F.); Noirhomme, Q. (Quentin); Nyirádi, J. (József); M. Oddo (Mauro); Oldenbeuving, A. (Annemarie); M. Oresic (Matej); Ortolano, F. (Fabrizio); A. Palotie (Aarno); P.M. Parizel; Patruno, A. (Adriana); J.-F. Payen (Jean-François); Perera, N. (Natascha); V. Perlbarg (Vincent); Persona, P. (Paolo); W.C. Peul (Wilco); N. Pichon (Nicolas); Piilgaard, H. (Henning); A. Piippo (Anna); Pili, F.S. (Floury Sébastien); M. Pirinen (Matti); H. Ples (Horia); Pomposo, I. (Inigo); M. Psota (Marek); P. Pullens (Pim); L. Puybasset (Louis); A. Ragauskas (Arminas); Raj, R. (Rahul); Rambadagalla, M. (Malinka); Rehorčíková, V. (Veronika); J.K.J. Rhodes (Jonathan K.J.); S. Richardson (Sylvia); S. Ripatti (Samuli); S. Rocka (Saulius); Rodier, N. (Nicolas); Roe, C. (Cecilie); Roise, O. (Olav); Roks, G. (Gerwin); Romegoux, P. (Pauline); J. Rosand (Jonathan); Rosenfeld, J. (Jeffrey); C. Rosenlund (Christina); G. Rosenthal (Guy); R. Rossaint (Rolf); S. Rossi (Sandra); Rostalski, T. (Tim); Rueckert, D.L. (Danie L.); Ruiz De Arcaute, F. (Felix); M. Rusnák (Martin); Sacchi, M. (Marco); Sahakian, B. (Barbara); J. Sahuquillo (Juan); O. Sakowitz (Oliver); Sala, F. (Francesca); Sanchez-Pena, P. (Paola); Sanchez-Porras, R. (Renan); Sandor, J. (Janos); Santos, E. (Edgar); N. Sasse (Nadine); Sasu, L. (Luminita); Savo, D. (Davide); I.B. Schipper (Inger); Schlößer, B. (Barbara); S. Schmidt (Silke); Schneider, A. (Annette); H. Schoechl (Herbert); G.G. Schoonman; R. Schou (Rico); E. Schwendenwein (Elisabeth); Schöll, M. (Michael); Sir, O. (Özcan); T. Skandsen (Toril); Smakman, L. (Lidwien); D. Smeets (Dirk); Smielewski, P. (Peter); Sorinola, A. (Abayomi); Stamatakis, E.L. (Emmanue L.); S. Stanworth (Simon); Stegemann, K. (Katrin); Steinbüchel, N. (Nicole); R. Stevens (Robert); W. Stewart (William); N. Stocchetti (Nino); Sundström, N. (Nina); Synnot, A. (Anneliese); J. Szabó (József); J. Söderberg (Jeannette); F.S. Taccone (Fabio); Tamás, V. (Viktória); Tanskanen, P. (Päivi); A. Tascu (Alexandru); Taylor, M.S. (Mark Steven); Te Ao, B. (Braden); O. Tenovuo (Olli); Teodorani, G. (Guido); A. Theadom (Alice); Thomas, M. (Matt); D. Tibboel (Dick); C.M. Tolias (Christos M.); Tshibanda, J.-F.L. (Jean-Flory Luaba); Tudora, C.M. (Cristina Maria); P. Vajkoczy (Peter); Valeinis, E. (Egils); W. van Hecke (Wim); D. Van Praag (Dominique); D. Van Roost (Dirk); Van Vlierberghe, E. (Eline); Vande Vyvere, T. (Thijs); Vanhaudenhuyse, A. (Audrey); A. Vargiolu (Alessia); E. Vega (Emmanuel); J. Verheyden (Jan); P.M. Vespa (Paul M.); A. Vik (Anne); R. Vilcinis (Rimantas); Vizzino, G. (Giacinta); C.L.A.M. Vleggeert-Lankamp (Carmen); V. Volovici (Victor); P. Vulekovic (Peter); Vámos, Z. (Zoltán); Wade, D. (Derick); Wang, K.K.W. (Kevin K.W.); Wang, L. (Lei); Wildschut, E. (Eno); G. Williams (Guy); Willumsen, L. (Lisette); Wilson, A. (Adam); L. Wilson (Lindsay); Winkler, M.K.L. (Maren K. L.); P. Ylén (Peter); Younsi, A. (Alexander); M. Zaaroor (Menashe); Zhang, Z. (Zhiqun); Zheng, Z. (Zelong); Zumbo, F. (Fabrizio); De Lange, S. (Stefanie); G.C.W. De Ruiter (Godard C.W.); Den Boogert, H. (Hugo); Van Dijck, J. (Jeroen); T.A. van Essen (T.); C.M. van Heugten (Caroline M.); M. van der Jagt (Mathieu); J. van der Naalt (Joukje)

2016-01-01

textabstractIntroduction: The strength of evidence underpinning care and treatment recommendations in traumatic brain injury (TBI) is low. Comparative effectiveness research (CER) has been proposed as a framework to provide evidence for optimal care for TBI patients. The first step in CER is to map

Therapeutic Sleep for Traumatic Brain Injury

Science.gov (United States)

2017-06-01

AWARD NUMBER: W81XWH-16-1-0166 TITLE: Therapeutic Sleep for Traumatic Brain Injury PRINCIPAL INVESTIGATOR: Ravi Allada CONTRACTING...1. REPORT DATE June 2017 2. REPORT TYPE Annual 3. DATES COVERED 1June2016 - 31May2017 4. TITLE AND SUBTITLE Therapeutic Sleep for Traumatic Brain ...proposal will test the hypothesis that correcting sleep disorders can have a therapeutic effect onTraumatic Brain Injury (TBI) The majority of TBI

Cerebral Vascular Injury in Traumatic Brain Injury.

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Kenney, Kimbra; Amyot, Franck; Haber, Margalit; Pronger, Angela; Bogoslovsky, Tanya; Moore, Carol; Diaz-Arrastia, Ramon

2016-01-01

Traumatic cerebral vascular injury (TCVI) is a very frequent, if not universal, feature after traumatic brain injury (TBI). It is likely responsible, at least in part, for functional deficits and TBI-related chronic disability. Because there are multiple pharmacologic and non-pharmacologic therapies that promote vascular health, TCVI is an attractive target for therapeutic intervention after TBI. The cerebral microvasculature is a component of the neurovascular unit (NVU) coupling neuronal metabolism with local cerebral blood flow. The NVU participates in the pathogenesis of TBI, either directly from physical trauma or as part of the cascade of secondary injury that occurs after TBI. Pathologically, there is extensive cerebral microvascular injury in humans and experimental animal, identified with either conventional light microscopy or ultrastructural examination. It is seen in acute and chronic TBI, and even described in chronic traumatic encephalopathy (CTE). Non-invasive, physiologic measures of cerebral microvascular function show dysfunction after TBI in humans and experimental animal models of TBI. These include imaging sequences (MRI-ASL), Transcranial Doppler (TCD), and Near InfraRed Spectroscopy (NIRS). Understanding the pathophysiology of TCVI, a relatively under-studied component of TBI, has promise for the development of novel therapies for TBI. Published by Elsevier Inc.

Head injuries (TBI) to adults and children in motor vehicle crashes.

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Viano, David C; Parenteau, Chantal S; Xu, Likang; Faul, Mark

2017-08-18

This is a descriptive study. It determined the annual, national incidence of head injuries (traumatic brain injury, TBI) to adults and children in motor vehicle crashes. It evaluated NASS-CDS for exposure and incidence of various head injuries in towaway crashes. It evaluated 3 health databases for emergency department (ED) visits, hospitalizations, and deaths due to TBI in motor vehicle occupants. Four databases were evaluated using 1997-2010 data on adult (15+ years old) and child (0-14 years old) occupants in motor vehicle crashes: (1) NASS-CDS estimated the annual incidence of various head injuries and outcomes in towaway crashes, (2) National Hospital Ambulatory Medical Care Survey (NHAMCS)-estimated ED visits for TBI, (3) National Hospital Discharge Survey (NHDS) estimated hospitalizations for TBI, and (4) National Vital Statistics System (NVSS) estimated TBI deaths. The 4 databases provide annual national totals for TBI related injury and death in motor vehicle crashes based on differing definitions with TBI coded by the Abbreviated Injury Scale (AIS) in NASS-CDS and by International Classification of Diseases (ICD) in the health data. Adults: NASS-CDS had 16,980 ± 2,411 (risk = 0.43 ± 0.06%) with severe head injury (AIS 4+) out of 3,930,543 exposed adults in towaway crashes annually. There were 49,881 ± 9,729 (risk = 1.27 ± 0.25%) hospitalized with AIS 2+ head injury, without death. There were 6,753 ± 882 (risk = 0.17 ± 0.02%) fatalities with a head injury cause. The public health data had 89,331 ± 6,870 ED visits, 33,598 ± 1,052 hospitalizations, and 6,682 ± 22 deaths with TBI. NASS-CDS estimated 48% more hospitalized with AIS 2+ head injury without death than NHDS occupants hospitalized with TBI. NASS-CDS estimated 29% more deaths with AIS 3+ head injury than NVSS occupant TBI deaths but only 1% more deaths with a head injury cause. Children: NASS-CDS had 1,453 ± 318 (risk = 0.32 ± 0.07%) with severe head injury (AIS 4+) out of 454,973 exposed

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...

Understanding Traumatic Brain Injury: An Introduction

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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,…

Review of the literature on the use of social media by people with traumatic brain injury (TBI).

Science.gov (United States)

Brunner, Melissa; Hemsley, Bronwyn; Palmer, Stuart; Dann, Stephen; Togher, Leanne

2015-01-01

To review the literature relating to use of social media by people with a traumatic brain injury (TBI), specifically its use for social engagement, information exchange or rehabilitation. A systematic review with a qualitative meta-synthesis of content themes was conducted. In June 2014, 10 databases were searched for relevant, peer-reviewed research studies in English that related to both TBI and social media. Sixteen studies met the inclusion criteria, with Facebook™ and Twitter™ being the most common social media represented in the included studies. Content analysis identified three major categories of meaning in relation to social media and TBI: (1) risks and benefits; (2) barriers and facilitators; and (3) purposes of use of social media. A greater emphasis was evident regarding potential risks and apparent barriers to social media use, with little focus on facilitators of successful use by people with TBI. Research to date reveals a range of benefits to the use of social media by people with TBI however there is little empirical research investigating its use. Further research focusing on ways to remove the barriers and increase facilitators for the use of social media by people with TBI is needed.

Parents and teachers reporting on a child's emotional and behavioural problems following severe traumatic brain injury (TBI): the moderating effect of time.

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Silberg, Tamar; Tal-Jacobi, Dana; Levav, Miriam; Brezner, Amichai; Rassovsky, Yuri

2015-01-01

Gathering information from parents and teachers following paediatric traumatic brain injury (TBI) has substantial clinical value for diagnostic decisions. Yet, a multi-informant approach has rarely been addressed when evaluating children at the chronic stage post-injury. In the current study, the goals were to examine (1) differences between parents' and teachers' reports on a child's emotional and behavioural problems and (2) the effect of time elapsed since injury on each rater's report. A sample of 42 parents and 42 teachers of children following severe TBI completed two standard rating scales. Receiver Operating Characteristic (ROC) curves were used to determine whether time elapsed since injury reliably distinguished children falling above and below clinical levels. Emotional-behavioural scores of children following severe TBI fell within normal range, according to both teachers and parents. Significant differences were found between parents' reports relatively close to the time of injury and 2 years post-injury. However, no such differences were observed in teachers' ratings. Parents and teachers of children following severe TBI differ in their reports on a child's emotional and behavioural problems. The present study not only underscores the importance of multiple informants, but also highlights, for the first time, the possibility that informants' perceptions may vary across time.

Behavioral and pathophysiological outcomes associated with caffeine consumption and repetitive mild traumatic brain injury (RmTBI) in adolescent rats.

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Yamakawa, Glenn R; Lengkeek, Connor; Salberg, Sabrina; Spanswick, Simon C; Mychasiuk, Richelle

2017-01-01

Given that caffeine consumption is exponentially rising in adolescents and they are at increased risk for repetitive mild traumatic brain injury (RmTBI), we sought to examine the pathophysiological outcomes associated with early life caffeine consumption and RmTBI. Adolescent male and female Sprague Dawley rats received either caffeine in the drinking water or normal water and were then randomly assigned to 3 mild injuries using our lateral impact device or 3 sham procedures. Following injury induction, behavioral outcomes were measured with a test battery designed to examine symptoms consistent with clinical manifestation of PCS (balance and motor coordination, anxiety, short-term working memory, and depressive-like behaviours). In addition, pathophysiological outcomes were examined with histological measures of volume and cellular proliferation in the dentate gyrus, as well as microglia activation in the ventromedial hypothalamus. Finally, modifications to expression of 12 genes (Adora2a, App, Aqp4, Bdnf, Bmal1, Clock, Cry, Gfap, Orx1, Orx2, Per, Tau), in the prefrontal cortex, hippocampus, and/or the hypothalamus were assessed. We found that chronic caffeine consumption in adolescence altered normal developmental trajectories, as well as recovery from RmTBI. Of particular importance, many of the outcomes exhibited sex-dependent responses whereby the sex of the animal modified response to caffeine, RmTBI, and the combination of the two. These results suggest that caffeine consumption in adolescents at high risk for RmTBI should be monitored.

Behavioral and pathophysiological outcomes associated with caffeine consumption and repetitive mild traumatic brain injury (RmTBI in adolescent rats.

Directory of Open Access Journals (Sweden)

Glenn R Yamakawa

Full Text Available Given that caffeine consumption is exponentially rising in adolescents and they are at increased risk for repetitive mild traumatic brain injury (RmTBI, we sought to examine the pathophysiological outcomes associated with early life caffeine consumption and RmTBI. Adolescent male and female Sprague Dawley rats received either caffeine in the drinking water or normal water and were then randomly assigned to 3 mild injuries using our lateral impact device or 3 sham procedures. Following injury induction, behavioral outcomes were measured with a test battery designed to examine symptoms consistent with clinical manifestation of PCS (balance and motor coordination, anxiety, short-term working memory, and depressive-like behaviours. In addition, pathophysiological outcomes were examined with histological measures of volume and cellular proliferation in the dentate gyrus, as well as microglia activation in the ventromedial hypothalamus. Finally, modifications to expression of 12 genes (Adora2a, App, Aqp4, Bdnf, Bmal1, Clock, Cry, Gfap, Orx1, Orx2, Per, Tau, in the prefrontal cortex, hippocampus, and/or the hypothalamus were assessed. We found that chronic caffeine consumption in adolescence altered normal developmental trajectories, as well as recovery from RmTBI. Of particular importance, many of the outcomes exhibited sex-dependent responses whereby the sex of the animal modified response to caffeine, RmTBI, and the combination of the two. These results suggest that caffeine consumption in adolescents at high risk for RmTBI should be monitored.

Medical Management of the Severe Traumatic Brain Injury Patient.

Science.gov (United States)

Marehbian, Jonathan; Muehlschlegel, Susanne; Edlow, Brian L; Hinson, Holly E; Hwang, David Y

2017-12-01

Severe traumatic brain injury (sTBI) is a major contributor to long-term disability and a leading cause of death worldwide. Medical management of the sTBI patient, beginning with prehospital triage, is aimed at preventing secondary brain injury. This review discusses prehospital and emergency department management of sTBI, as well as aspects of TBI management in the intensive care unit where advances have been made in the past decade. Areas of emphasis include intracranial pressure management, neuromonitoring, management of paroxysmal sympathetic hyperactivity, neuroprotective strategies, prognostication, and communication with families about goals of care. Where appropriate, differences between the third and fourth editions of the Brain Trauma Foundation guidelines for the management of severe traumatic brain injury are highlighted.

Characterizing brain structures and remodeling after TBI based on information content, diffusion entropy.

Science.gov (United States)

Fozouni, Niloufar; Chopp, Michael; Nejad-Davarani, Siamak P; Zhang, Zheng Gang; Lehman, Norman L; Gu, Steven; Ueno, Yuji; Lu, Mei; Ding, Guangliang; Li, Lian; Hu, Jiani; Bagher-Ebadian, Hassan; Hearshen, David; Jiang, Quan

2013-01-01

To overcome the limitations of conventional diffusion tensor magnetic resonance imaging resulting from the assumption of a Gaussian diffusion model for characterizing voxels containing multiple axonal orientations, Shannon's entropy was employed to evaluate white matter structure in human brain and in brain remodeling after traumatic brain injury (TBI) in a rat. Thirteen healthy subjects were investigated using a Q-ball based DTI data sampling scheme. FA and entropy values were measured in white matter bundles, white matter fiber crossing areas, different gray matter (GM) regions and cerebrospinal fluid (CSF). Axonal densities' from the same regions of interest (ROIs) were evaluated in Bielschowsky and Luxol fast blue stained autopsy (n = 30) brain sections by light microscopy. As a case demonstration, a Wistar rat subjected to TBI and treated with bone marrow stromal cells (MSC) 1 week after TBI was employed to illustrate the superior ability of entropy over FA in detecting reorganized crossing axonal bundles as confirmed by histological analysis with Bielschowsky and Luxol fast blue staining. Unlike FA, entropy was less affected by axonal orientation and more affected by axonal density. A significant agreement (r = 0.91) was detected between entropy values from in vivo human brain and histologically measured axonal density from post mortum from the same brain structures. The MSC treated TBI rat demonstrated that the entropy approach is superior to FA in detecting axonal remodeling after injury. Compared with FA, entropy detected new axonal remodeling regions with crossing axons, confirmed with immunohistological staining. Entropy measurement is more effective in distinguishing axonal remodeling after injury, when compared with FA. Entropy is also more sensitive to axonal density than axonal orientation, and thus may provide a more accurate reflection of axonal changes that occur in neurological injury and disease.

Characterizing Brain Structures and Remodeling after TBI Based on Information Content, Diffusion Entropy

Science.gov (United States)

Fozouni, Niloufar; Chopp, Michael; Nejad-Davarani, Siamak P.; Zhang, Zheng Gang; Lehman, Norman L.; Gu, Steven; Ueno, Yuji; Lu, Mei; Ding, Guangliang; Li, Lian; Hu, Jiani; Bagher-Ebadian, Hassan; Hearshen, David; Jiang, Quan

2013-01-01

Background To overcome the limitations of conventional diffusion tensor magnetic resonance imaging resulting from the assumption of a Gaussian diffusion model for characterizing voxels containing multiple axonal orientations, Shannon's entropy was employed to evaluate white matter structure in human brain and in brain remodeling after traumatic brain injury (TBI) in a rat. Methods Thirteen healthy subjects were investigated using a Q-ball based DTI data sampling scheme. FA and entropy values were measured in white matter bundles, white matter fiber crossing areas, different gray matter (GM) regions and cerebrospinal fluid (CSF). Axonal densities' from the same regions of interest (ROIs) were evaluated in Bielschowsky and Luxol fast blue stained autopsy (n = 30) brain sections by light microscopy. As a case demonstration, a Wistar rat subjected to TBI and treated with bone marrow stromal cells (MSC) 1 week after TBI was employed to illustrate the superior ability of entropy over FA in detecting reorganized crossing axonal bundles as confirmed by histological analysis with Bielschowsky and Luxol fast blue staining. Results Unlike FA, entropy was less affected by axonal orientation and more affected by axonal density. A significant agreement (r = 0.91) was detected between entropy values from in vivo human brain and histologically measured axonal density from post mortum from the same brain structures. The MSC treated TBI rat demonstrated that the entropy approach is superior to FA in detecting axonal remodeling after injury. Compared with FA, entropy detected new axonal remodeling regions with crossing axons, confirmed with immunohistological staining. Conclusions Entropy measurement is more effective in distinguishing axonal remodeling after injury, when compared with FA. Entropy is also more sensitive to axonal density than axonal orientation, and thus may provide a more accurate reflection of axonal changes that occur in neurological injury and disease

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...

Diverging volumetric trajectories following pediatric traumatic brain injury

Directory of Open Access Journals (Sweden)

Emily L. Dennis

2017-01-01

Full Text Available Traumatic brain injury (TBI is a significant public health concern, and can be especially disruptive in children, derailing on-going neuronal maturation in periods critical for cognitive development. There is considerable heterogeneity in post-injury outcomes, only partially explained by injury severity. Understanding the time course of recovery, and what factors may delay or promote recovery, will aid clinicians in decision-making and provide avenues for future mechanism-based therapeutics. We examined regional changes in brain volume in a pediatric/adolescent moderate-severe TBI (msTBI cohort, assessed at two time points. Children were first assessed 2–5 months post-injury, and again 12 months later. We used tensor-based morphometry (TBM to localize longitudinal volume expansion and reduction. We studied 21 msTBI patients (5 F, 8–18 years old and 26 well-matched healthy control children, also assessed twice over the same interval. In a prior paper, we identified a subgroup of msTBI patients, based on interhemispheric transfer time (IHTT, with significant structural disruption of the white matter (WM at 2–5 months post injury. We investigated how this subgroup (TBI-slow, N = 11 differed in longitudinal regional volume changes from msTBI patients (TBI-normal, N = 10 with normal WM structure and function. The TBI-slow group had longitudinal decreases in brain volume in several WM clusters, including the corpus callosum and hypothalamus, while the TBI-normal group showed increased volume in WM areas. Our results show prolonged atrophy of the WM over the first 18 months post-injury in the TBI-slow group. The TBI-normal group shows a different pattern that could indicate a return to a healthy trajectory.

Traumatic Brain Injury: Looking Back, Looking Forward

Science.gov (United States)

Bartlett, Sue; Lorenz, Laura; Rankin, Theresa; Elias, Eileen; Weider, Katie

2011-01-01

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

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. © 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice.

Science.gov (United States)

Ma, Elise L; Smith, Allen D; Desai, Neemesh; Cheung, Lumei; Hanscom, Marie; Stoica, Bogdan A; Loane, David J; Shea-Donohue, Terez; Faden, Alan I

2017-11-01

Traumatic brain injury (TBI) has complex effects on the gastrointestinal tract that are associated with TBI-related morbidity and mortality. We examined changes in mucosal barrier properties and enteric glial cell response in the gut after experimental TBI in mice, as well as effects of the enteric pathogen Citrobacter rodentium (Cr) on both gut and brain after injury. Moderate-level TBI was induced in C57BL/6mice by controlled cortical impact (CCI). Mucosal barrier function was assessed by transepithelial resistance, fluorescent-labelled dextran flux, and quantification of tight junction proteins. Enteric glial cell number and activation were measured by Sox10 expression and GFAP reactivity, respectively. Separate groups of mice were challenged with Cr infection during the chronic phase of TBI, and host immune response, barrier integrity, enteric glial cell reactivity, and progression of brain injury and inflammation were assessed. Chronic CCI induced changes in colon morphology, including increased mucosal depth and smooth muscle thickening. At day 28 post-CCI, increased paracellular permeability and decreased claudin-1 mRNA and protein expression were observed in the absence of inflammation in the colon. Colonic glial cell GFAP and Sox10 expression were significantly increased 28days after brain injury. Clearance of Cr and upregulation of Th1/Th17 cytokines in the colon were unaffected by CCI; however, colonic paracellular flux and enteric glial cell GFAP expression were significantly increased. Importantly, Cr infection in chronically-injured mice worsened the brain lesion injury and increased astrocyte- and microglial-mediated inflammation. These experimental studies demonstrate chronic and bidirectional brain-gut interactions after TBI, which may negatively impact late outcomes after brain injury. Copyright © 2017 Elsevier Inc. All rights reserved.

Technology and its role in rehabilitation for people with cognitive-communication disability following a traumatic brain injury (TBI).

Science.gov (United States)

Brunner, Melissa; Hemsley, Bronwyn; Togher, Leanne; Palmer, Stuart

2017-01-01

To review the literature on communication technologies in rehabilitation for people with a traumatic brain injury (TBI), and: (a) determine its application to cognitive-communicative rehabilitation, and b) develop a model to guide communication technology use with people after TBI. This integrative literature review of communication technology in TBI rehabilitation and cognitive-communication involved searching nine scientific databases and included 95 studies. Three major types of communication technologies (assistive technology, augmentative and alternative communication technology, and information communication technology) and multiple factors relating to use of technology by or with people after TBI were categorized according to: (i) individual needs, motivations and goals; (ii) individual impairments, activities, participation and environmental factors; and (iii) technologies. While there is substantial research relating to communication technologies and cognitive rehabilitation after TBI, little relates specifically to cognitive-communication rehabilitation. Further investigation is needed into the experiences and views of people with TBI who use communication technologies, to provide the 'user' perspective and influence user-centred design. Research is necessary to investigate the training interventions that address factors fundamental for success, and any impact on communication. The proposed model provides an evidence-based framework for incorporating technology into speech pathology clinical practice and research.

Prevalence of traumatic brain injury in juvenile offenders: a meta-analysis.

Science.gov (United States)

Farrer, Thomas J; Frost, R Brock; Hedges, Dawson W

2013-01-01

Studies of traumatic brain injury (TBI) among adult populations demonstrate that such injuries can lead to aggressive behaviors. Related findings suggest that incarcerated individuals have high rates of brain injuries. Such studies suggest that traumatic brain injury may be related to the etiology and recidivism of criminal behavior. Relatively few studies have examined the prevalence of TBI using a delinquent juvenile sample. In order to assess the relationship between TBI and juvenile offender status, the current study used meta-analytic techniques to examine the odds of having a TBI among juvenile offenders. Across 9 studies, we found that approximately 30% of juvenile offenders have sustained a previous brain injury. Across 5 studies that used a control group, a calculated summary odds ratio of 3.37 suggests that juvenile offenders are significantly more likely to have a TBI compared to controls. Results suggest that the rate of TBIs within the juvenile offender population is significant and that there may be a relationship between TBIs and juvenile criminal behavior.

Role of Melatonin in Traumatic Brain Injury and Spinal Cord Injury

Directory of Open Access Journals (Sweden)

Mehar Naseem

2014-01-01

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

Traumatic Brain Injury Induces Genome-Wide Transcriptomic, Methylomic, and Network Perturbations in Brain and Blood Predicting Neurological Disorders

Directory of Open Access Journals (Sweden)

Qingying Meng

2017-02-01

Full Text Available The complexity of the traumatic brain injury (TBI pathology, particularly concussive injury, is a serious obstacle for diagnosis, treatment, and long-term prognosis. Here we utilize modern systems biology in a rodent model of concussive injury to gain a thorough view of the impact of TBI on fundamental aspects of gene regulation, which have the potential to drive or alter the course of the TBI pathology. TBI perturbed epigenomic programming, transcriptional activities (expression level and alternative splicing, and the organization of genes in networks centered around genes such as Anax2, Ogn, and Fmod. Transcriptomic signatures in the hippocampus are involved in neuronal signaling, metabolism, inflammation, and blood function, and they overlap with those in leukocytes from peripheral blood. The homology between genomic signatures from blood and brain elicited by TBI provides proof of concept information for development of biomarkers of TBI based on composite genomic patterns. By intersecting with human genome-wide association studies, many TBI signature genes and network regulators identified in our rodent model were causally associated with brain disorders with relevant link to TBI. The overall results show that concussive brain injury reprograms genes which could lead to predisposition to neurological and psychiatric disorders, and that genomic information from peripheral leukocytes has the potential to predict TBI pathogenesis in the brain.

Facial Emotion Recognition Deficits following Moderate-Severe Traumatic Brain Injury (TBI): Re-examining the Valence Effect and the Role of Emotion Intensity

NARCIS (Netherlands)

Rosenberg, H.; McDonald, S.; Dethier, M.; Kessels, R.P.C.; Westbrook, R.F.

2014-01-01

Many individuals who sustain moderate-severe traumatic brain injuries (TBI) are poor at recognizing emotional expressions, with a greater impairment in recognizing negative (e.g., fear, disgust, sadness, and anger) than positive emotions (e.g., happiness and surprise). It has been questioned whether

"Help seniors live better, longer: prevent brain injury": an overview of CDC's education initiative to prevent fall-related TBI among older adults.

Science.gov (United States)

Sarmiento, Kelly; Langlois, Jean A; Mitchko, Jane

2008-01-01

Falls are the leading cause of traumatic brain injury (TBI) among older adults aged 75 and older. Despite this burden, many older adults, their caregivers, and professionals are not aware of the importance of TBI as an outcome of falls among older adults. To address this important public health problem, the Centers for Disease Control and Prevention (CDC) developed the "Help Seniors Live Better, Longer: Prevent Brain Injury" initiative to help raise awareness about methods to prevent, recognize and respond to fall-related TBIs among older adults aged 75 and older. The initiative was launched in March 2008, in collaboration with 26 participating organizations, and included a multipronged outreach strategy to help blanket the country with the messages of the initiative at the national, state, and local levels. Adherence to a logical, comprehensive health-education approach has proven to be highly effective in furthering the initial goals of the project.

Internet and Social Media Use After Traumatic Brain Injury: A Traumatic Brain Injury Model Systems Study.

Science.gov (United States)

Baker-Sparr, Christina; Hart, Tessa; Bergquist, Thomas; Bogner, Jennifer; Dreer, Laura; Juengst, Shannon; Mellick, David; OʼNeil-Pirozzi, Therese M; Sander, Angelle M; Whiteneck, Gale G

To characterize Internet and social media use among adults with moderate to severe traumatic brain injury (TBI) and to compare demographic and socioeconomic factors associated with Internet use between those with and without TBI. Ten Traumatic Brain Injury Model Systems centers. Persons with moderate to severe TBI (N = 337) enrolled in the TBI Model Systems National Database and eligible for follow-up from April 1, 2014, to March 31, 2015. Prospective cross-sectional observational cohort study. Internet usage survey. The proportion of Internet users with TBI was high (74%) but significantly lower than those in the general population (84%). Smartphones were the most prevalent means of Internet access for persons with TBI. The majority of Internet users with TBI had a profile account on a social networking site (79%), with more than half of the sample reporting multiplatform use of 2 or more social networking sites. Despite the prevalence of Internet use among persons with TBI, technological disparities remain in comparison with the general population. The extent of social media use among persons with TBI demonstrates the potential of these platforms for social engagement and other purposes. However, further research examining the quality of online activities and identifying potential risk factors of problematic use is recommended.

Tensor-Based Morphometry Reveals Volumetric Deficits in Moderate=Severe Pediatric Traumatic Brain Injury.

Science.gov (United States)

Dennis, Emily L; Hua, Xue; Villalon-Reina, Julio; Moran, Lisa M; Kernan, Claudia; Babikian, Talin; Mink, Richard; Babbitt, Christopher; Johnson, Jeffrey; Giza, Christopher C; Thompson, Paul M; Asarnow, Robert F

2016-05-01

Traumatic brain injury (TBI) can cause widespread and prolonged brain degeneration. TBI can affect cognitive function and brain integrity for many years after injury, often with lasting effects in children, whose brains are still immature. Although TBI varies in how it affects different individuals, image analysis methods such as tensor-based morphometry (TBM) can reveal common areas of brain atrophy on magnetic resonance imaging (MRI), secondary effects of the initial injury, which will differ between subjects. Here we studied 36 pediatric moderate to severe TBI (msTBI) participants in the post-acute phase (1-6 months post-injury) and 18 msTBI participants who returned for their chronic assessment, along with well-matched controls at both time-points. Participants completed a battery of cognitive tests that we used to create a global cognitive performance score. Using TBM, we created three-dimensional (3D) maps of individual and group differences in regional brain volumes. At both the post-acute and chronic time-points, the greatest group differences were expansion of the lateral ventricles and reduction of the lingual gyrus in the TBI group. We found a number of smaller clusters of volume reduction in the cingulate gyrus, thalamus, and fusiform gyrus, and throughout the frontal, temporal, and parietal cortices. Additionally, we found extensive associations between our cognitive performance measure and regional brain volume. Our results indicate a pattern of atrophy still detectable 1-year post-injury, which may partially underlie the cognitive deficits frequently found in TBI.

Isolated traumatic brain injury and venous thromboembolism.

Science.gov (United States)

Van Gent, Jan-Michael; Bandle, Jesse; Calvo, Richard Y; Zander, Ashley L; Olson, Erik J; Shackford, Steven R; Peck, Kimberly A; Sise, C Beth; Sise, Michael J

2014-08-01

Traumatic brain injury (TBI) is considered an independent risk factor of venous thromboembolism (VTE). However, the role of TBI severity in VTE risk has not been determined. We hypothesized that increased severity of brain injury in patients with isolated TBI (iTBI) is associated with an increased incidence of VTE. The records of patients admitted from June 2006 to December 2011 were reviewed for injury data, VTE risk factors, results of lower extremity surveillance ultrasound, and severity of TBI. Patients were identified by DRG International Classification of Diseases-9th Rev. codes for TBI, and only those with a nonhead Abbreviated Injury Scale (AIS) score of 1 or lower, indicating minimal associated injury, were included. The association of iTBI and VTE was determined using a case-control design. Among iTBI patients, those diagnosed with VTE (cases) were matched for age, sex, and admission year to those without VTE (controls). Data were analyzed using conditional logistic regression. There were 345 iTBI patients: 41 cases (12%) and 304 controls (88%). A total of 151 controls could not be matched to an appropriate case and were excluded. Of the remaining 153 controls, 1 to 16 controls were matched to each of the 41 VTE cases. Compared with the controls, the cases had a higher mean head-AIS score (4.4 vs. 3.9, p = 0.001) and overall Injury Severity Score (20.4 vs. 16.8, p = 0.001). Following adjustment for all factors found to be associated with VTE (ventilator days, central line placement, operative time > 2 hours, chemoprophylaxis, history of VTE, and history of cancer), the cases were significantly more likely to have a greater head injury severity (head-AIS score ≥ 5; odds ratio, 5.25; 95% confidence interval, 1.59-17.30; p = 0.006). The incidence of VTE in iTBI patients was significantly associated with the severity of TBI. VTE surveillance protocols may be warranted in these high-risk patients, as early detection of VTE could guide subsequent therapy

MRI patterns in prolonged low response states following traumatic brain injury in children and adolescents.

Science.gov (United States)

Patrick, Peter D; Mabry, Jennifer L; Gurka, Matthew J; Buck, Marcia L; Boatwright, Evelyn; Blackman, James A

2007-01-01

To explore the relationship between location and pattern of brain injury identified on MRI and prolonged low response state in children post-traumatic brain injury (TBI). This observational study compared 15 children who spontaneously recovered within 30 days post-TBI to 17 who remained in a prolonged low response state. 92.9% of children with brain stem injury were in the low response group. The predicted probability was 0.81 for brain stem injury alone, increasing to 0.95 with a regional pattern of injury to the brain stem, basal ganglia, and thalamus. Low response state in children post-TBI is strongly correlated with two distinctive regions of injury: the brain stem alone, and an injury pattern to the brain stem, basal ganglia, and thalamus. This study demonstrates the need for large-scale clinical studies using MRI as a tool for outcome assessment in children and adolescents following severe TBI.

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.

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…

Death following traumatic brain injury in Drosophila is associated with intestinal barrier dysfunction

Science.gov (United States)

Katzenberger, Rebeccah J; Chtarbanova, Stanislava; Rimkus, Stacey A; Fischer, Julie A; Kaur, Gulpreet; Seppala, Jocelyn M; Swanson, Laura C; Zajac, Jocelyn E; Ganetzky, Barry; Wassarman, David A

2015-01-01

Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Unfavorable TBI outcomes result from primary mechanical injuries to the brain and ensuing secondary non-mechanical injuries that are not limited to the brain. Our genome-wide association study of Drosophila melanogaster revealed that the probability of death following TBI is associated with single nucleotide polymorphisms in genes involved in tissue barrier function and glucose homeostasis. We found that TBI causes intestinal and blood–brain barrier dysfunction and that intestinal barrier dysfunction is highly correlated with the probability of death. Furthermore, we found that ingestion of glucose after a primary injury increases the probability of death through a secondary injury mechanism that exacerbates intestinal barrier dysfunction. Our results indicate that natural variation in the probability of death following TBI is due in part to genetic differences that affect intestinal barrier dysfunction. DOI: http://dx.doi.org/10.7554/eLife.04790.001 PMID:25742603

Family needs after brain injury

DEFF Research Database (Denmark)

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

2015-01-01

OBJECTIVE: The objective of this study was to explore differences by country in the importance of family needs after traumatic brain injury (TBI), as well as differences in met/unmet needs. METHOD: Two hundred and seventy-one family members of an individual with TBI in Mexico, Colombia, Spain...

Traumatic Brain Injury service (TBI) Service

Data.gov (United States)

Department of Veterans Affairs — This Service provides access to Tramatic Brain injury patient data consult notes. The service also provides one write service method writeNote. The Service supports...

Tensor-Based Morphometry Reveals Volumetric Deficits in Moderate=Severe Pediatric Traumatic Brain Injury

Science.gov (United States)

Hua, Xue; Villalon-Reina, Julio; Moran, Lisa M.; Kernan, Claudia; Babikian, Talin; Mink, Richard; Babbitt, Christopher; Johnson, Jeffrey; Giza, Christopher C.; Thompson, Paul M.; Asarnow, Robert F.

2016-01-01

Abstract Traumatic brain injury (TBI) can cause widespread and prolonged brain degeneration. TBI can affect cognitive function and brain integrity for many years after injury, often with lasting effects in children, whose brains are still immature. Although TBI varies in how it affects different individuals, image analysis methods such as tensor-based morphometry (TBM) can reveal common areas of brain atrophy on magnetic resonance imaging (MRI), secondary effects of the initial injury, which will differ between subjects. Here we studied 36 pediatric moderate to severe TBI (msTBI) participants in the post-acute phase (1–6 months post-injury) and 18 msTBI participants who returned for their chronic assessment, along with well-matched controls at both time-points. Participants completed a battery of cognitive tests that we used to create a global cognitive performance score. Using TBM, we created three-dimensional (3D) maps of individual and group differences in regional brain volumes. At both the post-acute and chronic time-points, the greatest group differences were expansion of the lateral ventricles and reduction of the lingual gyrus in the TBI group. We found a number of smaller clusters of volume reduction in the cingulate gyrus, thalamus, and fusiform gyrus, and throughout the frontal, temporal, and parietal cortices. Additionally, we found extensive associations between our cognitive performance measure and regional brain volume. Our results indicate a pattern of atrophy still detectable 1-year post-injury, which may partially underlie the cognitive deficits frequently found in TBI. PMID:26393494

Variation in Structure and Process of Care in Traumatic Brain Injury: Provider Profiles of European Neurotrauma Centers Participating in the CENTER-TBI Study.

Directory of Open Access Journals (Sweden)

Maryse C Cnossen

Full Text Available The strength of evidence underpinning care and treatment recommendations in traumatic brain injury (TBI is low. Comparative effectiveness research (CER has been proposed as a framework to provide evidence for optimal care for TBI patients. The first step in CER is to map the existing variation. The aim of current study is to quantify variation in general structural and process characteristics among centers participating in the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI study.We designed a set of 11 provider profiling questionnaires with 321 questions about various aspects of TBI care, chosen based on literature and expert opinion. After pilot testing, questionnaires were disseminated to 71 centers from 20 countries participating in the CENTER-TBI study. Reliability of questionnaires was estimated by calculating a concordance rate among 5% duplicate questions.All 71 centers completed the questionnaires. Median concordance rate among duplicate questions was 0.85. The majority of centers were academic hospitals (n = 65, 92%, designated as a level I trauma center (n = 48, 68% and situated in an urban location (n = 70, 99%. The availability of facilities for neuro-trauma care varied across centers; e.g. 40 (57% had a dedicated neuro-intensive care unit (ICU, 36 (51% had an in-hospital rehabilitation unit and the organization of the ICU was closed in 64% (n = 45 of the centers. In addition, we found wide variation in processes of care, such as the ICU admission policy and intracranial pressure monitoring policy among centers.Even among high-volume, specialized neurotrauma centers there is substantial variation in structures and processes of TBI care. This variation provides an opportunity to study effectiveness of specific aspects of TBI care and to identify best practices with CER approaches.

Effect of binasal occlusion (BNO) on the visual-evoked potential (VEP) in mild traumatic brain injury (mTBI).

Science.gov (United States)

Ciuffreda, Kenneth J; Yadav, Naveen K; Ludlam, Diana P

2013-01-01

The purpose of the experiment was to assess the effect of binasal occlusion (BNO) on the visually-evoked potential (VEP) in visually-normal (VN) individuals and in those with mild traumatic brain injury (mTBI) for whom BNO frequently reduces their primary symptoms related to abnormally-increased visual motion sensitivity (VMS). Subjects were comprised of asymptomatic VN adults (n = 10) and individuals with mTBI (n = 10) having the symptom of VMS. Conventional full-field VEP testing was employed under two conditions: without BNO and with opaque BNO which blocked regions on either side of the VEP test stimulus. Subjective impressions were also assessed. In VN, the mean VEP amplitude decreased significantly with BNO in all subjects. In contrast, in mTBI, the mean VEP amplitude increased significantly with BNO in all subjects. Latency was normal and unaffected in all cases. Repeat VEP testing in three subjects from each group revealed similar test-re-test findings. Visuomotor activities improved, with reduced symptoms, with BNO in the mTBI group. It is speculated that individuals with mTBI habitually attempt to suppress visual information in the near retinal periphery to reduce their abnormal VMS, with addition of the BNO negating the suppressive influence and thus producing a widespread disinhibition effect and resultant increase in VEP amplitude.

A Review of Magnetic Resonance Imaging and Diffusion Tensor Imaging Findings in Mild Traumatic Brain Injury

Science.gov (United States)

Shenton, ME; Hamoda, HM; Schneiderman, JS; Bouix, S; Pasternak, O; Rathi, Y; M-A, Vu; Purohit, MP; Helmer, K; Koerte, I; Lin, AP; C-F, Westin; Kikinis, R; Kubicki, M; Stern, RA; Zafonte, R

2013-01-01

Mild traumatic brain injury (mTBI), also referred to as concussion, remains a controversial diagnosis because the brain often appears quite normal on conventional computed tomography (CT) and magnetic resonance imaging (MRI) scans. Such conventional tools, however, do not adequately depict brain injury in mTBI because they are not sensitive to detecting diffuse axonal injuries (DAI), also described as traumatic axonal injuries (TAI), the major brain injuries in mTBI. Furthermore, for the 15 to 30% of those diagnosed with mTBI on the basis of cognitive and clinical symptoms, i.e., the “miserable minority,” the cognitive and physical symptoms do not resolve following the first three months post-injury. Instead, they persist, and in some cases lead to long-term disability. The explanation given for these chronic symptoms, i.e., postconcussive syndrome, particularly in cases where there is no discernible radiological evidence for brain injury, has led some to posit a psychogenic origin. Such attributions are made all the easier since both post-traumatic stress disorder (PTSD) and depression are frequently co-morbid with mTBI. The challenge is thus to use neuroimaging tools that are sensitive to DAI/TAI, such as diffusion tensor imaging (DTI), in order to detect brain injuries in mTBI. Of note here, recent advances in neuroimaging techniques, such as DTI, make it possible to characterize better extant brain abnormalities in mTBI. These advances may lead to the development of biomarkers of injury, as well as to staging of reorganization and reversal of white matter changes following injury, and to the ability to track and to characterize changes in brain injury over time. Such tools will likely be used in future research to evaluate treatment efficacy, given their enhanced sensitivity to alterations in the brain. In this article we review the incidence of mTBI and the importance of characterizing this patient population using objective radiological measures. Evidence

Antioxidant therapies in traumatic brain injury: a review

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Romero-Rivera Hector Rolando

2017-09-01

Full Text Available Oxidative stress constitute one of the commonest mechanism of the secondary injury contributing to neuronal death in traumatic brain injury cases. The oxidative stress induced secondary injury blockade may be considered as to be a good alternative to improve the outcome of traumatic brain injury (TBI treatment. Due to absence of definitive therapy of traumatic brain injury has forced researcher to utilize unconventional therapies and its roles investigated in the improvement of management and outcome in recent year. Antioxidant therapies are proven effective in many preclinical studies and encouraging results and the role of antioxidant mediaction may act as further advancement in the traumatic brain injury management it may represent aonr of newer moadlaity in neurosurgical aramamentorium, this kind of therapy could be a good alternative or adjuct to the previously established neuroprotection agents in TBI.

Glibenclamide reduces secondary brain damage after experimental traumatic brain injury.

Science.gov (United States)

Zweckberger, K; Hackenberg, K; Jung, C S; Hertle, D N; Kiening, K L; Unterberg, A W; Sakowitz, O W

2014-07-11

Following traumatic brain injury (TBI) SUR1-regulated NCCa-ATP (SUR1/TRPM4) channels are transcriptionally up-regulated in ischemic astrocytes, neurons, and capillaries. ATP depletion results in depolarization and opening of the channel leading to cytotoxic edema. Glibenclamide is an inhibitor of SUR-1 and, thus, might prevent cytotoxic edema and secondary brain damage following TBI. Anesthetized adult Sprague-Dawley rats underwent parietal craniotomy and were subjected to controlled cortical impact injury (CCI). Glibenclamide was administered as a bolus injection 15min after CCI injury and continuously via osmotic pumps throughout 7days. In an acute trial (180min) mean arterial blood pressure, heart rate, intracranial pressure, encephalographic activity, and cerebral metabolism were monitored. Brain water content was assessed gravimetrically 24h after CCI injury and contusion volumes were measured by MRI scanning technique at 8h, 24h, 72h, and 7d post injury. Throughout the entire time of observation neurological function was quantified using the "beam-walking" test. Glibenclamide-treated animals showed a significant reduction in the development of brain tissue water content(80.47%±0.37% (glibenclamide) vs. 80.83%±0.44% (control); pbeam-walking test throughout 7days. In accordance to these results and the available literature, glibenclamide seems to have promising potency in the treatment of TBI. Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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

Science.gov (United States)

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

2016-03-01

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

Impact of Single-Photon Emission Computed Tomography/Computed Tomography (SPECT/CT) and Positron Emission Tomography/Computed Tomography (PET/CT) in the Diagnosis of Traumatic Brain Injury (TBI): Case Report.

Science.gov (United States)

Molina-Vicenty, Irma L; Santiago-Sánchez, Michelaldemar; Vélez-Miró, Iván; Motta-Valencia, Keryl

2016-09-01

Traumatic brain injury (TBI) is defined as damage to the brain resulting from an external force. TBI, a global leading cause of death and disability, is associated with serious social, economic, and health problems. In cases of mild-to-moderate brain damage, conventional anatomical imaging modalities may or may not detect the cascade of metabolic changes that have occurred or are occurring at the intracellular level. Functional nuclear medicine imaging and neurophysiological parameters can be used to characterize brain damage, as the former provides direct visualization of brain function, even in the absence of overt behavioral manifestations or anatomical findings. We report the case of a 30-year-old Hispanic male veteran who, after 2 traumatic brain injury events, developed cognitive and neuropsychological problems with no clear etiology in the presence of negative computed tomography (CT) findings.

Driving, brain injury and assistive technology.

Science.gov (United States)

Lane, Amy K; Benoit, Dana

2011-01-01

Individuals with brain injury often present with cognitive, physical and emotional impairments which impact their ability to resume independence in activities of daily living. Of those activities, the resumption of driving privileges is cited as one of the greatest concerns by survivors of brain injury. The integration of driving fundamentals within the hierarchical model proposed by Keskinen represents the complexity of skills and behaviors necessary for driving. This paper provides a brief review of specific considerations concerning the driver with TBI and highlights current vehicle technology which has been developed by the automotive industry and by manufacturers of adaptive driving equipment that may facilitate the driving task. Adaptive equipment technology allows for compensation of a variety of operational deficits, whereas technological advances within the automotive industry provide drivers with improved safety and information systems. However, research has not yet supported the use of such intelligent transportation systems or advanced driving systems for drivers with brain injury. Although technologies are intended to improve the safety of drivers within the general population, the potential of negative consequences for drivers with brain injury must be considered. Ultimately, a comprehensive driving evaluation and training by a driving rehabilitation specialist is recommended for individuals with brain injury. An understanding of the potential impact of TBI on driving-related skills and knowledge of current adaptive equipment and technology is imperative to determine whether return-to-driving is a realistic and achievable goal for the individual with TBI.

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.

Psychiatric sequelae of traumatic brain injury: Retrospective ...

African Journals Online (AJOL)

Objective: Traumatic brain injury (TBI) is a public health problem and is associated with many complications. However little is known about the psychiatric sequelae of TBI in Nigeria. This study described the pattern and determinants of psychiatric sequelae among subjects with TBI. Materials and Methods: The study is a ...

Getting My Bearings, Returning to School: Issues Facing Adolescents with Traumatic Brain Injury

Science.gov (United States)

Schilling, Ethan J.; Getch, Yvette Q.

2012-01-01

Traumatic brain injury (TBI) is characterized by a blow to the head or other penetrating head injury resulting in impairment of the brain's functioning. Despite the high incidence of TBI in adolescents, many educators still consider TBI to be a low-incidence disability. In addition, school personnel often report receiving little to no pre-service…

Traumatic Brain Injury and Personality Change

Science.gov (United States)

Fowler, Marc; McCabe, Paul C.

2011-01-01

Traumatic brain injury (TBI) is the leading cause of death and lifelong disability in the United States for individuals below the age of 45. Current estimates from the Center for Disease Control (CDC) indicate that at least 1.4 million Americans sustain a TBI annually. TBI affects 475,000 children under age 14 each year in the United States alone.…

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....

The validity of the Brain Injury Cognitive Screen (BICS) as a neuropsychological screening assessment for traumatic and non-traumatic brain injury.

Science.gov (United States)

Vaughan, Frances L; Neal, Jo Anne; Mulla, Farzana Nizam; Edwards, Barbara; Coetzer, Rudi

2017-04-01

The Brain Injury Cognitive Screen (BICS) was developed as an in-service cognitive assessment battery for acquired brain injury patients entering community rehabilitation. The BICS focuses on domains that are particularly compromised following TBI, and provides a broader and more detailed assessment of executive function, attention and information processing than comparable screening assessments. The BICS also includes brief assessments of perception, naming, and construction, which were predicted to be more sensitive to impairments following non-traumatic brain injury. The studies reported here examine preliminary evidence for its validity in post-acute rehabilitation. In Study 1, TBI patients completed the BICS and were compared with matched controls. Patients with focal lesions and matched controls were compared in Study 2. Study 3 examined demographic effects in a sample of normative data. TBI and focal lesion patients obtained significantly lower composite memory, executive function and attention and information processing BICS scores than healthy controls. Injury severity effects were also obtained. Logistic regression analyses indicated that each group of BICS memory, executive function and attention measures reliably differentiated TBI and focal lesion participants from controls. Design Recall, Prospective Memory, Verbal Fluency, and Visual Search test scores showed significant independent regression effects. Other subtest measures showed evidence of sensitivity to brain injury. The study provides preliminary evidence of the BICS' sensitivity to cognitive impairment caused by acquired brain injury, and its potential clinical utility as a cognitive screen. Further validation based on a revised version of the BICS and more normative data are required.

Environmental Enrichment Mitigates Deficits after Repetitive Mild Traumatic Brain Injury.

Science.gov (United States)

Liu, Xixia; Qiu, Jianhua; Alcon, Sasha; Hashim, Jumana; Meehan, William P; Mannix, Rebekah

2017-08-15

Although environmental enrichment has been shown to improve functional and histologic outcomes in pre-clinical moderate-to-severe traumatic brain injury (TBI), there are a paucity of pre-clinical data regarding enrichment strategies in the setting of repetitive mild traumatic brain injury (rmTBI). Given the vast numbers of athletes and those in the military who sustain rmTBI, the mounting evidence of the long-term and progressive sequelae of rmTBI, and the lack of targeted therapies to mitigate these sequelae, successful enrichment interventions in rmTBI could have large public health significance. Here, we evaluated enrichment strategies in an established pre-clinical rmTBI model. Seventy-one male C57BL/6 mice were randomized to two different housing conditions, environmental enrichment (EE) or normal condition (NC), then subjected to rmTBI injury (seven injuries in 9 days) or sham injury (anesthesia only). Functional outcomes in all four groups (NC-TBI, EE-TBI, NC-sham, and EE-sham) were assessed by motor, exploratory/anxiety, and mnemonic behavioral tests. At the synaptic level, N-methyl d-aspartate receptor (NMDAR) subunit expression of phosphorylated glutamate receptor 1 (GluR1), phosphorylated Ca 2+ /calmodulin-dependent protein kinase II (CaMKII), and calpain were evaluated by western blot. Compared to injured NC-TBI mice, EE-TBI mice had improved memory and decreased anxiety and exploratory activity post-injury. Treatment with enrichment also corresponded to normal NMDAR subunit expression, decreased GluR1 phosphorylation, decreased phosphorylated CaMKII, and normal calpain expression post-rmTBI. These data suggest that enrichment strategies may improve functional outcomes and mitigate synaptic changes post-rmTBI. Given that enrichment strategies are feasible in the clinical setting, particularly for athletes and soldiers for whom the risk of repetitive injury is greatest, these data suggest that clinical trials may be warranted.

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…

Deep pockets or blueprint for change: traumatic brain injury (TBI) proactive strategy.

Science.gov (United States)

Wood, D W; Pohl, S; Lawler, S; Okamoto, G

1998-09-01

The Pacific Conference scheduled for October 1-3, 1988, is a critical event in the development of an integrated community-based plan for a comprehensive continuum of services to address the "silent epidemic," Traumatic Brain Injured (TBI). This paper provides insights of the complex nature and the special problems faced by the TBI survivors; their families, natural supports and caregivers, as well as the health, social and educational care providers in Hawaii. Process for the development of the community plan is presented.

Systems biomarkers as acute diagnostics and chronic monitoring tools for traumatic brain injury

Science.gov (United States)

Wang, Kevin K. W.; Moghieb, Ahmed; Yang, Zhihui; Zhang, Zhiqun

2013-05-01

Traumatic brain injury (TBI) is a significant biomedical problem among military personnel and civilians. There exists an urgent need to develop and refine biological measures of acute brain injury and chronic recovery after brain injury. Such measures "biomarkers" can assist clinicians in helping to define and refine the recovery process and developing treatment paradigms for the acutely injured to reduce secondary injury processes. Recent biomarker studies in the acute phase of TBI have highlighted the importance and feasibilities of identifying clinically useful biomarkers. However, much less is known about the subacute and chronic phases of TBI. We propose here that for a complex biological problem such as TBI, multiple biomarker types might be needed to harness the wide range of pathological and systemic perturbations following injuries, including acute neuronal death, neuroinflammation, neurodegeneration and neuroregeneration to systemic responses. In terms of biomarker types, they range from brain-specific proteins, microRNA, genetic polymorphism, inflammatory cytokines and autoimmune markers and neuro-endocrine hormones. Furthermore, systems biology-driven biomarkers integration can help present a holistic approach to understanding scenarios and complexity pathways involved in brain injury.

Traumatic Brain Injury: Caregivers’ Problems and Needs

OpenAIRE

syed tajjudin syed hassan; WF Khaw; AR Rosna; J Husna

2011-01-01

Traumatic brain injury (TBI) is an increasingly major world health problem. This short review using the most pertinent articles on TBI caregiving problems and needs highlights the pressing issues. Articles focusing on both TBI-caregivers’ problems and needs are rarely found, especially for developing countries. Most TBI-caregiving is done by family members, whose altered lives portend burden and stresses which add to the overwhelming demand of caring for the TBI-survivor. Lack of information,...

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.

OCT imaging of acute vascular changes following mild traumatic brain injury in mice (Conference Presentation)

Science.gov (United States)

Chico-Calero, Isabel; Shishkov, Milen; Welt, Jonathan; Blatter, Cedric; Vakoc, Benjamin J.

2016-03-01

While most people recover completely from mild traumatic brain injuries (mTBIs) and concussions, a subset develop lasting neurological disorders. Understanding the complex pathophysiology of these injuries is critical to developing improved prognostic and therapeutic approaches. Multiple studies have shown that the structure and perfusion of brain vessels are altered after mTBI. It is possible that these vascular injuries contribute to or trigger neurodegeneration. Intravital microscopy and mouse models of TBI offer a powerful platform to study the vascular component of mTBI. Because optical coherence tomography based angiography is based on perfusion contrast and is not significantly degraded by vessel leakage or blood brain barrier disruption, it is uniquely suited to studies of brain perfusion in the setting of trauma. However, existing TBI imaging models require surgical exposure of the brain at the time of injury which conflates TBI-related vascular changes with those caused by surgery. In this work, we describe a modified cranial window preparation based on a flexible, transparent polyurethane membrane. Impact injuries were delivered directly through this membrane, and imaging was performed immediately after injury without the need for additional surgical procedures. Using this model, we demonstrate that mTBI induces a transient cessation of flow in the capillaries and smaller vessels near the injury point. Reperfusion is observed in all animals within 3 hours of injury. This work describes new insight into the transient vascular changes induced by mTBI, and demonstrates more broadly the utility of the OCT/polyurethane window model platform in preclinical studies of mTBI.

Traumatic Brain Injury: Caregivers’ Problems and Needs

Directory of Open Access Journals (Sweden)

syed tajjudin syed hassan

2011-03-01

Full Text Available Traumatic brain injury (TBI is an increasingly major world health problem. This short review using the most pertinent articles on TBI caregiving problems and needs highlights the pressing issues. Articles focusing on both TBI-caregivers’ problems and needs are rarely found, especially for developing countries. Most TBI-caregiving is done by family members, whose altered lives portend burden and stresses which add to the overwhelming demand of caring for the TBI-survivor. Lack of information, fi nancial inadequacy, anxiety, distress, coping defi cits, poor adaptability, inadequate knowledge and skills, and a poor support system comprise the major problems. Dysfunctional communication between caregivers and care-receivers has been little researched. The major needs are focused on health and rehabilitation information, fi nancial advice and assistance, emotional and social support, and positive psychological encouragement. In time, health information needs may be met, but not emotional support. Information on TBI caregiving problems and unmet needs is critical to all relevant healthcare stakeholders. Keywords: caregivers, rehabilitation, traumatic brain injury

Novel Treatment for Patients with Traumatic Brain Injury (TBI)

Science.gov (United States)

2016-06-01

equieffectiv e dose of phenylephri ne (PE)? 18 Does AVP maintain brain and muscle tissue 02 during CPP managemen t after TBI relative to an... Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any...discuss the meeting dates. I can be reached by telephone or email as listed below. K nnet 1·0 t ,. ti .. P ofessor of Surgery Leonard M. Miller

Volumetric analysis of day of injury computed tomography is associated with rehabilitation outcomes after traumatic brain injury

Science.gov (United States)

Majercik, Sarah; Bledsoe, Joseph; Ryser, David; Hopkins, Ramona O.; Fair, Joseph E.; Frost, R. Brock; MacDonald, Joel; Barrett, Ryan; Horn, Susan; Pisani, David; Bigler, Erin D.; Gardner, Scott; Stevens, Mark; Larson, Michael J.

2016-01-01

Introduction Day-of-injury (DOI) brain lesion volumes in traumatic brain injury (TBI) patients are rarely used to predict long-term outcomes in the acute setting. The purpose of this study was to investigate the relationship between acute brain injury lesion volume and rehabilitation outcomes in patients with TBI at a Level One Trauma Center. Methods Patients with TBI who were admitted to our rehabilitation unit after the acute care trauma service from February 2009-July 2011 were eligible for the study. Demographic data and outcome variables including cognitive and motor FIM scores, length of stay (LOS) in the rehabilitation unit, and ability to return to home were obtained. DOI quantitative injury lesion volumes and degree of midline shift were obtained from day-of-injury (DOI) brain computed tomography (CT) scans. A multiple step-wise regression model including 13 independent variables was created. This model was used to predict post-rehabilitation outcomes, including FIM scores and ability to return to home. PInjury Severity Score 24.7±9.9, and head Abbreviated Injury Scale score 3.73±0.97. Acute hospital length of stay (LOS) was 12.3±8.9 days and rehabilitation LOS was 15.9±9.3 days. Day-of-injury TBI lesion volumes were inversely associated with cognitive FIM scores at rehabilitation admission (p=0.004) and discharge (p=0.004) and inversely associated with ability to be discharged to home after rehabilitation (p=0.006). Conclusion In a cohort of patients with moderate to severe TBI requiring a rehabilitation unit stay after the acute care hospital stay, DOI brain injury lesion volumes are associated with worse cognitive FIM scores at the time of rehabilitation admission and discharge. Smaller injury volumes were associated with eventual discharge to home. Volumetric neuroimaging in the acute injury phase may improve surgeons’ ultimate outcome predictions in TBI patients. Level of Evidence/Study Type Level V, case series, Prognostic/Epidemiological PMID

Psychometric properties of the college survey for students with brain injury: individuals with and without traumatic brain injury.

Science.gov (United States)

Kennedy, Mary R T; Krause, Miriam O; O'Brien, Katy H

2014-01-01

The psychometric properties of the college challenges sub-set from The College Survey for Students with Brain Injury (CSS-BI) were investigated with adults with and without traumatic brain injury (TBI). Adults with and without TBI completed the CSS-BI. A sub-set of participants with TBI were interviewed, intentional and convergent validity were investigated, and the internal structure of the college challenges was analysed with exploratory factor analysis/principle component analysis. Respondents with TBI understood the items describing college challenges with evidence of intentional validity. More individuals with TBI than controls endorsed eight of the 13 college challenges. Those who reported more health issues endorsed more college challenges, demonstrating preliminary convergent validity. Cronbach's alphas of >0.85 demonstrated acceptable internal reliability. Factor analysis revealed a four-factor model for those with TBI: studying and learning (Factor 1), time management and organization (Factor 2), social (Factor 3) and nervousness/anxiety (Factor 4). This model explained 72% and 69% of the variance for those with and without TBI, respectively. The college challenges sub-set from the CSS-BI identifies challenges that individuals with TBI face when going to college. Some challenges were related to two factors in the model, demonstrating the inter-connections of these experiences.

HMGB1 a-Box Reverses Brain Edema and Deterioration of Neurological Function in a Traumatic Brain Injury Mouse Model

Directory of Open Access Journals (Sweden)

Lijun Yang

2018-05-01

Full Text Available Background/Aims: Traumatic brain injury (TBI is a complex neurological injury in young adults lacking effective treatment. Emerging evidences suggest that inflammation contributes to the secondary brain injury following TBI, including breakdown of the blood brain barrier (BBB, subsequent edema and neurological deterioration. High mobility group box-1 (HMGB1 has been identified as a key cytokine in the inflammation reaction following TBI. Here, we investigated the therapeutic efficacy of HMGB1 A-box fragment, an antagonist competing with full-length HMGB1 for receptor binding, against TBI. Methods: TBI was induced by controlled cortical impact (CCI in adult male mice. HMGB1 A-box fragment was given intravenously at 2 mg/kg/day for 3 days after CCI. HMGB1 A-box-treated CCI mice were compared with saline-treated CCI mice and sham mice in terms of BBB disruption evaluated by Evan’s blue extravasation, brain edema by brain water content, cell death by propidium iodide staining, inflammation by Western blot and ELISA assay for cytokine productions, as well as neurological functions by the modified Neurological Severity Score, wire grip and beam walking tests. Results: HMGB1 A-box reversed brain damages in the mice following TBI. It significantly reduced brain edema by protecting integrity of the BBB, ameliorated cell degeneration, and decreased expression of pro-inflammatory cytokines released in injured brain after TBI. These cellular and molecular effects were accompanied by improved behavioral performance in TBI mice. Notably, HMGB1 A-box blocked IL-1β-induced HMGB1 release, and preferentially attenuated TLR4, Myd88 and P65 in astrocyte cultures. Conclusion: Our data suggest that HMGB1 is involved in CCI-induced TBI, which can be inhibited by HMGB1 A-box fragment. Therefore, HMGB1 A-box fragment may have therapeutic potential for the secondary brain damages in TBI.

HMGB1 a-Box Reverses Brain Edema and Deterioration of Neurological Function in a Traumatic Brain Injury Mouse Model.

Science.gov (United States)

Yang, Lijun; Wang, Feng; Yang, Liang; Yuan, Yunchao; Chen, Yan; Zhang, Gengshen; Fan, Zhenzeng

2018-01-01

Traumatic brain injury (TBI) is a complex neurological injury in young adults lacking effective treatment. Emerging evidences suggest that inflammation contributes to the secondary brain injury following TBI, including breakdown of the blood brain barrier (BBB), subsequent edema and neurological deterioration. High mobility group box-1 (HMGB1) has been identified as a key cytokine in the inflammation reaction following TBI. Here, we investigated the therapeutic efficacy of HMGB1 A-box fragment, an antagonist competing with full-length HMGB1 for receptor binding, against TBI. TBI was induced by controlled cortical impact (CCI) in adult male mice. HMGB1 A-box fragment was given intravenously at 2 mg/kg/day for 3 days after CCI. HMGB1 A-box-treated CCI mice were compared with saline-treated CCI mice and sham mice in terms of BBB disruption evaluated by Evan's blue extravasation, brain edema by brain water content, cell death by propidium iodide staining, inflammation by Western blot and ELISA assay for cytokine productions, as well as neurological functions by the modified Neurological Severity Score, wire grip and beam walking tests. HMGB1 A-box reversed brain damages in the mice following TBI. It significantly reduced brain edema by protecting integrity of the BBB, ameliorated cell degeneration, and decreased expression of pro-inflammatory cytokines released in injured brain after TBI. These cellular and molecular effects were accompanied by improved behavioral performance in TBI mice. Notably, HMGB1 A-box blocked IL-1β-induced HMGB1 release, and preferentially attenuated TLR4, Myd88 and P65 in astrocyte cultures. Our data suggest that HMGB1 is involved in CCI-induced TBI, which can be inhibited by HMGB1 A-box fragment. Therefore, HMGB1 A-box fragment may have therapeutic potential for the secondary brain damages in TBI. © 2018 The Author(s). Published by S. Karger AG, Basel.

Triple Peripheral Nerve Injury Accompanying to Traumatic Brain Injury: A Case Report

Directory of Open Access Journals (Sweden)

Ižlknur Can

2014-02-01

Full Text Available Secondary injuries especially extremity fractures may be seen concurrently with traumatic brain injury (TBI. Peripheral nerve damages may accompany to these fractures and may be missed out, especially in acute stage. In this case report; damage of radial, ulnar and median nerves which was developed secondarily to distal humerus fracture that could not be detected in acute stage, in a patient who had motor vehicle accident (MVA. 29-year-old male patient was admitted with weakness in the right upper extremity. 9 months ago, he had traumatic brain injury because of MVA, and fracture of distal humerus was detected in follow-ups. Upon the suspect of the peripheral nerve injury, the diagnosis was confirmed with ENMG. The patient responded well to the rehabilitation program treatment. In a TBI patient, it must be kept in mind that there might be a secondary trauma and therefore peripheral nerve lesions may accompany to TBI.

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

Metabolic alterations in patients who develop traumatic brain injury (TBI)-induced hypopituitarism.

Science.gov (United States)

Prodam, F; Gasco, V; Caputo, M; Zavattaro, M; Pagano, L; Marzullo, P; Belcastro, S; Busti, A; Perino, C; Grottoli, S; Ghigo, E; Aimaretti, G

2013-08-01

Hypopituitarism is associated with metabolic alterations but in TBI-induced hypopituitarism data are scanty. The aim of our study was to evaluate the prevalence of naïve hypertension, dyslipidemia, and altered glucose metabolism in TBI-induced hypopituitarism patients. Cross-sectional retrospective study in a tertiary care endocrinology center. 54 adult patients encountering a moderate or severe TBI were evaluated in the chronic phase (at least 12 months after injury) after-trauma. Presence of hypopituitarism, BMI, hypertension, fasting blood glucose and insulin levels, oral glucose tolerance test (if available) and a lipid profile were evaluated. The 27.8% of patients showed various degrees of hypopituitarism. In particular, 9.3% had total, 7.4% multiple and 11.1% isolated hypopituitarism. GHD was present in 22.2% of patients. BMI was similar between the two groups. Hypopituitaric patients presented a higher prevalence of dyslipidemia (phypopituitaric patients. In particular, triglycerides (phypopituitaric TBI patients. We showed that long-lasting TBI patients who develop hypopituitarism frequently present metabolic alterations, in particular altered glucose levels, insulin resistance and hypertriglyceridemia. In view of the risk of premature cardiovascular death in hypopituitaric patients, major attention has to been paid in those who encountered a TBI, because they suffer from the same comorbidities and may present other deterioration factors due to complex pharmacological treatments and restriction in participation in life activities and healthy lifestyle. Copyright © 2013 Elsevier Ltd. All rights reserved.

Variation in monitoring and treatment policies for intracranial hypertension in traumatic brain injury: A survey in 66 neurotrauma centers participating in the CENTER-TBI study

NARCIS (Netherlands)

M.C. Cnossen (Maryse); Huijben, J.A. (Jilske A.); van der Jagt, M. (Mathieu); Volovici, V. (Victor); van Essen, T. (Thomas); S. Polinder (Suzanne); D. Nelson (David); Ercole, A. (Ari); Stocchetti, N. (Nino); Citerio, G. (Giuseppe); W.C. Peul (Wilco); A.I.R. Maas (Andrew I.R.); D.K. Menon (David ); E.W. Steyerberg (Ewout W.); Lingsma, H.F. (Hester F.); Adams, H. (Hadie); Alessandro, M. (Masala); J.E. Allanson (Judith); Amrein, K. (Krisztina); Andaluz, N. (Norberto); N. Andelic (Nada); Andrea, N. (Nanni); L. Andreassen (Lasse); Anke, A. (Audny); Antoni, A. (Anna); Ardon, H. (Hilko); Audibert, G. (Gérard); Auslands, K. (Kaspars); Azouvi, P. (Philippe); Baciu, C. (Camelia); Bacon, A. (Andrew); Badenes, R. (Rafael); Baglin, T. (Trevor); R.H.M.A. Bartels (Ronald); P. Barzo (P.); Bauerfeind, U. (Ursula); R. Beer (Ronny); Belda, F.J. (Francisco Javier); B.-M. Bellander (Bo-Michael); A. Belli (Antonio); Bellier, R. (Rémy); H. Benali (Habib); Benard, T. (Thierry); M. Berardino (Maurizio); L. Beretta (Luigi); Beynon, C. (Christopher); Bilotta, F. (Federico); H. Binder (Harald); Biqiri, E. (Erta); Blaabjerg, M. (Morten); Lund, S.B. (Stine Borgen); Bouzat, P. (Pierre); Bragge, P. (Peter); Brazinova, A. (Alexandra); F. Brehar (Felix); Brorsson, C. (Camilla); Buki, A. (Andras); M. Bullinger (Monika); Bucková, V. (Veronika); Calappi, E. (Emiliana); P. Cameron (Peter); Carbayo, L.G. (Lozano Guillermo); Carise, E. (Elsa); K.L.H. Carpenter (Keri L.H.); Castaño-León, A.M. (Ana M.); Causin, F. (Francesco); Chevallard, G. (Giorgio); A. Chieregato (Arturo); G. Citerio (Giuseppe); Cnossen, M. (Maryse); M. Coburn (Mark); J.P. Coles (Jonathan P.); Cooper, J.D. (Jamie D.); Correia, M. (Marta); A. Covic (Amra); N. Curry (Nicola); E. Czeiter (Endre); M. Czosnyka (Marek); Dahyot-Fizelier, C. (Claire); F. Damas (François); P. Damas (Pierre); H. Dawes (Helen); De Keyser, V. (Véronique); F.D. Corte (Francesco); B. Depreitere (Bart); Ding, S. (Shenghao); D.W.J. Dippel (Diederik); K. Dizdarevic (Kemal); Dulière, G.-L. (Guy-Loup); Dzeko, A. (Adelaida); G. Eapen (George); Engemann, H. (Heiko); A. Ercole (Ari); P. Esser (Patrick); Ezer, E. (Erzsébet); M. Fabricius (Martin); V.L. Feigin (V.); Feng, J. (Junfeng); Foks, K. (Kelly); F. Fossi (Francesca); Francony, G. (Gilles); J. Frantzén (Janek); Freo, U. (Ulderico); S.K. Frisvold (Shirin Kordasti); Furmanov, A. (Alex); Gagliardo, P. (Pablo); D. Galanaud (Damien); G. Gao (Guoyi); K. Geleijns (Karin); A. Ghuysen (Alexandre); Giraud, B. (Benoit); Glocker, B. (Ben); Gomez, P.A. (Pedro A.); Grossi, F. (Francesca); R.L. Gruen (Russell); Gupta, D. (Deepak); J.A. Haagsma (Juanita); E. Hadzic (Ermin); I. Haitsma (Iain); J.A. Hartings (Jed); R. Helbok (Raimund); E. Helseth (Eirik); Hertle, D. (Daniel); S. Hill (Sean); Hoedemaekers, A. (Astrid); S. Hoefer (Stefan); P.J. Hutchinson (Peter J.); Håberg, K.A. (Kristine Asta); B.C. Jacobs (Bart); Janciak, I. (Ivan); K. Janssens (Koen); Jiang, J.-Y. (Ji-Yao); Jones, K. (Kelly); Kalala, J.-P. (Jean-Pierre); Kamnitsas, K. (Konstantinos); Karan, M. (Mladen); Karau, J. (Jana); A. Katila (Ari); M. Kaukonen (Maija); Keeling, D. (David); Kerforne, T. (Thomas); N. Ketharanathan (Naomi); Kettunen, J. (Johannes); Kivisaari, R. (Riku); A.G. Kolias (Angelos G.); Kolumbán, B. (Bálint); E.J.O. Kompanje (Erwin); D. Kondziella (Daniel); L.-O. Koskinen (Lars-Owe); Kovács, N. (Noémi); F. Kalovits (Ferenc); A. Lagares (Alfonso); L. Lanyon (Linda); S. Laureys (Steven); Lauritzen, M. (Martin); F.E. Lecky (Fiona); C. Ledig (Christian); R. Lefering; V. Legrand (Valerie); Lei, J. (Jin); L. Levi (Leon); R. Lightfoot (Roger); H.F. Lingsma (Hester); D. Loeckx (Dirk); Lozano, A. (Angels); Luddington, R. (Roger); Luijten-Arts, C. (Chantal); Maas, A.I.R. (Andrew I.R.); MacDonald, S. (Stephen); MacFayden, C. (Charles); M. Maegele (Marc); M. Majdan (Marek); Major, S. (Sebastian); A. Manara (Alex); Manhes, P. (Pauline); G. Manley (Geoffrey); Martin, D. (Didier); C. Martino (Costanza); Maruenda, A. (Armando); H. Maréchal (Hugues); Mastelova, D. (Dagmara); Mattern, J. (Julia); McMahon, C. (Catherine); Melegh, B. (Béla); Menon, D. (David); T. Menovsky (Tomas); Morganti-Kossmann, C. (Cristina); Mulazzi, D. (Davide); Mutschler, M. (Manuel); H. Mühlan (Holger); Negru, A. (Ancuta); Nelson, D. (David); E. Neugebauer (Eddy); V.F. Newcombe (Virginia F.); Noirhomme, Q. (Quentin); Nyirádi, J. (József); M. Oddo (Mauro); A.W. Oldenbeuving; M. Oresic (Matej); Ortolano, F. (Fabrizio); A. Palotie (Aarno); P.M. Parizel; Patruno, A. (Adriana); J.-F. Payen (Jean-François); Perera, N. (Natascha); V. Perlbarg (Vincent); Persona, P. (Paolo); Peul, W. (Wilco); N. Pichon (Nicolas); Piilgaard, H. (Henning); A. Piippo (Anna); S.P. Floury (Sébastien Pili); M. Pirinen (Matti); H. Ples (Horia); Polinder, S. (Suzanne); Pomposo, I. (Inigo); M. Psota (Marek); P. Pullens (Pim); L. Puybasset (Louis); A. Ragauskas (Arminas); R. Raj (Rahul); Rambadagalla, M. (Malinka); Rehorcíková, V. (Veronika); J.K.J. Rhodes (Jonathan K.J.); S. Richardson (Sylvia); S. Ripatti (Samuli); S. Rocka (Saulius); Rodier, N. (Nicolas); Roe, C. (Cecilie); Roise, O. (Olav); C.M.A.A. Roks (Gerwin); Romegoux, P. (Pauline); J. Rosand (Jonathan); Rosenfeld, J. (Jeffrey); C. Rosenlund (Christina); G. Rosenthal (Guy); R. Rossaint (Rolf); S. Rossi (Sandra); Rostalski, T. (Tim); D. Rueckert (Daniel); de Ruiz, A.F. (Arcaute Felix); M. Rusnák (Martin); Sacchi, M. (Marco); Sahakian, B. (Barbara); J. Sahuquillo (Juan); O. Sakowitz (Oliver); Sala, F. (Francesca); Sanchez-Pena, P. (Paola); Sanchez-Porras, R. (Renan); Sandor, J. (Janos); Santos, E. (Edgar); N. Sasse (Nadine); Sasu, L. (Luminita); Savo, D. (Davide); I.B. Schipper (Inger); Schlößer, B. (Barbara); S. Schmidt (Silke); Schneider, A. (Annette); H. Schoechl (Herbert); G.G. Schoonman; Rico, F.S. (Frederik Schou); E. Schwendenwein (Elisabeth); Schöll, M. (Michael); Sir, O. (özcan); T. Skandsen (Toril); Smakman, L. (Lidwien); D. Smeets (Dominique); Smielewski, P. (Peter); Sorinola, A. (Abayomi); E. Stamatakis (Emmanuel); S. Stanworth (Simon); Stegemann, K. (Katrin); Steinbüchel, N. (Nicole); R. Stevens (Robert); W. Stewart (William); E.W. Steyerberg (Ewout); N. Stocchetti (Nino); Sundström, N. (Nina); Synnot, A. (Anneliese); J. Szabó (József); J. Söderberg (Jeannette); F.S. Taccone (Fabio); Tamás, V. (Viktória); Tanskanen, P. (Päivi); A. Tascu (Alexandru); Taylor, M.S. (Mark Steven); Te, A.B. (Ao Braden); O. Tenovuo (Olli); Teodorani, G. (Guido); A. Theadom (Alice); Thomas, M. (Matt); D. Tibboel (Dick); C.M. Tolias (Christos M.); Tshibanda, J.-F.L. (Jean-Flory Luaba); Tudora, C.M. (Cristina Maria); P. Vajkoczy (Peter); Valeinis, E. (Egils); Hecke, W.V. (Wim Van); Praag, D.V. (Dominique Van); Dirk, V.R. (Van Roost); Vlierberghe, E.V. (Eline Van); Vyvere, T.V. (Thijs vande); Vanhaudenhuyse, A. (Audrey); A. Vargiolu (Alessia); E. Vega (Emmanuel); J. Verheyden (Jan); Vespa, P.M. (Paul M.); A. Vik (Anne); R. Vilcinis (Rimantas); Vizzino, G. (Giacinta); C.L.A.M. Vleggeert-Lankamp (Carmen); V. Volovici (Victor); P. Vulekovic (Peter); Vámos, Z. (Zoltán); Wade, D. (Derick); Wang, K.K.W. (Kevin K.W.); Wang, L. (Lei); E.D. Wildschut (Enno); G. Williams (Guy); Willumsen, L. (Lisette); Wilson, A. (Adam); Wilson, L. (Lindsay); Winkler, M.K.L. (Maren K.L.); P. Ylén (Peter); Younsi, A. (Alexander); M. Zaaroor (Menashe); Zhang, Z. (Zhiqun); Zheng, Z. (Zelong); Zumbo, F. (Fabrizio); de Lange, S. (Stefanie); G.C.W. De Ruiter (Godard C.W.); den Boogert, H. (Hugo); van Dijck, J. (Jeroen); T.A. van Essen (T.); C.M. van Heugten (Caroline M.); M. van der Jagt (Mathieu); J. van der Naalt (Joukje)

2017-01-01

textabstractBackground: No definitive evidence exists on how intracranial hypertension should be treated in patients with traumatic brain injury (TBI). It is therefore likely that centers and practitioners individually balance potential benefits and risks of different intracranial pressure (ICP)

Perioperative Care for Pediatric Patients With Penetrating Brain Injury: A Review.

Science.gov (United States)

Mikhael, Marco; Frost, Elizabeth; Cristancho, Maria

2017-05-19

Traumatic brain injury (TBI) continues to be the leading cause of death and acquired disability in young children and adolescents, due to blunt or penetrating trauma, the latter being less common but more lethal. Penetrating brain injury (PBI) has not been studied extensively, mainly reported as case reports or case series, due to the assumption that both types of brain injury have common pathophysiology and consequently common management. However, recommendations and guidelines for the management of PBI differ from those of blunt TBI in regards to neuroimaging, intracranial pressure (ICP) monitoring, and surgical management including those pertaining to vascular injury. PBI was one of the exclusion criteria in the second edition of guidelines for the acute medical management of severe TBI in infants, children, and adolescents that was published in 2012 (it is referred to as "pediatric guidelines" in this review). Many reviews of TBI do not differentiate between the mechanisms of injury. We present an overview of PBI, its presenting features, epidemiology, and causes as well as an analysis of case series and the conclusions that may be drawn from those and other studies. More clinical trials specific to penetrating head injuries in children, focusing mainly on pathophysiology and management, are needed. The term PBI is specific to penetrating injury only, whereas TBI, a more inclusive term, describes mainly, but not only, blunt injury.

What Can I Do to Help Prevent Traumatic Brain Injury?

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... TBI Online Concussion Training Press Room Guide to Writing about TBI in News and Social Media Living with TBI HEADS UP to Brain Injury Awareness Get Email Updates To receive email updates about this topic, ...

Facial emotion recognition deficits following moderate-severe Traumatic Brain Injury (TBI): re-examining the valence effect and the role of emotion intensity.

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Rosenberg, Hannah; McDonald, Skye; Dethier, Marie; Kessels, Roy P C; Westbrook, R Frederick

2014-11-01

Many individuals who sustain moderate-severe traumatic brain injuries (TBI) are poor at recognizing emotional expressions, with a greater impairment in recognizing negative (e.g., fear, disgust, sadness, and anger) than positive emotions (e.g., happiness and surprise). It has been questioned whether this "valence effect" might be an artifact of the wide use of static facial emotion stimuli (usually full-blown expressions) which differ in difficulty rather than a real consequence of brain impairment. This study aimed to investigate the valence effect in TBI, while examining emotion recognition across different intensities (low, medium, and high). Twenty-seven individuals with TBI and 28 matched control participants were tested on the Emotion Recognition Task (ERT). The TBI group was more impaired in overall emotion recognition, and less accurate recognizing negative emotions. However, examining the performance across the different intensities indicated that this difference was driven by some emotions (e.g., happiness) being much easier to recognize than others (e.g., fear and surprise). Our findings indicate that individuals with TBI have an overall deficit in facial emotion recognition, and that both people with TBI and control participants found some emotions more difficult than others. These results suggest that conventional measures of facial affect recognition that do not examine variance in the difficulty of emotions may produce erroneous conclusions about differential impairment. They also cast doubt on the notion that dissociable neural pathways underlie the recognition of positive and negative emotions, which are differentially affected by TBI and potentially other neurological or psychiatric disorders.

Traumatic brain injuries in the construction industry.

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Colantonio, Angela; McVittie, Doug; Lewko, John; Yin, Junlang

2009-10-01

This study analyses factors associated with work-related traumatic brain injury (TBI), specifically in the construction industry in Ontario, Canada. This cross-sectional study utilized data extracted from the Ontario Workplace Safety and Insurance Board (WSIB) records indicating concussion/intracranial injury that resulted in days off work in 2004-2005. Analyses of 218 TBI cases revealed that falls were the most common cause of injury, followed by being struck by or against an object. Mechanisms of injury and the temporal profile of injury also varied by age. For instance, a significantly higher proportion of injuries occurred in the mornings for young workers compared to older workers. The results of this study provide important information for prevention of TBI which suggest important age-specific strategies for workers in the construction industry.

Traumatic Brain Injury: An Overview of School Re-Entry.

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Tucker, Bonnie Foster; Colson, Steven E.

1992-01-01

This article presents a definition of traumatic brain injury (TBI); describes problem behavioral characteristics of students post-TBI and some possible solutions; examines academic, social, emotional, and cognitive factors; and outlines interventions to assist teachers in working constructively with TBI students. (JDD)

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

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Abdolreza Babaee

2015-09-01

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

Vascular impairment as a pathological mechanism underlying long-lasting cognitive dysfunction after pediatric traumatic brain injury.

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Ichkova, Aleksandra; Rodriguez-Grande, Beatriz; Bar, Claire; Villega, Frederic; Konsman, Jan Pieter; Badaut, Jerome

2017-12-01

Traumatic brain injury (TBI) is the leading cause of death and disability in children. Indeed, the acute mechanical injury often evolves to a chronic brain disorder with long-term cognitive, emotional and social dysfunction even in the case of mild TBI. Contrary to the commonly held idea that children show better recovery from injuries than adults, pediatric TBI patients actually have worse outcome than adults for the same injury severity. Acute trauma to the young brain likely interferes with the fine-tuned developmental processes and may give rise to long-lasting consequences on brain's function. This review will focus on cerebrovascular dysfunction as an important early event that may lead to long-term phenotypic changes in the brain after pediatric TBI. These, in turn may be associated with accelerated brain aging and cognitive dysfunction. Finally, since no effective treatments are currently available, understanding the unique pathophysiological mechanisms of pediatric TBI is crucial for the development of new therapeutic options. Copyright © 2017 Elsevier Ltd. All rights reserved.

Brain-Derived Neurotrophic Factor in TBI-related mortality: Interrelationships between Genetics and Acute Systemic and CNS BDNF Profiles

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Failla, Michelle D.; Conley, Yvette P.; Wagner, Amy K.

2015-01-01

Background Older adults have higher mortality rates after severe traumatic brain injury (TBI) compared to younger adults. Brain derived neurotrophic factor (BDNF) signaling is altered in aging and is important to TBI given its role in neuronal survival/plasticity and autonomic function. Following experimental TBI, acute BDNF administration has not been efficacious. Clinically, genetic variation in BDNF (reduced signaling alleles: rs6265, Met-carriers; rs7124442, C-carriers) were protective in acute mortality. Post-acutely, these genotypes carried lower mortality risk in older adults, and greater mortality risk among younger adults. Objective Investigate BDNF levels in mortality/outcome following severe TBI in the context of age and genetic risk. Methods CSF and serum BDNF were assessed prospectively during the first week following severe TBI (n=203), and in controls (n=10). Age, BDNF genotype, and BDNF levels were assessed as mortality/outcome predictors. Results CSF BDNF levels tended to be higher post-TBI (p=0.061) versus controls and were associated with time until death (p=0.042). In contrast, serum BDNF levels were reduced post-TBI versus controls (pBDNF serum and gene*age interactions were mortality predictors post-TBI in the same multivariate model. CSF and serum BDNF tended to be negatively correlated post-TBI (p=0.07). Conclusions BDNF levels predicted mortality, in addition to gene*age interactions, suggesting levels capture additional mortality risk. Higher CSF BDNF post-TBI may be detrimental due to injury and age-related increases in pro-apoptotic BDNF target receptors. Negative CSF and serum BDNF correlations post-TBI suggest blood-brain barrier transit alterations. Understanding BDNF signaling in neuronal survival, plasticity, and autonomic function may inform treatment. PMID:25979196

Mitochondrial targeted neuron focused genes in hippocampus of rats with traumatic brain injury.

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Sharma, Pushpa; Su, Yan A; Barry, Erin S; Grunberg, Neil E; Lei, Zhang

2012-09-01

Mild traumatic brain injury (mTBI) represents a major health problem in civilian populations as well as among the military service members due to (1) lack of effective treatments, and (2) our incomplete understanding about the progression of secondary cell injury cascades resulting in neuronal cell death due to deficient cellular energy metabolism and damaged mitochondria. The aim of this study was to identify and delineate the mitochondrial targeted genes responsible for altered brain energy metabolism in the injured brain. Rats were either grouped into naïve controls or received lateral fluid percussion brain injury (2-2.5 atm) and followed up for 7 days. Rats were either grouped into naïve controls or received lateral fluid percussion brain injury (2-2.5 atm) and followed for 7 days. The severity of brain injury was evaluated by the neurological severity scale-revised (NSS-R) at 3 and 5 days post TBI and immunohistochemical analyses at 7 days post TBI. The expression profiles of mitochondrial-targeted genes across the hippocampus from TBI and naïe rats were also examined by oligo-DNA microarrays. NSS-R scores of TBI rats (5.4 ± 0.5) in comparison to naïe rats (3.9 ± 0.5) and H and E staining of brain sections suggested a mild brain injury. Bioinformatics and systems biology analyses showed 31 dysregulated genes, 10 affected canonical molecular pathways including a number of genes involved in mitochondrial enzymes for oxidative phosphorylation, mitogen-activated protein Kinase (MAP), peroxisome proliferator-activated protein (PPAP), apoptosis signaling, and genes responsible for long-term potentiation of Alzheimer's and Parkinson's diseases. Our results suggest that dysregulated mitochondrial-focused genes in injured brains may have a clinical utility for the development of future therapeutic strategies aimed at the treatment of TBI.

Mild TBI Diagnosis and Management Strategies

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Department of Veterans Affairs — The Mild Traumatic Brain Injury (TBI) Diagnosis and Management Strategies will assist in the study of TBI issues, such as the Influence of Concussion on Persistent...

Defense Health Care: Research on Hyperbaric Oxygen Therapy to Treat Traumatic Brain Injury and Post-Traumatic Stress Disorder

Science.gov (United States)

2015-12-01

Traumatic Brain Injury and Post - Traumatic Stress Disorder Why GAO Did This Study TBI and PTSD are signature...injury (TBI) and post - traumatic stress disorder ( PTSD ), most of which were focused solely on TBI (29 articles). The 32 articles consisted of 7 case...Case Report Articles on Hyperbaric Oxygen Therapy to Treat Traumatic Brain Injury (TBI) or Post - Traumatic Stress Disorder ( PTSD ),

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

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Traumatic brain injury (TBI) has complex effects on the gastrointestinal tract that are associated with TBI-related morbidity and mortality. We examined changes in mucosal barrier properties and enteric glial cell response in the gut after experimental TBI in mice, as well as effects of the enteric...

Evaluation after Traumatic Brain Injury

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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…

Current Opportunities for Clinical Monitoring of Axonal Pathology in Traumatic Brain Injury

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Parmenion P. Tsitsopoulos

2017-11-01

Full Text Available Traumatic brain injury (TBI is a multidimensional and highly complex disease commonly resulting in widespread injury to axons, due to rapid inertial acceleration/deceleration forces transmitted to the brain during impact. Axonal injury leads to brain network dysfunction, significantly contributing to cognitive and functional impairments frequently observed in TBI survivors. Diffuse axonal injury (DAI is a clinical entity suggested by impaired level of consciousness and coma on clinical examination and characterized by widespread injury to the hemispheric white matter tracts, the corpus callosum and the brain stem. The clinical course of DAI is commonly unpredictable and it remains a challenging entity with limited therapeutic options, to date. Although axonal integrity may be disrupted at impact, the majority of axonal pathology evolves over time, resulting from delayed activation of complex intracellular biochemical cascades. Activation of these secondary biochemical pathways may lead to axonal transection, named secondary axotomy, and be responsible for the clinical decline of DAI patients. Advances in the neurocritical care of TBI patients have been achieved by refinements in multimodality monitoring for prevention and early detection of secondary injury factors, which can be applied also to DAI. There is an emerging role for biomarkers in blood, cerebrospinal fluid, and interstitial fluid using microdialysis in the evaluation of axonal injury in TBI. These biomarker studies have assessed various axonal and neuroglial markers as well as inflammatory mediators, such as cytokines and chemokines. Moreover, modern neuroimaging can detect subtle or overt DAI/white matter changes in diffuse TBI patients across all injury severities using magnetic resonance spectroscopy, diffusion tensor imaging, and positron emission tomography. Importantly, serial neuroimaging studies provide evidence for evolving axonal injury. Since axonal injury may be a key

Primary blast-induced traumatic brain injury: lessons from lithotripsy

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Nakagawa, A.; Ohtani, K.; Armonda, R.; Tomita, H.; Sakuma, A.; Mugikura, S.; Takayama, K.; Kushimoto, S.; Tominaga, T.

2017-11-01

Traumatic injury caused by explosive or blast events is traditionally divided into four mechanisms: primary, secondary, tertiary, and quaternary blast injury. The mechanisms of blast-induced traumatic brain injury (bTBI) are biomechanically distinct and can be modeled in both in vivo and in vitro systems. The primary bTBI injury mechanism is associated with the response of brain tissue to the initial blast wave. Among the four mechanisms of bTBI, there is a remarkable lack of information regarding the mechanism of primary bTBI. On the other hand, 30 years of research on the medical application of shock waves (SWs) has given us insight into the mechanisms of tissue and cellular damage in bTBI, including both air-mediated and underwater SW sources. From a basic physics perspective, the typical blast wave consists of a lead SW followed by shock-accelerated flow. The resultant tissue injury includes several features observed in primary bTBI, such as hemorrhage, edema, pseudo-aneurysm formation, vasoconstriction, and induction of apoptosis. These are well-described pathological findings within the SW literature. Acoustic impedance mismatch, penetration of tissue by shock/bubble interaction, geometry of the skull, shear stress, tensile stress, and subsequent cavitation formation are all important factors in determining the extent of SW-induced tissue and cellular injury. In addition, neuropsychiatric aspects of blast events need to be taken into account, as evidenced by reports of comorbidity and of some similar symptoms between physical injury resulting in bTBI and the psychiatric sequelae of post-traumatic stress. Research into blast injury biophysics is important to elucidate specific pathophysiologic mechanisms of blast injury, which enable accurate differential diagnosis, as well as development of effective treatments. Herein we describe the requirements for an adequate experimental setup when investigating blast-induced tissue and cellular injury; review SW physics

Pharmacologic resuscitation for hemorrhagic shock combined with traumatic brain injury

DEFF Research Database (Denmark)

Jin, Guang; Duggan, Michael; Imam, Ayesha

2012-01-01

[Hex]) after traumatic brain injury (TBI) decreases brain swelling, without affecting size of the lesion. This study was performed to determine whether addition of VPA to Hex would decrease the lesion size in a clinically relevant large animal model of TBI + HS....

Educational professionals' understanding of childhood traumatic brain injury.

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Linden, Mark A; Braiden, Hannah-Jane; Miller, Sarah

2013-01-01

To determine the understanding of educational professionals around the topic of childhood brain injury and explore the factor structure of the Common Misconceptions about Traumatic Brain Injury Questionnaire (CM-TBI). Cross-sectional postal survey. The CM-TBI was posted to all educational establishments in one region of the UK. One representative from each school was asked to complete and return the questionnaire (n = 388). Differences were demonstrated between those participants who knew someone with a brain injury and those who did not, with a similar pattern being shown for those educators who had taught a child with brain injury. Participants who had taught a child with brain injury demonstrated greater knowledge in areas such as seatbelts/prevention, brain damage, brain injury sequelae, amnesia, recovery and rehabilitation. Principal components analysis suggested the existence of four factors and the discarding of half the original items of the questionnaire. In the first European study to explore this issue, it is highlighted that teachers are ill-prepared to cope with children who have sustained a brain injury. Given the importance of a supportive school environment in return to life following hospitalization, the lack of understanding demonstrated by teachers in this research may significantly impact on a successful return to school.

Traumatic brain injury pharmacological treatment: recommendations

Directory of Open Access Journals (Sweden)

Renato Anghinah

Full Text Available ABSTRACT This article presents the recommendations on the pharmacological treatment employed in traumatic brain injury (TBI at the outpatient clinic of the Cognitive Rehabilitation after TBI Service of the Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Brazil. A systematic assessment of the consensus reached in other countries, and of articles on TBI available in the PUBMED and LILACS medical databases, was carried out. We offer recommendations of pharmacological treatments in patients after TBI with different symptoms.

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

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Zhao, Yan; Wang, Zheng-Guo

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 bTBI-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.

Enhanced Cognitive Rehabilitation to Treat Comorbid TBI and PTSD

Science.gov (United States)

2015-10-01

injury (TBI) and posttraumatic stress disorder ( PTSD ) benefit fully from interventions for both conditions. PTSD and TBI occur together frequently in...veterans with comorbid traumatic brain injury and posttraumatic stress disorder : study protocol for a randomized controlled trial. CONCLUSION: In...moderate TBI (mTBI) and PTSD . Emotional symptoms are likely a main cause of the persistence of post -concussive symptoms while thinking problems

A preliminary model for posttraumatic brain injury depression.

Science.gov (United States)

Malec, James F; Brown, Allen W; Moessner, Anne M; Stump, Timothy E; Monahan, Patrick

2010-07-01

To develop, based on previous research, and evaluate a model for depression after traumatic brain injury (TBI). Cross-sectional structural equation modeling (SEM) of data from consecutively recruited patients. Acute hospital and inpatient rehabilitation units. Adult patients (N=158) after hospital admission for moderate to severe TBI. Not applicable. External appraisal of ability in participants was measured by the Mayo-Portland Adaptability Inventory (MPAI-4) Ability Index completed by a TBI clinical nurse specialist. Patient self-appraisal of post-TBI ability and depression were measured by the Awareness Questionnaire and Beck Depression Inventory-II. Functional outcome 1 year after injury was assessed with the MPAI-4 Participation Index. Successive SEM resulted in a parsimonious model with excellent fit. Consistent with prior research, a moderately strong association between self-appraisal of post-TBI ability and depression was found. Injury severity, as measured by the duration of posttraumatic amnesia (PTA), was not significantly associated with post-TBI depression. The 1-year functional outcome was associated with depression and TBI severity. The strong association between self-appraisal of post-TBI ability and depression is consistent with the cognitive-behavioral model of depression and recommends consideration and further study of cognitive-behavioral therapy for post-TBI depression. The lack of association between TBI severity and depression may represent the indirect and proxy nature of current measures of TBI severity such as PTA. Emerging neuroimaging techniques (eg, diffusion tensor imaging, magnetic resonance imaging spectroscopy) may provide the more direct measures of disruption of brain function after TBI that are needed to advance this line of research. Copyright 2010 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.

Immersive virtual reality in traumatic brain injury rehabilitation: A literature review.

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Aida, Jared; Chau, Brian; Dunn, Justin

2018-04-07

Traumatic brain injury (TBI) is a common cause of morbidity and mortality in the United States with its sequelae often affecting individuals long after the initial injury. Innovations in virtual reality (VR) technology may offer potential therapy options in the recovery from such injuries. However, there is currently no consensus regarding the efficacy of VR in the setting of TBI rehabilitation. The aim of this review is to evaluate and summarize the current literature regarding immersive VR in the rehabilitation of those with TBI. A comprehensive literature search was conducted utilizing PubMed, Google Scholar, and the Cochrane Review using the search terms "virtual reality," "traumatic brain injury," "brain injury," and "immersive." A total of 11 studies were evaluated. These were primarily of low-level evidence, with the exception of two randomized, controlled trials. 10 of 11 studies demonstrated improvement with VR therapy. VR was most frequently used to address gait or cognitive deficits. While the current literature generally offers support for the use of VR in TBI recovery, there is a paucity of strong evidence to support its widespread use. The increasing availability of immersive VR technology offers the potential for engaging therapy in TBI rehabilitation, but its utility remains uncertain given the limited studies available at this time.

‘Studying Injured Minds’ - The Vietnam Head Injury Study and 40 years of brain injury research

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Vanessa eRaymont

2011-03-01

Full Text Available The study of those who have sustained traumatic brain injuries (TBI during military conflicts has greatly facilitated research in the fields of neuropsychology, neurosurgery, psychiatry, neurology and neuroimaging. The Vietnam Head Injury Study (VHIS is a prospective, long-term follow-up study of a cohort of 1,221 Vietnam veterans with mostly penetrating brain injuries, which has stretched over more than 40 years. The scope of this study, both in terms of the types of injury and fields of examination, has been extremely broad. It has been instrumental in extending the field of TBI research and in exposing pressing medical and social issues that affect those who suffer such injuries. This review summarizes the history of conflict-related TBI research and the VHIS to date, as well as the vast range of important findings the VHIS has established.

Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury

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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.

Clinically-Important Brain Injury and CT Findings in Pediatric Mild Traumatic Brain Injuries: A Prospective Study in a Chinese Reference Hospital

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Huiping Zhu

2014-03-01

Full Text Available This study investigated injury patterns and the use of computed tomography (CT among Chinese children with mild traumatic brain injury (MTBI. We enrolled children with MTBI who were treated within 24 hours of head trauma in the emergency department of Wuhan Medical Care Center for Women and Children in Wuhan, China. Characteristics of MTBIs were analyzed by age and gender. Results of cranial CT scan and clinically-important brain injury (ciTBI for children were obtained. The definition of ciTBI was: death from TBI, intubation for more than 24 h for TBI, neurosurgery, or hospital admission of 2 nights or more. Of 455 eligible patients with MTBI, ciTBI occurred in two, and no one underwent neurosurgical intervention. CT scans were performed for 441 TBI patients (96.9%, and abnormal findings were reported for 147 patients (33.3%, 95% CI 29.0–37.8. Falls were the leading cause of MTBI (61.5%, followed by blows (18.9% and traffic collisions (14.1% for children in the 0–2 group and 10–14 group. For children aged between 3 and 9, the top three causes of TBI were falls, traffic collisions and blows. Leisure activity was the most reported activity when injuries occurred for all age groups. Sleeping/resting and walking ranked in the second and third place for children between 0 and 2 years of age, and walking and riding for the other two groups. The places where the majority injuries occurred were the home for the 0–2 and 3–9 years of age groups, and school for the 10–14 years of age group. There was no statistical difference between boys and girls with regard to the activity that caused the MTBI. This study highlights the important roles that parents and school administrators in the development of preventive measures to reduce the risk of traumatic brain injury in children. Also, identifying children who had a head trauma at very low risk of clinically important TBI for whom CT might be unnecessary is a priority area of research in China.

Volumetric analysis of day of injury computed tomography is associated with rehabilitation outcomes after traumatic brain injury.

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Majercik, Sarah; Bledsoe, Joseph; Ryser, David; Hopkins, Ramona O; Fair, Joseph E; Brock Frost, R; MacDonald, Joel; Barrett, Ryan; Horn, Susan; Pisani, David; Bigler, Erin D; Gardner, Scott; Stevens, Mark; Larson, Michael J

2017-01-01

Day-of-injury (DOI) brain lesion volumes in traumatic brain injury (TBI) patients are rarely used to predict long-term outcomes in the acute setting. The purpose of this study was to investigate the relationship between acute brain injury lesion volume and rehabilitation outcomes in patients with TBI at a level one trauma center. Patients with TBI who were admitted to our rehabilitation unit after the acute care trauma service from February 2009-July 2011 were eligible for the study. Demographic data and outcome variables including cognitive and motor Functional Independence Measure (FIM) scores, length of stay (LOS) in the rehabilitation unit, and ability to return to home were obtained. The DOI quantitative injury lesion volumes and degree of midline shift were obtained from DOI brain computed tomography scans. A multiple stepwise regression model including 13 independent variables was created. This model was used to predict postrehabilitation outcomes, including FIM scores and ability to return to home. A p value less than 0.05 was considered significant. Ninety-six patients were enrolled in the study. Mean age was 43 ± 21 years, admission Glasgow Coma Score was 8.4 ± 4.8, Injury Severity Score was 24.7 ± 9.9, and head Abbreviated Injury Scale score was 3.73 ± 0.97. Acute hospital LOS was 12.3 ± 8.9 days, and rehabilitation LOS was 15.9 ± 9.3 days. Day-of-injury TBI lesion volumes were inversely associated with cognitive FIM scores at rehabilitation admission (p = 0.004) and discharge (p = 0.004) and inversely associated with ability to be discharged to home after rehabilitation (p = 0.006). In a cohort of patients with moderate to severe TBI requiring a rehabilitation unit stay after the acute care hospital stay, DOI brain injury lesion volumes are associated with worse cognitive FIM scores at the time of rehabilitation admission and discharge. Smaller-injury volumes were associated with eventual discharge to home. Volumetric neuroimaging in the acute

Direct cost associated with acquired brain injury in Ontario

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Chen Amy

2012-08-01

Full Text Available Abstract Background Acquired Brain Injury (ABI from traumatic and non traumatic causes is a leading cause of disability worldwide yet there is limited research summarizing the health system economic burden associated with ABI. The objective of this study was to determine the direct cost of publicly funded health care services from the initial hospitalization to three years post-injury for individuals with traumatic (TBI and non-traumatic brain injury (nTBI in Ontario Canada. Methods A population-based cohort of patients discharged from acute hospital with an ABI code in any diagnosis position in 2004 through 2007 in Ontario was identified from administrative data. Publicly funded health care utilization was obtained from several Ontario administrative healthcare databases. Patients were stratified according to traumatic and non-traumatic causes of brain injury and whether or not they were discharged to an inpatient rehabilitation center. Health system costs were calculated across a continuum of institutional and community settings for up to three years after initial discharge. The continuum of settings included acute care emergency departments inpatient rehabilitation (IR complex continuing care home care services and physician visits. All costs were calculated retrospectively assuming the government payer’s perspective. Results Direct medical costs in an ABI population are substantial with mean cost in the first year post-injury per TBI and nTBI patient being $32132 and $38018 respectively. Among both TBI and nTBI patients those discharged to IR had significantly higher treatment costs than those not discharged to IR across all institutional and community settings. This tendency remained during the entire three-year follow-up period. Annual medical costs of patients hospitalized with a brain injury in Ontario in the first follow-up year were approximately $120.7 million for TBI and $368.7 million for nTBI. Acute care cost accounted for 46

Long-Term Functional and Psychosocial Outcomes After Hypoxic-Ischemic Brain Injury: A Case-Controlled Comparison to Traumatic Brain Injury.

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Harbinson, Meredith; Zarshenas, Sareh; Cullen, Nora K

2017-12-01

Despite the increasing rate of survival from hypoxic-ischemic brain injury (HIBI), there is a paucity of evidence on the long-term functional outcomes after inpatient rehabilitation among these nontrauma patients compared to patients with traumatic brain injury (TBI). To compare functional and psychosocial outcomes of patients with HIBI to those of case-matched patients with TBI 4-11 years after brain insult. Retrospective, matched case-controlled study. Data at the time of rehabilitation admission and discharge were collected as part of a larger acquired brain injury (ABI) database at Toronto Rehabilitation Institute (TRI) between 1999 and 2009. This study consisted of 11 patients with HIBI and 11 patients with TBI that attended the neuro-rehabilitation day program at TRI during a similar time frame and were matched on age, admission Functional Independence Measure (FIM) scores, and acute care length of stay (ALOS). At 4-11 years following brain insult, patients were reassessed using the FIM, Disability Rating Scale (DRS), Personal Health Questionnaire Depression Scale (PHQ-9), and the Mayo-Portland Adaptability Inventory 4 (MPAI-4). At follow-up, patients with HIBI had significantly lower FIM motor and cognitive scores than patients with TBI (75.3 ± 20.6 versus 88.1 ± 4.78, P MPAI-4 at follow-up (P < .05). The study results suggest that patients with HIBI achieve less long-term functional improvements compared to patients with TBI. Further research is warranted to compare the components of inpatient rehabilitation while adjusting for demographics and clinical characteristics between these 2 groups of patients. III. Copyright © 2017 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.

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

Energy Technology Data Exchange (ETDEWEB)

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

2009-04-30

Traumatic brain injury [TBI] has become a signature injury of current military conflicts, with debilitating, costly, and long-lasting effects. Although mechanisms by which head impacts cause TBI have been well-researched, the mechanisms by which blasts cause TBI are not understood. From numerical hydrodynamic simulations, we have discovered that non-lethal blasts can induce sufficient skull flexure to generate potentially damaging loads in the brain, even without a head impact. The possibility that this mechanism may contribute to TBI has implications for injury diagnosis and armor design.

Traumatic Brain Injury Pathophysiology and Treatments: Early, Intermediate, and Late Phases Post-Injury

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Algattas, Hanna; Huang, Jason H.

2014-01-01

Traumatic Brain Injury (TBI) affects a large proportion and extensive array of individuals in the population. While precise pathological mechanisms are lacking, the growing base of knowledge concerning TBI has put increased emphasis on its understanding and treatment. Most treatments of TBI are aimed at ameliorating secondary insults arising from the injury; these insults can be characterized with respect to time post-injury, including early, intermediate, and late pathological changes. Early pathological responses are due to energy depletion and cell death secondary to excitotoxicity, the intermediate phase is characterized by neuroinflammation and the late stage by increased susceptibility to seizures and epilepsy. Current treatments of TBI have been tailored to these distinct pathological stages with some overlap. Many prophylactic, pharmacologic, and surgical treatments are used post-TBI to halt the progression of these pathologic reactions. In the present review, we discuss the mechanisms of the pathological hallmarks of TBI and both current and novel treatments which target the respective pathways. PMID:24381049

Longitudinal Examination of Resilience After Traumatic Brain Injury: A Traumatic Brain Injury Model Systems Study.

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Marwitz, Jennifer H; Sima, Adam P; Kreutzer, Jeffrey S; Dreer, Laura E; Bergquist, Thomas F; Zafonte, Ross; Johnson-Greene, Douglas; Felix, Elizabeth R

2018-02-01

To evaluate (1) the trajectory of resilience during the first year after a moderate-severe traumatic brain injury (TBI); (2) factors associated with resilience at 3, 6, and 12 months postinjury; and (3) changing relationships over time between resilience and other factors. Longitudinal analysis of an observational cohort. Five inpatient rehabilitation centers. Patients with TBI (N=195) enrolled in the resilience module of the TBI Model Systems study with data collected at 3-, 6-, and 12-month follow-up. Not applicable. Connor-Davidson Resilience Scale. Initially, resilience levels appeared to be stable during the first year postinjury. Individual growth curve models were used to examine resilience over time in relation to demographic, psychosocial, and injury characteristics. After adjusting for these characteristics, resilience actually declined over time. Higher levels of resilience were related to nonminority status, absence of preinjury substance abuse, lower anxiety and disability level, and greater life satisfaction. Resilience is a construct that is relevant to understanding brain injury outcomes and has potential value in planning clinical interventions. Copyright © 2017 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.

The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease

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Kokiko-Cochran, Olga N.; Godbout, Jonathan P.

2018-01-01

The post-injury inflammatory response is a key mediator in long-term recovery from traumatic brain injury (TBI). Moreover, the immune response to TBI, mediated by microglia and macrophages, is influenced by existing brain pathology and by secondary immune challenges. For example, recent evidence shows that the presence of beta-amyloid and phosphorylated tau protein, two hallmark features of AD that increase during normal aging, substantially alter the macrophage response to TBI. Additional data demonstrate that post-injury microglia are “primed” and become hyper-reactive following a subsequent acute immune challenge thereby worsening recovery. These alterations may increase the incidence of neuropsychiatric complications after TBI and may also increase the frequency of neurodegenerative pathology. Therefore, the purpose of this review is to summarize experimental studies examining the relationship between TBI and development of AD-like pathology with an emphasis on the acute and chronic microglial and macrophage response following injury. Furthermore, studies will be highlighted that examine the degree to which beta-amyloid and tau accumulation as well as pre- and post-injury immune stressors influence outcome after TBI. Collectively, the studies described in this review suggest that the brain’s immune response to injury is a key mediator in recovery, and if compromised by previous, coincident, or subsequent immune stressors, post-injury pathology and behavioral recovery will be altered. PMID:29686672

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.

Hypopituitarism after traumatic brain injury.

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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. Copyright © 2015 Elsevier Inc. All rights reserved.

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,

Vocational outcome 6-15 years after a traumatic brain injury.

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Lexell, J; Wihlney, A-K; Jacobsson, L J

2016-01-01

To describe vocational outcome 6-15 years after a traumatic brain injury (TBI) among individuals who were productive by working or studying at the time of their TBI and determine the associations with variables related to the time of injury and at follow-up. Thirty-four individuals with a mild TBI and 45 with a moderate-to-severe TBI were assessed on average 10 years post-injury. Logistic regression was used to determine the association between their current vocational situation and variables related to the time of injury (gender, age, injury severity and educational level) and at follow-up (time since injury, marital status and overall disability). A total of 67% were productive at follow-up. Age at injury, injury severity and the degree of disability at follow-up were strongly associated with being productive. Younger individuals with milder TBI and less severe disability were significantly more likely to be fully productive. No significant associations were found between productivity and gender, education, time since injury or marital status. This study indicates that return to productivity in a long-term perspective after a TBI is possible, in particular when the individual is young, has sustained a mild TBI and has a milder form of overall disability.

Functional MRI in the Investigation of Blast-Related Traumatic Brain Injury

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Graner, John; Oakes, Terrence R.; French, Louis M.; Riedy, Gerard

2012-01-01

This review focuses on the application of functional magnetic resonance imaging (fMRI) to the investigation of blast-related traumatic brain injury (bTBI). Relatively little is known about the exact mechanisms of neurophysiological injury and pathological and functional sequelae of bTBI. Furthermore, in mild bTBI, standard anatomical imaging techniques (MRI and computed tomography) generally fail to show focal lesions and most of the symptoms present as subjective clinical functional deficits. Therefore, an objective test of brain functionality has great potential to aid in patient diagnosis and provide a sensitive measurement to monitor disease progression and treatment. The goal of this review is to highlight the relevant body of blast-related TBI literature and present suggestions and considerations in the development of fMRI studies for the investigation of bTBI. The review begins with a summary of recent bTBI publications followed by discussions of various elements of blast-related injury. Brief reviews of some fMRI techniques that focus on mental processes commonly disrupted by bTBI, including working memory, selective attention, and emotional processing, are presented in addition to a short review of resting state fMRI. Potential strengths and weaknesses of these approaches as regards bTBI are discussed. Finally, this review presents considerations that must be made when designing fMRI studies for bTBI populations, given the heterogeneous nature of bTBI and its high rate of comorbidity with other physical and psychological injuries. PMID:23460082

Interleukin-1 Receptor in Seizure Susceptibility after Traumatic Injury to the Pediatric Brain.

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Semple, Bridgette D; O'Brien, Terence J; Gimlin, Kayleen; Wright, David K; Kim, Shi Eun; Casillas-Espinosa, Pablo M; Webster, Kyria M; Petrou, Steven; Noble-Haeusslein, Linda J

2017-08-16

Epilepsy after pediatric traumatic brain injury (TBI) is associated with poor quality of life. This study aimed to characterize post-traumatic epilepsy in a mouse model of pediatric brain injury, and to evaluate the role of interleukin-1 (IL-1) signaling as a target for pharmacological intervention. Male mice received a controlled cortical impact or sham surgery at postnatal day 21, approximating a toddler-aged child. Mice were treated acutely with an IL-1 receptor antagonist (IL-1Ra; 100 mg/kg, s.c.) or vehicle. Spontaneous and evoked seizures were evaluated from video-EEG recordings. Behavioral assays tested for functional outcomes, postmortem analyses assessed neuropathology, and brain atrophy was detected by ex vivo magnetic resonance imaging. At 2 weeks and 3 months post-injury, TBI mice showed an elevated seizure response to the convulsant pentylenetetrazol compared with sham mice, associated with abnormal hippocampal mossy fiber sprouting. A robust increase in IL-1β and IL-1 receptor were detected after TBI. IL-1Ra treatment reduced seizure susceptibility 2 weeks after TBI compared with vehicle, and a reduction in hippocampal astrogliosis. In a chronic study, IL-1Ra-TBI mice showed improved spatial memory at 4 months post-injury. At 5 months, most TBI mice exhibited spontaneous seizures during a 7 d video-EEG recording period. At 6 months, IL-1Ra-TBI mice had fewer evoked seizures compared with vehicle controls, coinciding with greater preservation of cortical tissue. Findings demonstrate this model's utility to delineate mechanisms underlying epileptogenesis after pediatric brain injury, and provide evidence of IL-1 signaling as a mediator of post-traumatic astrogliosis and seizure susceptibility. SIGNIFICANCE STATEMENT Epilepsy is a common cause of morbidity after traumatic brain injury in early childhood. However, a limited understanding of how epilepsy develops, particularly in the immature brain, likely contributes to the lack of efficacious treatments

MicroRNAs as diagnostic markers and therapeutic targets for traumatic brain injury

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Bridget Martinez

2017-01-01

Full Text Available Traumatic brain injury (TBI is characterized by primary damage to the brain from the external mechanical force and by subsequent secondary injury due to various molecular and pathophysiological responses that eventually lead to neuronal cell death. Secondary brain injury events may occur minutes, hours, or even days after the trauma, and provide valuable therapeutic targets to prevent further neuronal degeneration. At the present time, there is no effective treatment for TBI due, in part, to the widespread impact of numerous complex secondary biochemical and pathophysiological events occurring at different time points following the initial injury. MicroRNAs control a range of physiological and pathological functions such as development, differentiation, apoptosis and metabolism, and may serve as potential targets for progress assessment and intervention against TBI to mitigate secondary damage to the brain. This has implications regarding improving the diagnostic accuracy of brain impairment and long-term outcomes as well as potential novel treatments. Recent human studies have identified specific microRNAs in serum/plasma (miR-425-p, -21, -93, -191 and -499 and cerebro-spinal fluid (CSF (miR-328, -362-3p, -451, -486a as possible indicators of the diagnosis, severity, and prognosis of TBI. Experimental animal studies have examined specific microRNAs as biomarkers and therapeutic targets for moderate and mild TBI (e.g., miR-21, miR-23b. MicroRNA profiling was altered by voluntary exercise. Differences in basal microRNA expression in the brain of adult and aged animals and alterations in response to TBI (e.g., miR-21 have also been reported. Further large-scale studies with TBI patients are needed to provide more information on the changes in microRNA profiles in different age groups (children, adults, and elderly.

Patient Effort in Traumatic Brain Injury Inpatient Rehabilitation: Course and Associations With Age, Brain Injury Severity, and Time Postinjury

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Seel, Ronald T.; Corrigan, John D.; Dijkers, Marcel P.; Barrett, Ryan S.; Bogner, Jennifer; Smout, Randall J.; Garmoe, William; Horn, Susan D.

2016-01-01

Objective To describe patients' level of effort in occupational, physical, and speech therapy sessions during traumatic brain injury (TBI) inpatient rehabilitation and to evaluate how age, injury severity, cognitive impairment, and time are associated with effort. Design Prospective, multicenter, longitudinal cohort study. Setting Acute TBI rehabilitation programs. Participants Patients (N=1946) receiving 138,555 therapy sessions. Interventions Not applicable. Main Outcome Measures Effort in rehabilitation sessions rated on the Rehabilitation Intensity of Therapy Scale, FIM, Comprehensive Severity Index brain injury severity score, posttraumatic amnesia (PTA), and Agitated Behavior Scale (ABS). Results The Rehabilitation Intensity of Therapy Scale effort ratings in individual therapy sessions closely conformed to a normative distribution for all 3 disciplines. Mean Rehabilitation Intensity of Therapy Scale ratings for patients' therapy sessions were higher in the discharge week than in the admission week (Prehabilitation, differences in effort ratings (Pcognitive scores and over time. In linear mixed-effects modeling, age and Comprehensive Severity Index brain injury severity score at admission, days from injury to rehabilitation admission, days from admission, and daily ratings of PTA and ABS score were predictors of level of effort (Prehabilitation setting using the Rehabilitation Intensity of Therapy Scale. Patients who sustain TBI show varying levels of effort in rehabilitation therapy sessions, with effort tending to increase over the stay. PTA and agitated behavior are primary risk factors that substantially reduce patient effort in therapies. PMID:26212400

Brain and Serum Androsterone is Elevated in Response to Stress in Rats with Mild Traumatic Brain Injury

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Richard J Servatius

2016-08-01

Full Text Available Exposure to lateral fluid percussion (LFP injury consistent with mild traumatic brain injury (mTBI persistently attenuates acoustic startle responses (ASRs in rats. Here, we examined whether the experience of head trauma affects stress reactivity. Male Sprague-Dawley rats were matched for ASRs and randomly assigned to receive mTBI through LFP or experience a sham surgery (SHAM. ASRs were measured post injury days (PIDs 1, 3, 7, 14, 21 and 28. To assess neurosteroids, rats received a single 2.0 mA, 0.5 s foot shock on PID 34 (S34, PID 35 (S35, on both days (2S, or the experimental context (CON. Levels of the neurosteroids pregnenolone (PREG, allopregnanolone (ALLO, and androsterone (ANDRO were determined for the prefrontal cortex, hippocampus and cerebellum. For 2S rats, repeated blood samples were obtained at 15, 30 and 60 min post-stressor for determination of corticosterone (CORT levels after stress or context on PID 34. Similar to earlier work, ASRs were severely attenuated in mTBI rats without remission for 28 days after injury. No differences were observed between mTBI and SHAM rats in basal CORT, peak CORT levels or its recovery. In serum and brain, ANDRO levels were the most stress-sensitive. Stress-induced ANDRO elevations were greater than those in mTBI rats. As a positive allosteric modulator of gamma-aminobutyric acid (GABAA receptors, increased brain ANDRO levels are expected to be anxiolytic. The impact of brain ANDRO elevations in the aftermath of mTBI on coping warrants further elaboration.

Effect of chromatic filters on visual performance in individuals with mild traumatic brain injury (mTBI): A pilot study.

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Fimreite, Vanessa; Willeford, Kevin T; Ciuffreda, Kenneth J

2016-01-01

Spectral filters have been used clinically in patients with mild traumatic brain injury (mTBI). However, they have not been formally assessed using objective techniques in this population. Thus, the aim of the present pilot study was to determine the effect of spectral filters on reading performance and visuo-cortical responsivity in adults with mTBI. 12 adults with mTBI/concussion were tested. All reported photosensitivity and reading problems. They were compared to 12 visually-normal, asymptomatic adults. There were several test conditions: three luminance-matched control filters (gray neutral density, blue, and red), the patient-selected 'precision tint lens' that provided the most comfort and clarity of text using the Intuitive Colorimeter System, and baseline without any filters. The Visagraph was used to assess reading eye movements and reading speed objectively with each filter. In addition, both the amplitude and latency of the visual-evoked potential (VEP) were assessed with the same filters. There were few significant group differences in either the reading-related parameters or VEP latency for any of the test filter conditions. Subjective improvements were noted in most with mTBI (11/12). The majority of patients with mTBI chose a tinted filter that resulted in increased visual comfort. While significant findings based on the objective testing were found for some conditions, the subjective results suggest that precision tints should be considered as an adjunctive treatment in patients with mTBI and photosensitivity. Copyright © 2016 Spanish General Council of Optometry. Published by Elsevier España, S.L.U. All rights reserved.

The spectrum and outcome of paediatric traumatic brain injury in ...

African Journals Online (AJOL)

The spectrum and outcome of paediatric traumatic brain injury in ... to develop a comprehensive overview of traumatic brain injury (TBI) in children ... We reviewed the age, gender, outcomes, radiological findings and treatment of the patients.

Glucose and oxygen metabolism after penetrating ballistic-like brain injury

Science.gov (United States)

Gajavelli, Shyam; Kentaro, Shimoda; Diaz, Julio; Yokobori, Shoji; Spurlock, Markus; Diaz, Daniel; Jackson, Clayton; Wick, Alexandra; Zhao, Weizhao; Leung, Lai Y; Shear, Deborah; Tortella, Frank; Bullock, M Ross

2015-01-01

Traumatic brain injury (TBI) is a major cause of death and disability in all age groups. Among TBI, penetrating traumatic brain injuries (PTBI) have the worst prognosis and represent the leading cause of TBI-related morbidity and death. However, there are no specific drugs/interventions due to unclear pathophysiology. To gain insights we looked at cerebral metabolism in a PTBI rat model: penetrating ballistic-like brain injury (PBBI). Early after injury, regional cerebral oxygen tension and consumption significantly decreased in the ipsilateral cortex in the PBBI group compared with the control group. At the same time point, glucose uptake was significantly reduced globally in the PBBI group compared with the control group. Examination of Fluorojade B-stained brain sections at 24 hours after PBBI revealed an incomplete overlap of metabolic impairment and neurodegeneration. As expected, the injury core had the most severe metabolic impairment and highest neurodegeneration. However, in the peri-lesional area, despite similar metabolic impairment, there was lesser neurodegeneration. Given our findings, the data suggest the presence of two distinct zones of primary injury, of which only one recovers. We anticipate the peri-lesional area encompassing the PBBI ischemic penumbra, could be salvaged by acute therapies. PMID:25669903

Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death

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Sang Hwon Lee

2017-11-01

Full Text Available Protocatechuic acid (PCA was first purified from green tea and has shown numerous biological activities, including anti-apoptotic, anti-inflammatory, and anti-atherosclerotic effects. The effect of PCA on traumatic brain injury (TBI-induced neuronal death has not previously been evaluated. TBI is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile. TBI causes neuronal death in the hippocampus and cerebral cortex. The present study aimed to evaluate the therapeutic potential of PCA on TBI-induced neuronal death. Here, TBI was induced by a controlled cortical impact model using rats. PCA (30 mg/kg was injected into the intraperitoneal (ip space immediately after TBI. Neuronal death was evaluated with Fluoro Jade-B (FJB staining at 24 h after TBI. Oxidative injury was detected by 4-hydroxy-2-nonenal (4HNE, glutathione (GSH concentration was analyzed by glutathione adduct with N-ethylmaleimide (GS-NEM staining at 24 h after TBI, and microglial activation in the hippocampus was detected by CD11b immunohistochemistry at one week after TBI. We found that the proportion of degenerating neurons, oxidative injury, GSH depletion, and microglia activation in the hippocampus and cortex were all reduced by PCA treatment following TBI. Therefore, our study suggests that PCA may have therapeutic potential in preventing TBI-induced neuronal death.

Electroencephalography and quantitative electroencephalography in mild traumatic brain injury.

Science.gov (United States)

Haneef, Zulfi; Levin, Harvey S; Frost, James D; Mizrahi, Eli M

2013-04-15

Mild traumatic brain injury (mTBI) causes brain injury resulting in electrophysiologic abnormalities visible in electroencephalography (EEG) recordings. Quantitative EEG (qEEG) makes use of quantitative techniques to analyze EEG characteristics such as frequency, amplitude, coherence, power, phase, and symmetry over time independently or in combination. QEEG has been evaluated for its use in making a diagnosis of mTBI and assessing prognosis, including the likelihood of progressing to the postconcussive syndrome (PCS) phase. We review the EEG and qEEG changes of mTBI described in the literature. An attempt is made to separate the findings seen during the acute, subacute, and chronic phases after mTBI. Brief mention is also made of the neurobiological correlates of qEEG using neuroimaging techniques or in histopathology. Although the literature indicates the promise of qEEG in making a diagnosis and indicating prognosis of mTBI, further study is needed to corroborate and refine these methods.

Intelligence after traumatic brain injury: meta-analysis of outcomes and prognosis.

Science.gov (United States)

Königs, M; Engenhorst, P J; Oosterlaan, J

2016-01-01

Worldwide, 54-60 million individuals sustain traumatic brain injury (TBI) each year. This meta-analysis aimed to quantify intelligence impairments after TBI and to determine the value of age and injury severity in the prognosis of TBI. An electronic database search identified 81 relevant peer-reviewed articles encompassing 3890 patients. Full-scale IQ (FSIQ), performance IQ (PIQ) and verbal IQ (VIQ) impairments were quantified (Cohen's d) for patients with mild, moderate and severe TBI in the subacute phase of recovery and the chronic phase. Meta-regressions explored prognostic values of age and injury severity measures for intelligence impairments. The results showed that, in the subacute phase, FSIQ impairments were absent for patients with mild TBI, medium-sized for patients with moderate TBI (d = -0.61, P intelligence impairments, where children may have better recovery from mild TBI and poorer recovery from severe TBI than adults. Injury severity measures predict intelligence impairments and do not outperform one another. © 2015 EAN.

Posttraining Epinephrine Reverses Memory Deficits Produced by Traumatic Brain Injury in Rats

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Alejandro Lorón-Sánchez

2016-01-01

Full Text Available The aim of this research is to evaluate whether posttraining systemic epinephrine is able to improve object recognition memory in rats with memory deficits produced by traumatic brain injury. Forty-nine two-month-old naïve male Wistar rats were submitted to surgical procedures to induce traumatic brain injury (TBI or were sham-operated. Rats were trained in an object recognition task and, immediately after training, received an intraperitoneal injection of distilled water (Sham-Veh and TBI-Veh group or 0.01 mg/kg epinephrine (TBI-Epi group or no injection (TBI-0 and Sham-0 groups. Retention was tested 3 h and 24 h after acquisition. The results showed that brain injury produced severe memory deficits and that posttraining administration of epinephrine was able to reverse them. Systemic administration of distilled water also had an enhancing effect, but of a lower magnitude. These data indicate that posttraining epinephrine and, to a lesser extent, vehicle injection reduce memory deficits associated with TBI, probably through induction of a low-to-moderate emotional arousal.

Posttraining Epinephrine Reverses Memory Deficits Produced by Traumatic Brain Injury in Rats

Science.gov (United States)

Lorón-Sánchez, Alejandro; Torras-Garcia, Meritxell; Coll-Andreu, Margalida; Costa-Miserachs, David; Portell-Cortés, Isabel

2016-01-01

The aim of this research is to evaluate whether posttraining systemic epinephrine is able to improve object recognition memory in rats with memory deficits produced by traumatic brain injury. Forty-nine two-month-old naïve male Wistar rats were submitted to surgical procedures to induce traumatic brain injury (TBI) or were sham-operated. Rats were trained in an object recognition task and, immediately after training, received an intraperitoneal injection of distilled water (Sham-Veh and TBI-Veh group) or 0.01 mg/kg epinephrine (TBI-Epi group) or no injection (TBI-0 and Sham-0 groups). Retention was tested 3 h and 24 h after acquisition. The results showed that brain injury produced severe memory deficits and that posttraining administration of epinephrine was able to reverse them. Systemic administration of distilled water also had an enhancing effect, but of a lower magnitude. These data indicate that posttraining epinephrine and, to a lesser extent, vehicle injection reduce memory deficits associated with TBI, probably through induction of a low-to-moderate emotional arousal. PMID:27127685

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)....

Clinical treatment of traumatic brain injury complicated by cranial nerve injury.

Science.gov (United States)

Jin, Hai; Wang, Sumin; Hou, Lijun; Pan, Chengguang; Li, Bo; Wang, Hui; Yu, Mingkun; Lu, Yicheng

2010-09-01

To discuss the epidemiology, diagnosis and surgical treatment of cranial nerve injury following traumatic brain injury (TBI) for the sake of raising the clinical treatment of this special category of TBI. A retrospective analysis was made of 312 patients with cranial nerve injury among 3417 TBI patients, who were admitted for treatment in this hospital. A total of 312 patients (9.1%) involving either a single nerve or multiple nerves among the 12 pairs of cranial nerves were observed. The extent of nerve injury varied and involved the olfactory nerve (66 cases), optic nerve (78 cases), oculomotor nerve (56 cases), trochlear nerve (8 cases), trigeminal nerve (4 cases), abducent nerve (12 cases), facial nerve (48 cases), acoustic nerve (10 cases), glossopharyngeal nerve (8 cases), vagus nerve (6 cases), accessory nerve (10 cases) and hypoglossal nerve (6 cases). Imaging examination revealed skull fracture in 217 cases, complicated brain contusion in 232 cases, epidural haematoma in 194 cases, subarachnoid haemorrhage in 32 cases, nasal cerebrospinal fluid (CSF) leakage in 76 cases and ear CSF leakage in 8 cases. Of the 312 patients, 46 patients died; the mortality rate associated with low cranial nerve injury was as high as 73.3%. Among the 266 surviving patients, 199 patients received conservative therapy and 67 patients received surgical therapy; the curative rates among these two groups were 61.3% (122 patients) and 86.6% (58 patients), respectively. TBI-complicated cranial nerve injury is subject to a high incidence rate, a high mortality rate and a high disability rate. Our findings suggest that the chance of recovery may be increased in cases where injuries are amenable to surgical decompression. It is necessary to study all 12 pairs of cranial nerves systematically. Clinically, it is necessary to standardise surgical indications, operation timing, surgical approaches and methods for the treatment of TBI-complicated cranial nerve injury. 2010 Elsevier Ltd. All

Primary Blast Injury Criteria for Animal/Human TBI Models using Field Validated Shock Tubes

Science.gov (United States)

2017-09-01

acute hemorrhage characterized by partial filling of small groups of alveoli by blood . 240 kPa: Mild multifocal pools of acute hemorrhage which...Neurotrauma, Blast TBI, Primary blast brain injury, Blast overpressure, Blood -brain barrier, Neuroinflammation, Oxidative stress, Neuroproteomics 16...stress, neuroinflammation and BBB damage as a result of blast overpressure in the acute phase (0, 4 and 24 hours post-exposure). Our group

Pediatric acquired brain injury.

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Bodack, Marie I

2010-10-01

Although pediatric patients are sometimes included in studies about visual problems in patients with acquired brain injury (ABI), few studies deal solely with children. Unlike studies dealing with adult patients, in which mechanisms of brain injury are divided into cerebral vascular accident (CVA) and traumatic brain injury (TBI), studies on pediatric patients deal almost exclusively with traumatic brain injury, specifically caused by accidents. Here we report on the vision problems of 4 pediatric patients, ages 3 to 18 years, who were examined in the ophthalmology/optometry clinic at a children's hospital. All patients had an internally caused brain injury and after the initial insult manifested problems in at least one of the following areas: acuity, binocularity, motility (tracking or saccades), accommodation, visual fields, and visual perceptual skills. Pediatric patients can suffer from a variety of oculo-visual problems after the onset of head injury. These patients may or may not be symptomatic and can benefit from optometric intervention. Copyright © 2010 American Optometric Association. Published by Elsevier Inc. All rights reserved.

Top-cited articles in traumatic brain injury.

Directory of Open Access Journals (Sweden)

Bhanu eSharma

2014-11-01

Full Text Available 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, respectively, 1990 ± 14.9 years and 2003 ± 6.7 years. 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 TBI. 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 TBI

Traumatic Brain Injury Increases Cortical Glutamate Network Activity by Compromising GABAergic Control.

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Cantu, David; Walker, Kendall; Andresen, Lauren; Taylor-Weiner, Amaro; Hampton, David; Tesco, Giuseppina; Dulla, Chris G

2015-08-01

Traumatic brain injury (TBI) is a major risk factor for developing pharmaco-resistant epilepsy. Although disruptions in brain circuitry are associated with TBI, the precise mechanisms by which brain injury leads to epileptiform network activity is unknown. Using controlled cortical impact (CCI) as a model of TBI, we examined how cortical excitability and glutamatergic signaling was altered following injury. We optically mapped cortical glutamate signaling using FRET-based glutamate biosensors, while simultaneously recording cortical field potentials in acute brain slices 2-4 weeks following CCI. Cortical electrical stimulation evoked polyphasic, epileptiform field potentials and disrupted the input-output relationship in deep layers of CCI-injured cortex. High-speed glutamate biosensor imaging showed that glutamate signaling was significantly increased in the injured cortex. Elevated glutamate responses correlated with epileptiform activity, were highest directly adjacent to the injury, and spread via deep cortical layers. Immunoreactivity for markers of GABAergic interneurons were significantly decreased throughout CCI cortex. Lastly, spontaneous inhibitory postsynaptic current frequency decreased and spontaneous excitatory postsynaptic current increased after CCI injury. Our results suggest that specific cortical neuronal microcircuits may initiate and facilitate the spread of epileptiform activity following TBI. Increased glutamatergic signaling due to loss of GABAergic control may provide a mechanism by which TBI can give rise to post-traumatic epilepsy. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Oligodendrogenesis after Cerebral Ischaemia and Traumatic Brain Injury

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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.

Psychological Characteristics in Acute Mild Traumatic Brain Injury: An MMPI-2 Study.

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Gass, Carlton S; Rogers, David; Kinne, Erica

2017-01-01

The psychological characteristics of acute traumatic brain injury (TBI) have received limited research focus, despite empirical evidence of their relevance for subsequent psychological adjustment and early therapeutic intervention. This study addressed a wide range of psychological features in 47 individuals who were hospitalized as a result of acute mild TBI (mTBI). Participants were screened from amongst consecutive TBI admissions for moderate to severe brain injury, and for pre-injury neurological, psychiatric, or substance abuse histories. Clinical and content scale scores on the MMPI-2 were explored in relation to patient gender, age, level of education, and extent of cognitive complaints. The results revealed diverse psychosocial problem areas across the sample, the most common of which were somatic and cognitive complaints, compromised insight, and a naively optimistic self-perception. The mediating roles of injury severity and demographic variables are discussed. Clinical implications and specific recommendations are presented.

Anaemia worsens early functional outcome after traumatic brain injury: a preliminary study.

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Litofsky, N Scott; Miller, Douglas C; Chen, Zhenzhou; Simonyi, Agnes; Klakotskaia, Diana; Giritharan, Andrew; Feng, Qi; McConnell, Diane; Cui, Jiankun; Gu, Zezong

2018-01-01

To determine early effects on outcome from traumatic brain injury (TBI) induced by controlled cortical impact (CCI) associated with anaemia in mice. Outcome from TBI with concomitant anaemia would be worse than TBI without anaemia. CCI was induced with electromagnetic impaction in four groups of C57BL/6J mice: sham, sham+anaemia; TBI; and TBI+anaemia. Anaemia was created by withdrawal of 30% of calculated intravascular blood volume and saline replacement of equal volume. Functional outcome was assessed by beam-walking test and open field test (after pre-injury training) on post-injury days 3 and 7. After functional assessment, brains removed from sacrificed animals were pathological reviewed with haematoxylin and eosin, cresyl violet, Luxol Fast Blue, and IBA-1 immunostains. Beam-walking was similar between animals with TBI and TBI+anaemia (p = 0.9). In open field test, animals with TBI+anaemia walked less distance than TBI alone or sham animals on days 3 (p < 0.001) and 7 (p < 0.05), indicating less exploratory and locomotion behaviours. No specific pathologic differences could be identified. Anaemia associated with TBI from CCI is associated with worse outcome as measured by less distance travelled in the open field test at three days than if anaemia is not present.

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)....

Comparative Effectiveness of Family Problem-Solving Therapy (F-PST) for Adolescent TBI

Science.gov (United States)

2018-01-25

Tbi; Intracranial Edema; Brain Edema; Craniocerebral Trauma; Head Injury; Brain Hemorrhage, Traumatic; Subdural Hematoma; Brain Concussion; Head Injuries, Closed; Epidural Hematoma; Cortical Contusion; Wounds and Injuries; Disorders of Environmental Origin; Trauma, Nervous System; Brain Injuries

Role of Intravenous Levetiracetam in Seizure Prophylaxis of Severe Traumatic Brain Injury Patients

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BATOOL F. KIRMANI

2013-11-01

Full Text Available Traumatic brain injury (TBI can cause seizures and the development of epilepsy. The incidence of seizures varies from 21% in patients with severe brain injuries to 50% in patients with war-related penetrating TBI. In the acute and sub-acute periods following injury, seizures can lead to increased intracranial pressure and cerebral edema, further complicating TBI management. Anticonvulsants should be used for seizure prophylaxis and treatment. Phenytoin is the most widely prescribed anticonvulsant in these patients. Intravenous levetiracetam, made available in 2006, is now being considered as an alternative to phenytoin in acute care settings. When compared with phenytoin, levetiracetam has fewer side-effects and drug-drug interactions. In the following, the role of levetiracetam in TBI care and the supporting evidence is discussed.

Tribes and tribulations: interdisciplinary eHealth in providing services for people with a traumatic brain injury (TBI).

Science.gov (United States)

Hines, M; Brunner, M; Poon, S; Lam, M; Tran, V; Yu, D; Togher, L; Shaw, T; Power, E

2017-11-21

eHealth has potential for supporting interdisciplinary care in contemporary traumatic brain injury (TBI) rehabilitation practice, yet little is known about whether this potential is being realised, or what needs to be done to further support its implementation. The purpose of this study was to explore health professionals' experiences of, and attitudes towards eHealth technologies to support interdisciplinary practice within rehabilitation for people after TBI. A qualitative study using narrative analysis was conducted. One individual interview and three focus groups were conducted with health professionals (n = 17) working in TBI rehabilitation in public and private healthcare settings across regional and metropolitan New South Wales, Australia. Narrative analysis revealed that participants held largely favourable views about eHealth and its potential to support interdisciplinary practice in TBI rehabilitation. However, participants encountered various issues related to (a) the design of, and access to electronic medical records, (b) technology, (c) eHealth implementation, and (d) information and communication technology processes that disconnected them from the work they needed to accomplish. In response, health professionals attempted to make the most of unsatisfactory eHealth systems and processes, but were still mostly unsuccessful in optimising the quality, efficiency, and client-centredness of their work. Attention to sources of disconnection experienced by health professionals, specifically design of, and access to electronic health records, eHealth resourcing, and policies and procedures related to eHealth and interdisciplinary practice are required if the potential of eHealth for supporting interdisciplinary practice is to be realised.

Mild traumatic brain injury results in depressed cerebral glucose uptake: An (18)FDG PET study.

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Selwyn, Reed; Hockenbury, Nicole; Jaiswal, Shalini; Mathur, Sanjeev; Armstrong, Regina C; Byrnes, Kimberly R

2013-12-01

Moderate to severe traumatic brain injury (TBI) in humans and rats induces measurable metabolic changes, including a sustained depression in cerebral glucose uptake. However, the effect of a mild TBI on brain glucose uptake is unclear, particularly in rodent models. This study aimed to determine the glucose uptake pattern in the brain after a mild lateral fluid percussion (LFP) TBI. Briefly, adult male rats were subjected to a mild LFP and positron emission tomography (PET) imaging with (18)F-fluorodeoxyglucose ((18)FDG), which was performed prior to injury and at 3 and 24 h and 5, 9, and 16 days post-injury. Locomotor function was assessed prior to injury and at 1, 3, 7, 14, and 21 days after injury using modified beam walk tasks to confirm injury severity. Histology was performed at either 10 or 21 days post-injury. Analysis of function revealed a transient impairment in locomotor ability, which corresponds to a mild TBI. Using reference region normalization, PET imaging revealed that mild LFP-induced TBI depresses glucose uptake in both the ipsilateral and contralateral hemispheres in comparison with sham-injured and naïve controls from 3 h to 5 days post-injury. Further, areas of depressed glucose uptake were associated with regions of glial activation and axonal damage, but no measurable change in neuronal loss or gross tissue damage was observed. In conclusion, we show that mild TBI, which is characterized by transient impairments in function, axonal damage, and glial activation, results in an observable depression in overall brain glucose uptake using (18)FDG-PET.

Traumatic Brain Injury: Persistent Misconceptions and Knowledge Gaps among Educators

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Ettel, Deborah; Glang, Ann E.; Todis, Bonnie; Davies, Susan C.

2016-01-01

Each year approximately 700,000 U.S. children aged 0-19 years sustain a traumatic brain injury (TBI) placing them at risk for academic, cognitive, and behavioural challenges. Although TBI has been a special education disability category for 25 years, prevalence studies show that of the 145,000 students each year who sustain long-term injury from…

Invisible Bleeding: The Command Team’s Role in the Identification, Understanding, and Treatment of Traumatic Brain Injury and Post Traumatic Stress Disorder

Science.gov (United States)

2013-04-11

Traumatic Brain Injury, Post Traumatic Stress Disorder , TBI, PTSD , Wounded...Brain Injury (TBI) and Post Traumatic Stress Disorder ( PTSD ). Command teams must leverage the existing programs and infrastructure while demonstrating a...subsequent struggle with Traumatic Brain Injury (TBI) and Post Traumatic Stress Disorder ( PTSD ) have given me the unique insight to tackle

Oxidative burst of circulating neutrophils following traumatic brain injury in human.

Directory of Open Access Journals (Sweden)

Yiliu Liao

Full Text Available Besides secondary injury at the lesional site, Traumatic brain injury (TBI can cause a systemic inflammatory response, which may cause damage to initially unaffected organs and potentially further exacerbate the original injury. Here we investigated plasma levels of important inflammatory mediators, oxidative activity of circulating leukocytes, particularly focusing on neutrophils, from TBI subjects and control subjects with general trauma from 6 hours to 2 weeks following injury, comparing with values from uninjured subjects. We observed increased plasma level of inflammatory cytokines/molecules TNF-α, IL-6 and CRP, dramatically increased circulating leukocyte counts and elevated expression of TNF-α and iNOS in circulating leukocytes from TBI patients, which suggests a systemic inflammatory response following TBI. Our data further showed increased free radical production in leukocyte homogenates and elevated expression of key oxidative enzymes iNOS, COX-2 and NADPH oxidase (gp91(phox in circulating leukocytes, indicating an intense induction of oxidative burst following TBI, which is significantly greater than that in control subjects with general trauma. Furthermore, flow cytometry assay proved neutrophils as the largest population in circulation after TBI and showed significantly up-regulated oxidative activity and suppressed phagocytosis rate for circulating neutrophils following brain trauma. It suggests that the highly activated neutrophils might play an important role in the secondary damage, even outside the injured brain. Taken together, the potent systemic inflammatory response induced by TBI, especially the intensively increase oxidative activity of circulating leukocytes, mainly neutrophils, may lead to a systemic damage, dysfunction/damage of bystander tissues/organs and even further exacerbate secondary local damage. Controlling these pathophysiological processes may be a promising therapeutic strategy and will protect unaffected

Impact of Posttraumatic Stress Disorder and Injury Severity on Recovery in Children with Traumatic Brain Injury

Science.gov (United States)

Kenardy, Justin; Le Brocque, Robyne; Hendrikz, Joan; Iselin, Greg; Anderson, Vicki; McKinlay, Lynne

2012-01-01

The adverse impact on recovery of posttraumatic stress disorder (PTSD) in mild traumatic brain injury (TBI) has been demonstrated in returned veterans. The study assessed this effect in children's health outcomes following TBI and extended previous work by including a full range of TBI severity, and improved assessment of PTSD within a…

Neuroprotective effect of hyperbaric oxygen therapy in a juvenile rat model of repetitive mild traumatic brain injury

Directory of Open Access Journals (Sweden)

Lei Huang

2016-01-01

Full Text Available Repetitive mild traumatic brain injury (rmTBI is an important medical concern for adolescent athletes that can lead to long-term disabilities. Multiple mild injuries may exacerbate tissue damage resulting in cumulative brain injury and poor functional recovery. In the present study, we investigated the increased brain vulnerability to rmTBI and the effect of hyperbaric oxygen treatment using a juvenile rat model of rmTBI. Two episodes of mild cortical controlled impact (3 days apart were induced in juvenile rats. Hyperbaric oxygen (HBO was applied 1 hour/day × 3 days at 2 atmosphere absolute consecutively, starting at 1 day after initial mild traumatic brain injury (mTBI. Neuropathology was assessed by multi-modal magnetic resonance imaging (MRI and tissue immunohistochemistry. After repetitive mTBI, there were increases in T2-weighted imaging-defined cortical lesions and susceptibility weighted imaging-defined cortical microhemorrhages, correlated with brain tissue gliosis at the site of impact. HBO treatment significantly decreased the MRI-identified abnormalities and tissue histopathology. Our findings suggest that HBO treatment improves the cumulative tissue damage in juvenile brain following rmTBI. Such therapy regimens could be considered in adolescent athletes at the risk of repeated concussions exposures.

Molecular mechanisms of cognitive dysfunction following traumatic brain injury

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Walker, Kendall R.; Tesco, Giuseppina

2013-01-01

Traumatic brain injury (TBI) results in significant disability due to cognitive deficits particularly in attention, learning and memory, and higher-order executive functions. The role of TBI in chronic neurodegeneration and the development of neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic Lateral Sclerosis (ALS) and most recently chronic traumatic encephalopathy (CTE) is of particular importance. However, despite significant effort very few therapeutic options exist to prevent or reverse cognitive impairment following TBI. In this review, we present experimental evidence of the known secondary injury mechanisms which contribute to neuronal cell loss, axonal injury, and synaptic dysfunction and hence cognitive impairment both acutely and chronically following TBI. In particular we focus on the mechanisms linking TBI to the development of two forms of dementia: AD and CTE. We provide evidence of potential molecular mechanisms involved in modulating Aβ and Tau following TBI and provide evidence of the role of these mechanisms in AD pathology. Additionally we propose a mechanism by which Aβ generated as a direct result of TBI is capable of exacerbating secondary injury mechanisms thereby establishing a neurotoxic cascade that leads to chronic neurodegeneration. PMID:23847533

Molecular mechanisms of cognitive dysfunction following traumatic brain injury.

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Walker, Kendall R; Tesco, Giuseppina

2013-01-01

Traumatic brain injury (TBI) results in significant disability due to cognitive deficits particularly in attention, learning and memory, and higher-order executive functions. The role of TBI in chronic neurodegeneration and the development of neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic Lateral Sclerosis (ALS) and most recently chronic traumatic encephalopathy (CTE) is of particular importance. However, despite significant effort very few therapeutic options exist to prevent or reverse cognitive impairment following TBI. In this review, we present experimental evidence of the known secondary injury mechanisms which contribute to neuronal cell loss, axonal injury, and synaptic dysfunction and hence cognitive impairment both acutely and chronically following TBI. In particular we focus on the mechanisms linking TBI to the development of two forms of dementia: AD and CTE. We provide evidence of potential molecular mechanisms involved in modulating Aβ and Tau following TBI and provide evidence of the role of these mechanisms in AD pathology. Additionally we propose a mechanism by which Aβ generated as a direct result of TBI is capable of exacerbating secondary injury mechanisms thereby establishing a neurotoxic cascade that leads to chronic neurodegeneration.

Patients with the most severe traumatic brain injury benefit from rehabilitation

DEFF Research Database (Denmark)

Poulsen, Ingrid; Norup, Anne; Liebach, Annette

2014-01-01

Patients with the most severe traumatic brain injury benefit from rehabilitation Ingrid Poulsen, Anne Norup, Annette Liebach, Lars Westergaard, Karin Spangsberg Kristensen, Tina Haren, & Lars Peter Kammersgaard Department for Neurorehabilitation, TBI Unit, Copenhagen University, Glostrup Hospital......., Hvidovre, Denmark Objectives: During the last couple of years, studies have indicated that even patients with the most severe traumatic brain injuries (TBI) benefit from rehabilitation despite what initially appears to be dismal prognosis. In Denmark, all patients with severe TBI have had an opportunity......-acute inpatient rehabilitation during a 12-year period followed an intensive interdisciplinary rehabilitation programme. Severity of injury was defined by Glasgow Coma Scale (GCS) score on rehabilitation admission and duration of post-traumatic amnesia (PTA). Patients were routinely measured...

Neuropsychology of traumatic brain injury: An expert overview.

Science.gov (United States)

Azouvi, P; Arnould, A; Dromer, E; Vallat-Azouvi, C

Traumatic brain injury (TBI) is a serious healthcare problem, and this report is a selective review of recent findings on the epidemiology, pathophysiology and neuropsychological impairments following TBI. Patients who survive moderate-to-severe TBI frequently suffer from a wide range of cognitive deficits and behavioral changes due to diffuse axonal injury. These deficits include slowed information-processing and impaired long-term memory, attention, working memory, executive function, social cognition and self-awareness. Mental fatigue is frequently also associated and can exacerbate the consequences of neuropsychological deficits. Personality and behavioral changes can include combinations of impulsivity and apathy. Even mild TBI raises specific problems: while most patients recover within a few weeks or months, a minority of patients may suffer from long-lasting symptoms (post-concussion syndrome). The pathophysiology of such persistent problems remains a subject of debate, but seems to be due to both injury-related and non-injury-related factors. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury

OpenAIRE

Loane, David J; Pocivavsek, Ana; Moussa, Charbel E-H; Thompson, Rachel; Matsuoka, Yasuji; Faden, Alan I; Rebeck, G William; Burns, Mark P

2009-01-01

Amyloid-β (Aβ) peptides, found in Alzheimer’s disease brain, accumulate rapidly after traumatic brain injury (TBI) in both humans and animals. Here we show that blocking either β- or γ-secretase, enzymes required for production of Aβ from amyloid precursor protein (APP), can ameliorate motor and cognitive deficits and reduce cell loss after experimental TBI in mice. Thus, APP secretases are promising targets for treatment of TBI.

Recent neuroimaging techniques in mild traumatic brain injury.

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Belanger, Heather G; Vanderploeg, Rodney D; Curtiss, Glenn; Warden, Deborah L

2007-01-01

Mild traumatic brain injury (TBI) is characterized by acute physiological changes that result in at least some acute cognitive difficulties and typically resolve by 3 months postinjury. Because the majority of mild TBI patients have normal structural magnetic resonance imaging (MRI)/computed tomography (CT) scans, there is increasing attention directed at finding objective physiological correlates of persistent cognitive and neuropsychiatric symptoms through experimental neuroimaging techniques. The authors review studies utilizing these techniques in patients with mild TBI; these techniques may provide more sensitive assessment of structural and functional abnormalities following mild TBI. Particular promise is evident with fMRI, PET, and SPECT scanning, as demonstrated by associations between brain activation and clinical outcomes.

Current understanding of neuroinflammation after traumatic brain injury and cell-based therapeutic opportunities.

Science.gov (United States)

Xiong, Ye; Mahmood, Asim; Chopp, Michael

2018-04-24

Traumatic brain injury (TBI) remains a major cause of death and disability worldwide. Increasing evidence indicates that TBI is an important risk factor for neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. Despite improved supportive and rehabilitative care of TBI patients, unfortunately, all late phase clinical trials in TBI have yet to yield a safe and effective neuroprotective treatment. The disappointing clinical trials may be attributed to variability in treatment approaches and heterogeneity of the population of TBI patients as well as a race against time to prevent or reduce inexorable cell death. TBI is not just an acute event but a chronic disease. Among many mechanisms involved in secondary injury after TBI, emerging preclinical studies indicate that posttraumatic prolonged and progressive neuroinflammation is associated with neurodegeneration which may be treatable long after the initiating brain injury. This review provides an overview of recent understanding of neuroinflammation in TBI and preclinical cell-based therapies that target neuroinflammation and promote functional recovery after TBI. Copyright © 2018 Daping Hospital and the Research Institute of Surgery of the Third Military Medical University. Production and hosting by Elsevier B.V. All rights reserved.

Insomnia symptoms and behavioural health symptoms in veterans 1 year after traumatic brain injury.

Science.gov (United States)

Farrell-Carnahan, Leah; Barnett, Scott; Lamberty, Gregory; Hammond, Flora M; Kretzmer, Tracy S; Franke, Laura M; Geiss, Meghan; Howe, Laura; Nakase-Richardson, Risa

2015-01-01

Insomnia and behavioural health symptoms 1 year after traumatic brain injury (TBI) were examined in a clinical sample representative of veterans who received inpatient treatment for TBI-related issues within the Veterans Health Administration. This was a cross-sectional sub-study (n = 112) of the Polytrauma Rehabilitation Centres' traumatic brain injury model system programme. Prevalence estimates of insomnia, depression, general anxiety, nightmares, headache and substance use, stratified by injury severity, were derived. Univariate logistic regression was used to examine unadjusted effects for each behavioural health problem and insomnia by injury severity. Participants were primarily male, insomnia; those with mild TBI were significantly more likely to meet criteria (43%) than those with moderate/severe TBI (22%), χ(2)(1, n = 112) = 5.088, p ≤ 0.05. Univariable logistic regression analyses revealed depressive symptoms and general anxiety were significantly associated with insomnia symptoms after TBI of any severity. Headache and binge drinking were significantly inversely related to insomnia symptoms after moderate/severe TBI, but not MTBI. Veterans with history of TBI, of any severity, and current insomnia symptoms may be at increased risk for depression and anxiety 1 year after TBI.

Brain injury impairs working memory and prefrontal circuit function

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Colin James Smith

2015-11-01

Full Text Available More than 2.5 million Americans suffer a traumatic brain injury (TBI each year. Even mild to moderate traumatic brain injury causes long-lasting neurological effects. Despite its prevalence, no therapy currently exists to treat the underlying cause of cognitive impairment suffered by TBI patients. Following lateral fluid percussion injury (LFPI, the most widely used experimental model of TBI, we investigated alterations in working memory and excitatory/inhibitory synaptic balance in the prefrontal cortex. LFPI impaired working memory as assessed with a T-maze behavioral task. Field excitatory postsynaptic potentials recorded in the prefrontal cortex were reduced in slices derived from brain-injured mice. Spontaneous and miniature excitatory postsynaptic currents onto layer 2/3 neurons were more frequent in slices derived from LFPI mice while inhibitory currents onto layer 2/3 neurons were smaller after LFPI. Additionally, an increase in action potential threshold and concomitant decrease in firing rate was observed in layer 2/3 neurons in slices from injured animals. Conversely, no differences in excitatory or inhibitory synaptic transmission onto layer 5 neurons were observed; however, layer 5 neurons demonstrated a decrease in input resistance and action potential duration after LFPI. These results demonstrate synaptic and intrinsic alterations in prefrontal circuitry that may underlie working memory impairment caused by TBI.

Insomnia in workers with delayed recovery from mild traumatic brain injury

DEFF Research Database (Denmark)

Mollayeva, Tatyana; Mollayeva, Shirin; Shapiro, Colin M

2016-01-01

Objective/Background/Aim Insomnia has not been explored as it relates to recovery after mild traumatic brain injury (mTBI). We aimed to evaluate the prevalence of insomnia among Ontario workers with delayed recovery from mTBI, and its relationship with sociodemographic, TBI- and claim-related, be...

Estrone is neuroprotective in rats after traumatic brain injury.

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Gatson, Joshua W; Liu, Ming-Mei; Abdelfattah, Kareem; Wigginton, Jane G; Smith, Scott; Wolf, Steven; Simpkins, James W; Minei, Joseph P

2012-08-10

In various animal and human studies, early administration of 17β-estradiol, a strong antioxidant, anti-inflammatory, and anti-apoptotic agent, significantly decreases the severity of injury in the brain associated with cell death. Estrone, the predominant estrogen in postmenopausal women, has been shown to be a promising neuroprotective agent. The overall goal of this project was to determine if estrone mitigates secondary injury following traumatic brain injury (TBI) in rats. Male rats were given either placebo (corn oil) or estrone (0.5 mg/kg) at 30 min after severe TBI. Using a controlled cortical impact device in rats that underwent a craniotomy, the right parietal cortex was injured using the impactor tip. Non-injured control and sham animals were also included. At 72 h following injury, the animals were perfused intracardially with 0.9% saline followed by 10% phosphate-buffered formalin. The whole brain was removed, sliced, and stained for TUNEL-positive cells. Estrone decreased cortical lesion volume (pcerebral cortical levels of TUNEL-positive staining (pprotective pathways such as the ERK1/2 and BDNF pathways, decreases ischemic secondary injury, and decreases apoptotic-mediated cell death. These results suggest that estrone may afford protection to those suffering from TBI.

Changes in brain-behavior relationships following a 3-month pilot cognitive intervention program for adults with traumatic brain injury

Directory of Open Access Journals (Sweden)

S. Porter

2017-08-01

Full Text Available Facilitating functional recovery following brain injury is a key goal of neurorehabilitation. Direct, objective measures of changes in the brain are critical to understanding how and when meaningful changes occur, however, assessing neuroplasticity using brain based results remains a significant challenge. Little is known about the underlying changes in functional brain networks that correlate with cognitive outcomes in traumatic brain injury (TBI. The purpose of this pilot study was to assess the feasibility of an intensive three month cognitive intervention program in individuals with chronic TBI and to evaluate the effects of this intervention on brain-behavioral relationships. We used tools from graph theory to evaluate changes in global and local brain network features prior to and following cognitive intervention. Network metrics were calculated from resting state electroencephalographic (EEG recordings from 10 adult participants with mild to severe brain injury and 11 age and gender matched healthy controls. Local graph metrics showed hyper-connectivity in the right inferior frontal gyrus and hypo-connectivity in the left inferior frontal gyrus in the TBI group at baseline in comparison with the control group. Following the intervention, there was a statistically significant increase in the composite cognitive score in the TBI participants and a statistically significant decrease in functional connectivity in the right inferior frontal gyrus. In addition, there was evidence of changes in the brain-behavior relationships following intervention. The results from this pilot study provide preliminary evidence for functional network reorganization that parallels cognitive improvements after cognitive rehabilitation in individuals with chronic TBI.

Changes in brain-behavior relationships following a 3-month pilot cognitive intervention program for adults with traumatic brain injury.

Science.gov (United States)

Porter, S; Torres, I J; Panenka, W; Rajwani, Z; Fawcett, D; Hyder, A; Virji-Babul, N

2017-08-01

Facilitating functional recovery following brain injury is a key goal of neurorehabilitation. Direct, objective measures of changes in the brain are critical to understanding how and when meaningful changes occur, however, assessing neuroplasticity using brain based results remains a significant challenge. Little is known about the underlying changes in functional brain networks that correlate with cognitive outcomes in traumatic brain injury (TBI). The purpose of this pilot study was to assess the feasibility of an intensive three month cognitive intervention program in individuals with chronic TBI and to evaluate the effects of this intervention on brain-behavioral relationships. We used tools from graph theory to evaluate changes in global and local brain network features prior to and following cognitive intervention. Network metrics were calculated from resting state electroencephalographic (EEG) recordings from 10 adult participants with mild to severe brain injury and 11 age and gender matched healthy controls. Local graph metrics showed hyper-connectivity in the right inferior frontal gyrus and hypo-connectivity in the left inferior frontal gyrus in the TBI group at baseline in comparison with the control group. Following the intervention, there was a statistically significant increase in the composite cognitive score in the TBI participants and a statistically significant decrease in functional connectivity in the right inferior frontal gyrus. In addition, there was evidence of changes in the brain-behavior relationships following intervention. The results from this pilot study provide preliminary evidence for functional network reorganization that parallels cognitive improvements after cognitive rehabilitation in individuals with chronic TBI.

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…

Immediate, but Not Delayed, Microsurgical Skull Reconstruction Exacerbates Brain Damage in Experimental Traumatic Brain Injury Model

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Lau, Tsz; Kaneko, Yuji; van Loveren, Harry; Borlongan, Cesario V.

2012-01-01

Moderate to severe traumatic brain injury (TBI) often results in malformations to the skull. Aesthetic surgical maneuvers may offer normalized skull structure, but inconsistent surgical closure of the skull area accompanies TBI. We examined whether wound closure by replacement of skull flap and bone wax would allow aesthetic reconstruction of the TBI-induced skull damage without causing any detrimental effects to the cortical tissue. Adult male Sprague-Dawley rats were subjected to TBI using the controlled cortical impact (CCI) injury model. Immediately after the TBI surgery, animals were randomly assigned to skull flap replacement with or without bone wax or no bone reconstruction, then were euthanized at five days post-TBI for pathological analyses. The skull reconstruction provided normalized gross bone architecture, but 2,3,5-triphenyltetrazolium chloride and hematoxylin and eosin staining results revealed larger cortical damage in these animals compared to those that underwent no surgical maneuver at all. Brain swelling accompanied TBI, especially the severe model, that could have relieved the intracranial pressure in those animals with no skull reconstruction. In contrast, the immediate skull reconstruction produced an upregulation of the edema marker aquaporin-4 staining, which likely prevented the therapeutic benefits of brain swelling and resulted in larger cortical infarcts. Interestingly, TBI animals introduced to a delay in skull reconstruction (i.e., 2 days post-TBI) showed significantly reduced edema and infarcts compared to those exposed to immediate skull reconstruction. That immediate, but not delayed, skull reconstruction may exacerbate TBI-induced cortical tissue damage warrants a careful consideration of aesthetic repair of the skull in TBI. PMID:22438975

Current status of fluid biomarkers in mild traumatic brain injury

Science.gov (United States)

Kulbe, Jacqueline R.; Geddes, James W.

2015-01-01

Mild traumatic brain injury (mTBI) affects millions of people annually and is difficult to diagnose. Mild injury is insensitive to conventional imaging techniques and diagnoses are often made using subjective criteria such as self-reported symptoms. Many people who sustain a mTBI develop persistent post-concussive symptoms. Athletes and military personnel are at great risk for repeat injury which can result in second impact syndrome or chronic traumatic encephalopathy. An objective and quantifiable measure, such as a serum biomarker, is needed to aid in mTBI diagnosis, prognosis, return to play/duty assessments, and would further elucidate mTBI pathophysiology. The majority of TBI biomarker research focuses on severe TBI with few studies specific to mild injury. Most studies use a hypothesis-driven approach, screening biofluids for markers known to be associated with TBI pathophysiology. This approach has yielded limited success in identifying markers that can be used clinically, additional candidate biomarkers are needed. Innovative and unbiased methods such as proteomics, microRNA arrays, urinary screens, autoantibody identification and phage display would complement more traditional approaches to aid in the discovery of novel mTBI biomarkers. PMID:25981889

Making waves in the brain: What are oscillations, and why modulating them makes sense for brain injury

Directory of Open Access Journals (Sweden)

Aleksandr ePevzner

2016-04-01

Full Text Available Traumatic brain injury (TBI can result in persistent cognitive, behavioral and emotional deficits. However, the vast majority of patients are not chronically hospitalized; rather they have to manage their disabilities once they are discharged to home. Promoting recovery to pre-injury level is important from a patient care as well as a societal perspective. Electrical neuromodulation is one approach that has shown promise in alleviating symptoms associated with neurological disorders such as in Parkinson’s disease and epilepsy. Consistent with this perspective, both animal and clinical studies have revealed that TBI alters physiological oscillatory rhythms. More recently several studies demonstrated that low frequency stimulation improves cognitive outcome in models of TBI. Specifically, stimulation of the septohippocampal circuit in the theta frequency entrained oscillations and improved spatial learning following traumatic brain injury. In order to evaluate the potential of electrical deep brain stimulation for clinical translation we review the basic neurophysiology of oscillations, their role in cognition and how they are changed post-TBI. Furthermore, we highlight several factors for future pre-clinical and clinical studies to consider, with the hope that it will promote a hypothesis driven approach to subsequent experimental designs and ultimately successful translation to improve outcome in patients with TBI.

ECONOMIC LOSSES CAUSED BY TRAUMATIC BRAIN INJURY IN CHILDREN

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S. A. Valiulina

2015-01-01

Full Text Available Background: Currently, analyzing the economic losses caused by health problems in population is of particular importance since it stipulates calculations of the volumes invested in healthcare systems in order to improve population’s health. Objective: The aim of our study was to find out economic losses caused by traumatic brain injury (TBI in children. Methods: The given work has utilized governmental statistical reports for Russia, for federal regions as well as for individual subjects. Direct medical expenses (medical services and indirect expenses (losses due to a temporary disability of parents having a sick child were calculated both in general and per patient. Results: Among all the direct medical costs of treatment of children with TBI inpatient care costs account for 85%. In the Central and Volga Federal District accounted for half of nationwide spending in general, brain injury and to provide certain kinds of healthcare. The structure of Russian costs as a result of the incidence of TBI children Moscow accounts for 20%. In Moscow, the cost of treating cases of traumatic brain injury in children is 3.2 times higher than the average for Russia. The resulting calculations of the value of health care costs attributable to a case of child head injury, behind the cost of treatment of the case of a child with head trauma, calculated according to the standards of Russia and the territories. This difference in the whole RF is 23%. Conclusion: The obtained findings have shown that in 2010 in Russia the magnitude of losses caused by TBI incidence in children amounted to 3 billion roubles or 0.008% of the gross product 1.2 billion roubles of which were direct expenses. However, this figure is considerably lower of the real amount; it becomes evident after the analysis of direct medical expenses per one case of pediatric TBI. Our calculations have shown that in Russia and in its regions the amount of expenses per one TBI patient is a quarter less

Efficacy of legal judgments for defendants with traumatic brain injury.

Science.gov (United States)

St Pierre, Maria E; Parente, Rick

2016-06-23

Literature has compared the frequency of aggressive behaviors of the TBI population and the non-TBI population, suggesting that the TBI population is predisposed to aggressive tendencies because the injury enables impulsivity, loss of self-control, and the inability to modify behaviors. These behavior changes have consequently, been found to lead to criminal involvement. In fact, the majority of the prison population has sustained at least one TBI in their lifetime compared to the prevalence of brain injuries in the general population. However, there is little research investigating the perceptions of criminality and guilt of these individuals. Two experiments were conducted that investigated the perceptions of morality, level of guilt, and appropriate sentencing of crimes committed by defendants with different severities of TBI (i.e., mild, severe, and no TBI). Participants were asked to read scenarios about crimes being committed by the defendant. Experiment 1 used a 1-between (crime), 1-within (TBI) mixed design ANOVA testing three dependent variables (morality, guilt, and sentencing). Using a more in vivo jury approach, Experiment 2 used a 3 (TBI)×2 (crime) independent groups factorial design testing the three dependent measures. Overall, defendants with TBI were found less guilty of their crime, perceived as behaving morally to the crime, and receiving a milder punishment relative to the no-TBI defendants. In the courtroom, the defense attorney should educate the judge and/or the jury on the effects brain injuries have on the cognition, behavior, and emotions of an individual. Thus, this education will ensure the best verdict is being reached.

An update on substance use and treatment following traumatic brain injury.

Science.gov (United States)

Graham, David P; Cardon, Aaron L

2008-10-01

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity among young adults. Substance abusers constitute a disproportionate percentage of these patients. A history of substance abuse predicts increased disability, poorer prognosis, and delayed recovery. While consensus in the literature indicates that substance-abuse rates decline following injury, conflicting literature shows a significant history of brain injury in addicts. We reviewed the literature on substance abuse after TBI to explore the state of knowledge on TBI as a risk factor for substance abuse. While recent reviews regarding substance abuse in TBI patients concur that substance-abuse rates decline even after mild TBI, an emerging literature suggests mild TBI may cause subtle impairments in cognitive, executive, and decision-making functions that are often poorly recognized in early diagnosis and treatment. When combined with difficulties in psychosocial adjustment and coping skills, these impairments may increase the risk for chronic substance abuse in a subset of TBI patients. Preliminary results from veterans indicate these patterns hold in a combat-related post-traumatic stress disorder population with TBI. This increasingly prevalent combination presents a specific challenge in rehabilitation. While this comorbidity presents a challenge for the successful treatment and rehabilitation of both disorders, there is sparse evidence to recommend any specific treatment strategy for these individuals. Mild TBI and substance abuse are bidirectionally related both for risks and treatment. Further understanding the neuropsychiatric pathology and different effects of different types of injuries will likely improve the implementation of effective treatments for each of these two conditions.

Estrogen provides neuroprotection against brain edema and blood brain barrier disruption through both estrogen receptors α and β following traumatic brain injury

Directory of Open Access Journals (Sweden)

Vida Naderi

2015-02-01

Full Text Available Objective(s:Estrogen (E2 has neuroprotective effects on blood-brain-barrier (BBB after traumatic brain injury (TBI. In order to investigate the roles of estrogen receptors (ERs in these effects, ER-α antagonist (MPP and, ER-β antagonist (PHTPP, or non-selective estrogen receptors antagonist (ICI 182780 were administered. Materials and Methods: Ovariectomized rats were divided into 10 groups, as follows: Sham, TBI, E2, oil, MPP+E2, PHTPP+E2, MPP+PHTPP+E2, ICI+E2, MPP, and DMSO. E2 (33.3 µg/Kg or oil were administered 30 min after TBI. 1 dose (150 µg/Kg of each of MPP, PHTPP, and (4 mg/kg ICI182780 was injected two times, 24 hr apart, before TBI and estrogen treatment. BBB disruption (Evans blue content and brain edema (brain water content evaluated 5 hr and 24 hr after the TBI were evaluated, respectively. Results: The results showed that E2 reduced brain edema after TBI compared to vehicle (P

Experimental Traumatic Brain Injury Induces Bone Loss in Rats.

Science.gov (United States)

Brady, Rhys D; Shultz, Sandy R; Sun, Mujun; Romano, Tania; van der Poel, Chris; Wright, David K; Wark, John D; O'Brien, Terence J; Grills, Brian L; McDonald, Stuart J

2016-12-01

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

A review of the International Brain Research Foundation novel approach to mild traumatic brain injury presented at the International Conference on Behavioral Health and Traumatic Brain Injury.

Science.gov (United States)

Polito, Mary Zemyan; Thompson, James W G; DeFina, Philip A

2010-09-01

"The International Conference on Behavioral Health and Traumatic Brain Injury" held at St. Joseph's Regional Medical Center in Paterson, NJ., from October 12 to 15, 2008, included a presentation on the novel assessment and treatment approach to mild traumatic brain injury (mTBI) by Philip A. DeFina, PhD, of the International Brain Research Foundation (IBRF). Because of the urgent need to treat a large number of our troops who are diagnosed with mTBI and post-traumatic stress disorder (PTSD), the conference was held to create a report for Congress titled "Recommendations to Improve the Care of Wounded Warriors NOW. March 12, 2009." This article summarizes and adds greater detail to Dr. DeFina's presentation on the current standard and novel ways to approach assessment and treatment of mTBI and PTSD. Pilot data derived from collaborative studies through the IBRF have led to the development of clinical and research protocols utilizing currently accepted, valid, and reliable neuroimaging technologies combined in novel ways to develop "neuromarkers." These neuromarkers are being evaluated in the context of an "Integrity-Deficit Matrix" model to demonstrate their ability to improve diagnostic accuracy, guide treatment programs, and possibly predict outcomes for patients suffering from traumatic brain injury.

Viewing the functional consequences of traumatic brain injury by using brain SPECT.

Science.gov (United States)

Pavel, D; Jobe, T; Devore-Best, S; Davis, G; Epstein, P; Sinha, S; Kohn, R; Craita, I; Liu, P; Chang, Y

2006-03-01

High-resolution brain SPECT is increasingly benefiting from improved image processing software and multiple complementary display capabilities. This enables detailed functional mapping of the disturbances in relative perfusion occurring after TBI. The patient population consisted of 26 cases (ages 8-61 years)between 3 months and 6 years after traumatic brain injury.A very strong case can be made for the routine use of Brain SPECT in TBI. Indeed it can provide a detailed evaluation of multiple functional consequences after TBI and is thus capable of supplementing the clinical evaluation and tailoring the therapeutic strategies needed. In so doing it also provides significant additional information beyond that available from MRI/CT. The critical factor for Brain SPECT's clinical relevance is a carefully designed technical protocol, including displays which should enable a comprehensive description of the patterns found, in a user friendly mode.

Preventing Older Adult Falls and TBI

Centers for Disease Control (CDC) Podcasts

2008-03-05

This podcast provides tips on how older adults can prevent falls and related injuries, such as traumatic brain injuries (TBI).  Created: 3/5/2008 by National Center for Injury Prevention and Control (NCIPC).   Date Released: 3/7/2008.

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.

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

DEFF Research Database (Denmark)

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

2013-01-01

Combination of traumatic brain injury (TBI) and hemorrhagic shock (HS) can result in significant morbidity and mortality. We have previously shown that early administration of fresh frozen plasma (FFP) in a large animal model of TBI and HS reduces the size of the brain lesion as well as the assoc...... as the associated edema. However, FFP is a perishable product that is not well suited for use in the austere prehospital settings. In this study, we tested whether a shelf-stable, low-volume, lyophilized plasma (LSP) product was as effective as FFP.......Combination of traumatic brain injury (TBI) and hemorrhagic shock (HS) can result in significant morbidity and mortality. We have previously shown that early administration of fresh frozen plasma (FFP) in a large animal model of TBI and HS reduces the size of the brain lesion as well...

Neuroinflammatory responses to traumatic brain injury: etiology, clinical consequences, and therapeutic opportunities

Directory of Open Access Journals (Sweden)

Lozano D

2015-01-01

Full Text Available Diego Lozano,* Gabriel S Gonzales-Portillo,* Sandra Acosta, Ike de la Pena, Naoki Tajiri, Yuji Kaneko, Cesar V Borlongan Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA *These authors contributed equally to this work Abstract: Traumatic brain injury (TBI is a serious public health problem accounting for 1.4 million emergency room visits by US citizens each year. Although TBI has been traditionally considered an acute injury, chronic symptoms reminiscent of neurodegenerative disorders have now been recognized. These progressive neurodegenerative-like symptoms manifest as impaired motor and cognitive skills, as well as stress, anxiety, and mood affective behavioral alterations. TBI, characterized by external bumps or blows to the head exceeding the brain’s protective capacity, causes physical damage to the central nervous system with accompanying neurological dysfunctions. The primary impact results in direct neural cell loss predominantly exhibiting necrotic death, which is then followed by a wave of secondary injury cascades including excitotoxicity, oxidative stress, mitochondrial dysfunction, blood–brain barrier disruption, and inflammation. All these processes exacerbate the damage, worsen the clinical outcomes, and persist as an evolving pathological hallmark of what we now describe as chronic TBI. Neuroinflammation in the acute stage of TBI mobilizes immune cells, astrocytes, cytokines, and chemokines toward the site of injury to mount an antiinflammatory response against brain damage; however, in the chronic stage, excess activation of these inflammatory elements contributes to an “inflamed” brain microenvironment that principally contributes to secondary cell death in TBI. Modulating these inflammatory cells by changing their phenotype from proinflammatory to antiinflammatory would likely promote therapeutic effects on TBI. Because neuroinflammation occurs at

Neuroinflammation, myelin and behavior: Temporal patterns following mild traumatic brain injury in mice.

Directory of Open Access Journals (Sweden)

Toufik Taib

Full Text Available Traumatic brain injury (TBI results in white matter injury (WMI that is associated with neurological deficits. Neuroinflammation originating from microglial activation may participate in WMI and associated disorders. To date, there is little information on the time courses of these events after mild TBI. Therefore we investigated (i neuroinflammation, (ii WMI and (iii behavioral disorders between 6 hours and 3 months after mild TBI. For that purpose, we used experimental mild TBI in mice induced by a controlled cortical impact. (i For neuroinflammation, IL-1b protein as well as microglial phenotypes, by gene expression for 12 microglial activation markers on isolated CD11b+ cells from brains, were studied after TBI. IL-1b protein was increased at 6 hours and 1 day. TBI induced a mixed population of microglial phenotypes with both pro-inflammatory, anti-inflammatory and immunomodulatory markers from 6 hours to 3 days post-injury. At 7 days, microglial activation was completely resolved. (ii Three myelin proteins were assessed after TBI on ipsi- and contralateral corpus callosum, as this structure is enriched in white matter. TBI led to an increase in 2',3'-cyclic-nucleotide 3'-phosphodiesterase, a marker of immature and mature oligodendrocyte, at 2 days post-injury; a bilateral demyelination, evaluated by myelin basic protein, from 7 days to 3 months post-injury; and an increase in myelin oligodendrocyte glycoprotein at 6 hours and 3 days post-injury. Transmission electron microscopy study revealed various myelin sheath abnormalities within the corpus callosum at 3 months post-TBI. (iii TBI led to sensorimotor deficits at 3 days post-TBI, and late cognitive flexibility disorder evidenced by the reversal learning task of the Barnes maze 3 months after injury. These data give an overall invaluable overview of time course of neuroinflammation that could be involved in demyelination and late cognitive disorder over a time-scale of 3 months in a model

Pituitary dysfunction following traumatic brain injury: clinical perspectives

Science.gov (United States)

Tanriverdi, Fatih; Kelestimur, Fahrettin

2015-01-01

Traumatic brain injury (TBI) is a well recognized public health problem worldwide. TBI has previously been considered as a rare cause of hypopituitarism, but an increased prevalence of neuroendocrine dysfunction in patients with TBI has been reported during the last 15 years in most of the retrospective and prospective studies. Based on data in the current literature, approximately 15%–20% of TBI patients develop chronic hypopituitarism, which clearly suggests that TBI-induced hypopituitarism is frequent in contrast with previous assumptions. This review summarizes the current data on TBI-induced hypopituitarism and briefly discusses some clinical perspectives on post-traumatic anterior pituitary hormone deficiency. PMID:26251600

Ccr2 deletion dissociates cavity size and tau pathology after mild traumatic brain injury.

Science.gov (United States)

Gyoneva, Stefka; Kim, Daniel; Katsumoto, Atsuko; Kokiko-Cochran, O Nicole; Lamb, Bruce T; Ransohoff, Richard M

2015-12-03

Millions of people experience traumatic brain injury (TBI) as a result of falls, car accidents, sports injury, and blast. TBI has been associated with the development of neurodegenerative conditions such as Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE). In the initial hours and days, the pathology of TBI comprises neuronal injury, breakdown of the blood-brain barrier, and inflammation. At the cellular level, the inflammatory reaction consists of responses by brain-resident microglia, astrocytes, and vascular elements as well as infiltration of peripheral cells. After TBI, signaling by chemokine (C-C motif) ligand 2 (CCL2) to the chemokine (C-C motif) receptor 2 (CCR2) is a key regulator of brain infiltration by monocytes. We utilized mice with one or both copies of Ccr2 disrupted by red fluorescent protein (RFP, Ccr2 (RFP/+) and Ccr2 (RFP/RFP) ). We subjected these mice to the mild lateral fluid percussion model of TBI and examined several pathological outcomes 3 days later in order to determine the effects of altered monocyte entry into the brain. Ccr2 deletion reduced monocyte infiltration, diminished lesion cavity volume, and lessened axonal damage after mild TBI, but the microglial reaction to the lesion was not affected. We further examined phosphorylation of the microtubule-associated protein tau, which aggregates in brains of people with TBI, AD, and CTE. Surprisingly, Ccr2 deletion was associated with increased tau mislocalization to the cell body in the cortex and hippocampus by tissue staining and increased levels of phosphorylated tau in the hippocampus by Western blot. Disruption of CCR2 enhanced tau pathology and reduced cavity volume in the context of TBI. The data reveal a complex role for CCR2(+) monocytes in TBI, as monitored by cavity volume, axonal damage, and tau phosphorylation.

Outcome and comparative effectiveness research in traumatic brain injury : a methodological perspective

NARCIS (Netherlands)

M.C. Cnossen (Maryse)

2017-01-01

markdownabstractTraumatic brain injury (TBI) is one of the leading causes of death and disability worldwide. Although research activity in TBI has expanded rapidly, all these endeavors have not yet resulted in major advances in our understanding of TBI. This thesis addresses two important topics

Dietary Docosahexaenoic Acid Improves Cognitive Function, Tissue Sparing, and Magnetic Resonance Imaging Indices of Edema and White Matter Injury in the Immature Rat after Traumatic Brain Injury

OpenAIRE

Schober, Michelle E.; Requena, Daniela F.; Abdullah, Osama M.; Casper, T. Charles; Beachy, Joanna; Malleske, Daniel; Pauly, James R.

2016-01-01

Traumatic brain injury (TBI) is the leading cause of acquired neurologic disability in children. Specific therapies to treat acute TBI are lacking. Cognitive impairment from TBI may be blunted by decreasing inflammation and oxidative damage after injury. Docosahexaenoic acid (DHA) decreases cognitive impairment, oxidative stress, and white matter injury in adult rats after TBI. Effects of DHA on cognitive outcome, oxidative stress, and white matter injury in the developing rat after experimen...

Omega-3 Fatty Acids Could Alleviate the Risks of Traumatic Brain Injury – A Mini Review

Directory of Open Access Journals (Sweden)

Parvathy R. Kumar

2014-04-01

Full Text Available Traumatic brain injury (TBI is an acquired brain trauma that occurs when any sudden trauma/injury causes damage to the brain. TBI is characterized by tissue damage and imbalance in the cerebral blood flow and metabolism. It has been established through laboratory experiments that the dietary supplementation of omega-3 fatty acids (FAs could reduce the oxidative stress developed in brain due to TBI. The inclusion of omega-3 FA in diet could normalize the levels of brain-derived neurotrophic factor (BDNF, and thus, it could restore the survival of neuronal cells. BDNF improves the synaptic transmission by regulating synapsin 1 and cyclic adenosine monophosphate (cAMP response element binding protein. The brain tissue analysis of TBI models supplemented with omega-3 polyunsaturated fatty acids (PUFAs showed significantly reduced lipid peroxidation, nucleic acid and protein oxidation, thereby promoting neuronal and glial cell survival. Thus, omega-3 FA intake could be considered as a therapeutic option to reduce the secondary neuronal damages initiated by TBI.

Inter-Subject Variability of Axonal Injury in Diffuse Traumatic Brain Injury.

Science.gov (United States)

Ware, Jeffrey B; Hart, Tessa; Whyte, John; Rabinowitz, Amanda; Detre, John A; Kim, Junghoon

2017-07-15

Traumatic brain injury (TBI) is a leading cause of cognitive morbidity worldwide for which reliable biomarkers are needed. Diffusion tensor imaging (DTI) is a promising biomarker of traumatic axonal injury (TAI); however, existing studies have been limited by a primary reliance on group-level analytic methods not well suited to account for inter-subject variability. In this study, 42 adults with TBI of at least moderate severity were examined 3 months following injury and compared with 35 healthy controls. DTI data were used for both traditional group-level comparison and subject-specific analysis using the distribution-corrected Z-score (DisCo-Z) approach. Inter-subject variation in TAI was assessed in a threshold-invariant manner using a threshold-weighted overlap map derived from subject-specific analysis. Receiver operator curve analysis was used to examine the ability of subject-specific DTI analysis to identify TBI subjects with significantly impaired processing speed in comparison with region of interest-based fractional anisotropy (FA) measurements and clinical characteristics. Traditional group-wise analysis demonstrated widespread reductions of white matter FA within the TBI group (voxel-wise p traumatic deficits in processing speed. Significant group-level effects do not necessarily represent consistent effects at the individual level. Better accounting for inter-subject variability in neurobiological manifestations of TBI may substantially improve the ability to detect and classify patterns of injury.

Validating Multidimensional Outcome Assessment Using the TBI Common Data Elements: An Analysis of the TRACK-TBI Pilot Sample.

Science.gov (United States)

Nelson, Lindsay D; Ranson, Jana; Ferguson, Adam R; Giacino, Joseph; Okonkwo, David O; Valadka, Alex; Manley, Geoffrey; McCrea, Michael

2017-06-08

The Glasgow Outcome Scale-Extended (GOSE) is often the primary outcome measure in clinical trials for traumatic brain injury (TBI). Although the GOSE's capture of global function outcome has several strengths, concerns have been raised about its limited ability to identify mild disability and failure to capture the full scope of problems patients exhibit after TBI. This analysis examined the convergence of disability ratings across a multidimensional set of outcome domains in the Transforming Research and Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) Pilot study. The study collected measures recommended by the TBI Common Data Elements (CDE) Workgroup. Patients presenting to 3 emergency departments with a TBI of any severity enrolled in TRACK-TBI prospectively after injury; outcome measures were collected at 3 and six months postinjury. Analyses examined frequency of impairment and overlap between impairment status across the CDE outcome domains of Global Level of Functioning (GOSE), Neuropsychological (cognitive) Impairment, Psychological Status, TBI Symptoms, and Quality of Life. GOSE score correlated in the expected direction with other outcomes (M Spearman's rho = .21 and .49 with neurocognitive and self-report outcomes, respectively). The subsample in the Upper Good Recovery (GOSE 8) category appeared quite healthy across most other outcomes, although 19.0% had impaired executive functioning (Trail Making Test Part B). A significant minority of participants in the Lower Good Recovery subgroup (GOSE 7) met criteria for impairment across numerous other outcome measures. The findings highlight the multidimensional nature of TBI recovery and the limitations of applying only a single outcome measure.

Investigating nystagmus in patients with traumatic brain injury: A ...

African Journals Online (AJOL)

Background. Traumatic brain injury (TBI) is a health and socioeconomic concern worldwide. In patients with TBI, post-traumatic balance problems are often the result of damage to the vestibular system. Nystagmus is common in these patients, and can provide insight into the damage that has resulted from the trauma.

Effect of glycyrrhizin on traumatic brain injury in rats and its mechanism

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Gu Xiangjin

2014-02-01

Full Text Available 【Abstract】Objective: To investigate the neuroprotective effects of glycyrrhizin (Gly as well as its effect on expression of high-mobility group box 1 (HMGB1 in rats after traumatic brain injury (TBI. Methods: Male Sprague-Dawley rats were randomly divided into three groups: sham group, TBI group, and TBI+Gly group (n=36 per group. Rat TBI model was made by using the modified Feeney’s method. In TBI+Gly group, Gly was administered intravenously at a dosage of 10 mg/kg 30 min after TBI. At 24 h after TBI, motor function and brain water content were evaluated. Meanwhile, HMGB1/HMGB1 receptors including toll-like receptor 4 (TLR4 and receptor for advanced glycation end products (RAGE/nuclear factor- κB(NF- κB signaling pathway and inflammatory cytokines in the injured brain tissues were detected using quantitative real-time polymerase chain reaction, western blot, electrophoretic mobility shift assay and enzyme-linked immunosorbent assay. Furthermore, HMGB1, RAGE and TLR4 immunohistochemistry and apoptosis were analyzed. Results: Beam walking performance impairment and brain edema were significantly reduced in TBI+Gly group compared with TBI group; meanwhile, the over-expressions of HMGB1/HMGB1 receptors (TLR4 and RAGE/NF-κB DNA-binding activity and inflammatory cytokines were inhibited. The percentages of HMGB1, RAGE and TLR4- positive cells and apoptotic cells were respectively 58.37%±5.06%, 54.15%±4.65%, 65.50%± 4.83%, 52.02%± 4.63% in TBI group and 39.99%±4.99%, 34.87%±5.02%, 43.33%±4.54%, 37.84%±5.16% in TBI+Gly group (all P<0.01 compared with TBI group. Conclusion: Gly can reduce secondary brain injury and improve outcomes in rat following TBI by down-regulation of HMGB1/HMGB1 receptors (TLR4 and RAGE/NF-κB - mediated inflammatory responses in the injured rat brain.

Increased CD147 (EMMPRIN) expression in the rat brain following traumatic brain injury.

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Wei, Ming; Li, Hong; Shang, Yanguo; Zhou, Ziwei; Zhang, Jianning

2014-10-17

The extracellular matrix metalloproteinase inducer (EMMPRIN), or CD147, has been known to play a key regulatory role in vascular permeability and leukocyte activation by inducing the expression of matrix metalloproteinases (MMPs). The effects of traumatic brain injury on the expression of EMMPRIN remain poorly understood. In this study, we investigated changes in EMMPRIN expression in a rat model of fluid percussion injury (FPI) and examined the potential association between EMMPRIN and MMP-9 expression. Adult male rats were subjected to FPI. EMMPRIN expression was markedly up-regulated in the brain tissue surrounding the injured region 6-48 h after TBI, as measured by immunoblot and immunohistochemistry. EMMPRIN expression was localized to inflammatory cells. The increase in EMMPRIN expression was temporally correlated with an increase in MMP-9 levels. These data demonstrate, for the first time, changes in CD147 and MMP-9 expression following TBI. These data also suggest that CD147 and MMP-9 may play a role in vascular injuries after TBI. Copyright © 2014 Elsevier B.V. All rights reserved.

Melatonin Secretion Is Increased in Children with Severe Traumatic Brain Injury.

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Marseglia, Lucia; D'Angelo, Gabriella; Manti, Sara; Rulli, Immacolata; Salvo, Vincenzo; Buonocore, Giuseppe; Reiter, Russel J; Gitto, Eloisa

2017-05-13

Traumatic brain injury (TBI) is a leading cause of death and disability in children. Oxidative stress plays a significant role in brain damage and melatonin exhibits both direct and indirect antioxidant effects. The primary aim of the present study was to evaluate serum melatonin levels in children with severe TBI in comparison to critically ill children admitted to the Pediatric Intensive Care Unit for conditions other than TBI. Twenty-four children were evaluated, equally divided into severe TBI and no-TBI. Blood samples for serum melatonin analysis were collected at 22:00, 01:00, 03:00, 05:00, 08:00, and 12:00. Mean serum melatonin peaks in children of the TBI group were higher compared to the values of no-TBI critically ill children (495 ± 102 vs. 294 ± 119 pg/mL, p = 0.0002). Furthermore, the difference was even more significant in comparison to values reported in literature for healthy age-matched children (495 ± 102 vs. 197 ± 71 pg/mL, p melatonin levels dramatically increase in children after severe TBI. This elevation is likely to represent a response to oxidative stress and/or inflammation due to severe head injury.

Post-traumatic amnesia predicts intelligence impairment following traumatic brain injury: a meta-analysis

NARCIS (Netherlands)

Konigs, M.; de Kieviet, J.F.; Oosterlaan, J.

2012-01-01

Context: Worldwide, millions of patients with traumatic brain injury (TBI) suffer from persistent and disabling intelligence impairment. Post-traumatic amnesia (PTA) duration is a promising predictor of intelligence following TBI. Objectives: To determine (1) the impact of TBI on intelligence

Chronic traumatic encephalopathy-integration of canonical traumatic brain injury secondary injury mechanisms with tau pathology.

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Kulbe, Jacqueline R; Hall, Edward D

2017-11-01

In recent years, a new neurodegenerative tauopathy labeled Chronic Traumatic Encephalopathy (CTE), has been identified that is believed to be primarily a sequela of repeated mild traumatic brain injury (TBI), often referred to as concussion, that occurs in athletes participating in contact sports (e.g. boxing, American football, Australian football, rugby, soccer, ice hockey) or in military combatants, especially after blast-induced injuries. Since the identification of CTE, and its neuropathological finding of deposits of hyperphosphorylated tau protein, mechanistic attention has been on lumping the disorder together with various other non-traumatic neurodegenerative tauopathies. Indeed, brains from suspected CTE cases that have come to autopsy have been confirmed to have deposits of hyperphosphorylated tau in locations that make its anatomical distribution distinct for other tauopathies. The fact that these individuals experienced repetitive TBI episodes during their athletic or military careers suggests that the secondary injury mechanisms that have been extensively characterized in acute TBI preclinical models, and in TBI patients, including glutamate excitotoxicity, intracellular calcium overload, mitochondrial dysfunction, free radical-induced oxidative damage and neuroinflammation, may contribute to the brain damage associated with CTE. Thus, the current review begins with an in depth analysis of what is known about the tau protein and its functions and dysfunctions followed by a discussion of the major TBI secondary injury mechanisms, and how the latter have been shown to contribute to tau pathology. The value of this review is that it might lead to improved neuroprotective strategies for either prophylactically attenuating the development of CTE or slowing its progression. Copyright © 2017 Elsevier Ltd. All rights reserved.

Sleep-wake disturbances after traumatic brain injury.

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Ouellet, Marie-Christine; Beaulieu-Bonneau, Simon; Morin, Charles M

2015-07-01

Sleep-wake disturbances are extremely common after a traumatic brain injury (TBI). The most common disturbances are insomnia (difficulties falling or staying asleep), increased sleep need, and excessive daytime sleepiness that can be due to the TBI or other sleep disorders associated with TBI, such as sleep-related breathing disorder or post-traumatic hypersomnia. Sleep-wake disturbances can have a major effect on functional outcomes and on the recovery process after TBI. These negative effects can exacerbate other common sequelae of TBI-such as fatigue, pain, cognitive impairments, and psychological disorders (eg, depression and anxiety). Sleep-wake disturbances associated with TBI warrant treatment. Although evidence specific to patients with TBI is still scarce, cognitive-behavioural therapy and medication could prove helpful to alleviate sleep-wake disturbances in patients with a TBI. Copyright © 2015 Elsevier Ltd. All rights reserved.

Therapeutic effects of ellagic acid on memory, hippocampus electrophysiology deficits, and elevated TNF-α level in brain due to experimental traumatic brain injury

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Shahram Mashhadizadeh

2017-04-01

Full Text Available Objective(s: Cognitive defects such as learning and memory impairment are amongst the most repetitious sequelae after sever and moderate traumatic brain injury (TBI. It was suggested that ellagic acid (EA, an innate phenol product, display neuroprotective properties against oxidative and inflammatory damages after brain injury. The object of the current study was therapeutic properties of EA on blood-brain barrier (BBB interruption and elevated content of TNF-α in brain tissue followed by neurologic aftereffects, cognitive and brain electrophysiology deficits as outcomes of diffuse TBI in rat. Materials and Methods: TBI was induced by a 200 g weight falling by a 2-m height through a free-falling tube onto the head of anesthetized rat. TBI rats treated immediately after trauma with EA             (100 mg/kg, IP once every 8 hr until 48 hr later. Neurologic outcomes, passive avoidance task (PAT, hippocampal long-term potentiation (LTP, BBB permeability and content of TNF-α in brain tissue were evaluated. Results: TBI induced significant impairments in neurological score, BBB function, PAT and hippocampal LTP in TBI+Veh group in compare with Sham+Veh (P

The correlation of insulin resistance with the cerebral injury and stress reaction in patients with traumatic brain injury

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Zhan Lan

2017-04-01

Full Text Available Objective: To study the correlation of insulin resistance with the cerebral injury and stress reaction in patients with traumatic brain injury (TBI. Methods: 78 patients who were diagnosed with acute traumatic brain injury in our hospital between May 2014 and August 2016 were selected as the TBI group, and 90 healthy volunteers who received physical examination during the same period were selected as the control group. The peripheral blood was collected to detect glucose, insulin and nerve injury marker molecules, stress hormones as well as oxidative stress reaction products, and the insulin resistance index (HOMA-IR was calculated. Results: The HOMA-IR index of TBI group was significantly higher than that of control group (P<0.05; serum neuron-specific enolase (NSE, ubiquitin carboxy-terminal hydrolase L1 (UCH-L1, S100β, myelin basic protein (MBP, glucagon, growth hormone, cortisol, malondialdehyde (MDA and 8-hydroxy-deoxyguanosine (8-OHdGlevels of TBI group were significantly higher than those of control group (P<0.05; serum NSE, UCH-L1, S100β, MBP, glucagon, growth hormone, cortisol, MDA and 8-OHdG levels of patients with high HOMA-IR were significantly higher than those of patients with low HOMA-IR (P<0.05. Conclusion: The insulin resistance increases significantly in patients with traumatic brain injury, and is closely related to the degree of cerebral injury and stress reaction.

Role of Non-neuronal Cells in Tauopathies After Brain Injury

Science.gov (United States)

2017-09-01

AWARD NUMBER: W81XWH-15-1-0422 TITLE: Role of Nonneuronal Cells in Tauopathies After Brain Injury PRINCIPAL INVESTIGATOR: Sally A. Frautschy...AND SUBTITLE 5a. CONTRACT NUMBER Role of Non-neuronal Cells in Tauopathies After Brain Injury 5b. GRANT NUMBER W81XWH-15-1-0422 5c. PROGRAM...traumatic brain injury (TBI), specific inflammatory factors (complement proteins) elevated during long asymptomatic prodromal period are responsible

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...

Structural imaging of mild traumatic brain injury may not be enough: overview of functional and metabolic imaging of mild traumatic brain injury.

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Shin, Samuel S; Bales, James W; Edward Dixon, C; Hwang, Misun

2017-04-01

A majority of patients with traumatic brain injury (TBI) present as mild injury with no findings on conventional clinical imaging methods. Due to this difficulty of imaging assessment on mild TBI patients, there has been much emphasis on the development of diffusion imaging modalities such as diffusion tensor imaging (DTI). However, basic science research in TBI shows that many of the functional and metabolic abnormalities in TBI may be present even in the absence of structural damage. Moreover, structural damage may be present at a microscopic and molecular level that is not detectable by structural imaging modality. The use of functional and metabolic imaging modalities can provide information on pathological changes in mild TBI patients that may not be detected by structural imaging. Although there are various differences in protocols of positron emission tomography (PET), single photon emission computed tomography (SPECT), functional magnetic resonance imaging (fMRI), electroencephalography (EEG), and magnetoencephalography (MEG) methods, these may be important modalities to be used in conjunction with structural imaging in the future in order to detect and understand the pathophysiology of mild TBI. In this review, studies of mild TBI patients using these modalities that detect functional and metabolic state of the brain are discussed. Each modality's advantages and disadvantages are compared, and potential future applications of using combined modalities are explored.

Traumatic brain injury, the hidden pandemic: A focused response to ...

African Journals Online (AJOL)

Introduction: Traumatic brain injury (TBI) has many potential cognitive, behavioural and psychological consequences, and contributes significantly to the national burden of disease and to ongoing violent behaviour. Few resources are available for the rehabilitation of patients with TBI in South Africa, and access to ...

Fatigue following mild Traumatic Brain Injury : A six-month prospective cohort study

NARCIS (Netherlands)

Rakers, Sandra; Scheenen, Myrthe; de Koning, Myrthe; van der Horn, Harm J.; van der Naalt, Joukje; Spikman, Jacoba

2017-01-01

Objective: Fatigue is a frequent and profoundly disabling symptom following mild traumatic brain injury (mTBI), that may even persist for years. Approximately 85–90% of thepatients with TBI sustain a mild TBI, and among these patients, about 68% experience complaints of fatigue in the acute phase

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

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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. Copyright © 2015 the authors 0270-6474/15/350518-09$15.00/0.

Preservation of general intelligence following traumatic brain injury: contributions of the Met66 brain-derived neurotrophic factor.

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Aron K Barbey

Full Text Available Brain-derived neurotrophic factor (BDNF promotes survival and synaptic plasticity in the human brain. The Val66Met polymorphism of the BDNF gene interferes with intracellular trafficking, packaging, and regulated secretion of this neurotrophin. The human prefrontal cortex (PFC shows lifelong neuroplastic adaption implicating the Val66Met BDNF polymorphism in the recovery of higher-order executive functions after traumatic brain injury (TBI. In this study, we examined the effect of this BDNF polymorphism on the preservation of general intelligence following TBI. We genotyped a sample of male Vietnam combat veterans (n = 156 consisting of a frontal lobe lesion group with focal penetrating head injuries for the Val66Met BDNF polymorphism. Val/Met did not differ from Val/Val genotypes in general cognitive ability before TBI. However, we found substantial average differences between these groups in general intelligence (≈ half a standard deviation or 8 IQ points, verbal comprehension (6 IQ points, perceptual organization (6 IQ points, working memory (8 IQ points, and processing speed (8 IQ points after TBI. These results support the conclusion that Val/Met genotypes preserve general cognitive functioning, whereas Val/Val genotypes are largely susceptible to TBI.

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

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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.

Clinical Predictors of Progressive Hemorrhagic Injury in Children with Mild Traumatic Brain Injury

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Guangfu Di

2017-11-01

Full Text Available ObjectiveTraumatic brain injury (TBI occurs commonly in children. Repeat computed tomography (CT follow up of TBI patients is often scheduled to identify progressive hemorrhagic injury (PHI. However, the utility of repeated CT scans, especially in children with mild TBI [Glasgow Coma Scale (GCS scores of 13–15], has been debated. The purposes of the present study were to identify clinical predictors of PHI in children with mild TBI and to clarify relevant clinical factors via radiological examination.MethodsFrom 2014 to 2016, we retrospectively enrolled children <15 years of age with mild TBI. We recorded age, sex, GCS scores on admission, causes of head injury, timing of initial CT, any loss of consciousness, vomiting and seizure data, and type of TBI. Based on repeat CT findings, patients were dichotomized into either a PHI group or a non-PHI group. Also, clinical data were comparatively reviewed. Multivariate logistic regression analysis was used to identify clinical predictors of PHI.ResultsOf the 175 enrolled children, 15 (8.6% experienced PHI. Univariate analysis revealed that GCS score on admission, cause of head injury, vomiting, seizure, and TBI type were associated with PHI. Multivariate logistic regression analysis showed that a GCS score of 13 and epidural hemorrhage (EDH were independently associated with PHI (hazard ratio = 0.131, P = 0.018; hazard ratio = 6.612, P = 0.027, respectively.ConclusionA GCS score of 13 and EDH were associated with PHI. These factors should be considered when deciding whether to repeat CT on children with mild TBI.

Association Between Traumatic Brain Injury and Risk of Posttraumatic Stress Disorder in Active-Duty Marines

Science.gov (United States)

2013-01-01

traumatic brain injury (TBI) is a risk factor for posttraumatic stress disorder ( PTSD ) has been difficult to determine because of the prevalence of...Qualification Test; CAPS, Clinician-Administered PTSD Scale; PTSD , posttraumatic stress disorder ; TBI, traumatic brain injury. a For the zeromodel, base...New onset and persistent symptoms of post - traumatic stress disorder self reported after deployment and combat exposures. BMJ.

Brain network disturbance related to posttraumatic stress and traumatic brain injury in veterans.

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Spielberg, Jeffrey M; McGlinchey, Regina E; Milberg, William P; Salat, David H

2015-08-01

Understanding the neural causes and consequences of posttraumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI) is a high research priority, given the high rates of associated disability and suicide. Despite remarkable progress in elucidating the brain mechanisms of PTSD and mTBI, a comprehensive understanding of these conditions at the level of brain networks has yet to be achieved. The present study sought to identify functional brain networks and topological properties (measures of network organization and function) related to current PTSD severity and mTBI. Graph theoretic tools were used to analyze resting-state functional magnetic resonance imaging data from 208 veterans of Operation Enduring Freedom, Operation Iraqi Freedom, and Operation New Dawn, all of whom had experienced a traumatic event qualifying for PTSD criterion A. Analyses identified brain networks and topological network properties linked to current PTSD symptom severity, mTBI, and the interaction between PTSD and mTBI. Two brain networks were identified in which weaker connectivity was linked to higher PTSD re-experiencing symptoms, one of which was present only in veterans with comorbid mTBI. Re-experiencing was also linked to worse functional segregation (necessary for specialized processing) and diminished influence of key regions on the network, including the hippocampus. Findings of this study demonstrate that PTSD re-experiencing symptoms are linked to weakened connectivity in a network involved in providing contextual information. A similar relationship was found in a separate network typically engaged in the gating of working memory, but only in veterans with mTBI. Published by Elsevier Inc.

4: Rehabilitation after traumatic brain injury.

Science.gov (United States)

Khan, Fary; Baguley, Ian J; Cameron, Ian D

2003-03-17

Traumatic brain injury (TBI) commonly affects younger people and causes life-long impairments in physical, cognitive, behavioural and social function. The cognitive, behavioural and personality deficits are usually more disabling than the residual physical deficits. Recovery from TBI can continue for at least 5 years after injury. Rehabilitation is effective using an interdisciplinary approach, and close liaison with the patient, family and carers. The focus is on issues such as retraining in activities of daily living, pain management, cognitive and behavioural therapies, and pharmacological management. The social burden of TBI is significant, and therefore family education and counselling, and support of patient and carers, is important. General practitioners play an important role in providing ongoing support in the community, monitoring for medical complications, behavioural and personality issues, social reintegration, carer coping skills and return-to-work issues.

A SPECT study of language and brain reorganization three years after pediatric brain injury.

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Chiu Wong, Stephanie B; Chapman, Sandra B; Cook, Lois G; Anand, Raksha; Gamino, Jacquelyn F; Devous, Michael D

2006-01-01

Using single photon emission computed tomography (SPECT), we investigated brain plasticity in children 3 years after sustaining a severe traumatic brain injury (TBI). First, we assessed brain perfusion patterns (i.e., the extent of brain blood flow to regions of the brain) at rest in eight children who suffered severe TBI as compared to perfusion patterns in eight normally developing children. Second, we examined differences in perfusion between children with severe TBI who showed good versus poor recovery in complex discourse skills. Specifically, the children were asked to produce and abstract core meaning for two stories in the form of a lesson. Inconsistent with our predictions, children with severe TBI showed areas of increased perfusion as compared to normally developing controls. Adult studies have shown the reverse pattern with TBI associated with reduced perfusion. With regard to the second aim and consistent with previously identified brain-discourse relations, we found a strong positive association between perfusion in right frontal regions and discourse abstraction abilities, with higher perfusion linked to better discourse outcomes and lower perfusion linked to poorer discourse outcomes. Furthermore, brain-discourse patterns of increased perfusion in left frontal regions were associated with lower discourse abstraction ability. The results are discussed in terms of how brain changes may represent adaptive and maladaptive plasticity. The findings offer direction for future studies of brain plasticity in response to neurocognitive treatments.

Fish oil improves motor function, limits blood-brain barrier disruption, and reduces Mmp9 gene expression in a rat model of juvenile traumatic brain injury.

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Russell, K L; Berman, N E J; Gregg, P R A; Levant, B

2014-01-01

The effects of an oral fish oil treatment regimen on sensorimotor, blood-brain barrier, and biochemical outcomes of traumatic brain injury (TBI) were investigated in a juvenile rat model. Seventeen-day old Long-Evans rats were given a 15mL/kg fish oil (2.01g/kg EPA, 1.34g/kg DHA) or soybean oil dose via oral gavage 30min prior to being subjected to a controlled cortical impact injury or sham surgery, followed by daily doses for seven days. Fish oil treatment resulted in less severe hindlimb deficits after TBI as assessed with the beam walk test, decreased cerebral IgG infiltration, and decreased TBI-induced expression of the Mmp9 gene one day after injury. These results indicate that fish oil improved functional outcome after TBI resulting, at least in part from decreased disruption of the blood-brain barrier through a mechanism that includes attenuation of TBI-induced expression of Mmp9. © 2013 Elsevier Ltd. All rights reserved.

Microdialysis Monitoring in Clinical Traumatic Brain Injury and Its Role in Neuroprotective Drug Development.

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Thelin, Eric Peter; Carpenter, Keri L H; Hutchinson, Peter J; Helmy, Adel

2017-03-01

Injuries to the central nervous system continue to be vast contributors to morbidity and mortality; specifically, traumatic brain injury (TBI) is the most common cause of death during the first four decades of life. Several modalities are used to monitor patients suffering from TBI in order to prevent detrimental secondary injuries. The microdialysis (MD) technique, introduced during the 1990s, presents the treating physician with a robust monitoring tool for brain chemistry in addition to conventional intracranial pressure monitoring. Nevertheless, some limitations remain, such as limited spatial resolution. Moreover, while there have been several attempts to develop new potential pharmacological therapies in TBI, there are currently no available drugs which have shown clinical efficacy that targets the underlying pathophysiology, despite various trials investigating a plethora of pharmaceuticals. Specifically in the brain, MD is able to demonstrate penetration of the drug through the blood-brain barrier into the brain extracellular space at potential site of action. In addition, the downstream effects of drug action can be monitored directly. In the future, clinical MD, together with other monitoring modalities, can identify specific pathological substrates which require tailored treatment strategies for patients suffering from TBI.

Repeated mild traumatic brain injury in female rats increases lipid peroxidation in neurons.

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Yates, Nathanael J; Lydiard, Stephen; Fehily, Brooke; Weir, Gillian; Chin, Aaron; Bartlett, Carole A; Alderson, Jacqueline; Fitzgerald, Melinda

2017-07-01

Negative outcomes of mild traumatic brain injury (mTBI) can be exacerbated by repeated insult. Animal models of repeated closed-head mTBI provide the opportunity to define acute pathological mechanisms as the number of mTBI increases. Furthermore, little is known about the effects of mTBI impact site, and how this may affect brain function. We use a closed head, weight drop model of mTBI that allows head movement following impact, in adult female rats to determine the role of the number and location of mTBI on brain pathology and behaviour. Biomechanical assessment of two anatomically well-defined mTBI impact sites were used, anterior (bregma) and posterior (lambda). Location of the impact had no significant effect on impact forces (450 N), and the weight impact locations were on average 5.4 mm from the desired impact site. No between location vertical linear head kinematic differences were observed immediately following impact, however, in the 300 ms post-impact, significantly higher mean vertical head displacement and velocity were observed in the mTBI lambda trials. Breaches of the blood brain barrier were observed with three mTBI over bregma, associated with immunohistochemical indicators of damage. However, an increased incidence of hairline fractures of the skull and macroscopic haemorrhaging made bregma an unsuitable impact location to model repeated mTBI. Repeated mTBI over lambda did not cause skull fractures and were examined more comprehensively, with outcomes following one, two or three mTBI or sham, delivered at 1 day intervals, assessed on days 1-4. We observe a mild behavioural phenotype, with subtle deficits in cognitive function, associated with no identifiable neuroanatomical or inflammatory changes. However, an increase in lipid peroxidation in a subset of cortical neurons following two mTBI indicates increasing oxidative damage with repeated injury in female rats, supported by increased amyloid precursor protein immunoreactivity with three mTBI

A qualitative investigation of masculine identity after traumatic brain injury.

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MacQueen, Ruth; Fisher, Paul; Williams, Deirdre

2018-04-30

Men are twice as likely as women to experience a traumatic brain injury (TBI), suggesting that aspects of masculine identity contribute to how people acquire their brain injuries. Research also suggests that masculine identity impacts on how people manage their health experiences. The current study aimed to explore the experience of masculine identity following TBI. Individual interviews were conducted with 10 men aged 21-67 years who had experienced a TBI. All were living in the community. Interpretative phenomenological analysis was used to consider lived experiences and to explore the meaning of the TBI experience in relation to masculine identity. Three superordinate themes emerged from the analysis: doing life and relationships differently, self-perceptions and the perceived view of others, and managing the impact of TBI as a man. These themes are considered in relation to how participants' experiences interacted with dominant social ideals of masculine identity. The findings highlighted how masculine identity may be a valuable aspect of self in considering threats to and reconstruction of self-identity after TBI. Aspects of gender identity should be considered in order to promote engagement, support adjustment and achieve meaningful outcomes in rehabilitation.

Effect of binasal occlusion (BNO) and base-in prisms on the visual-evoked potential (VEP) in mild traumatic brain injury (mTBI).

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Yadav, Naveen K; Ciuffreda, Kenneth J

2014-01-01

To assess quantitatively the effect and relative contribution of binasal occlusion (BNO) and base-in prisms (BI) on visually-evoked potential (VEP) responsivity in persons with mild traumatic brain injury (mTBI) and the symptom of visual motion sensitivity (VMS), as well as in visually-normal (VN) individuals. Subjects were comprised of 20 VN adults and 15 adults with mTBI and VMS. There were four test conditions: (1) conventional pattern VEP, which served as the baseline comparison condition; (2) VEP with BNO alone; (3) VEP with 2 pd BI prisms before each eye; and (4) VEP with the above BNO and BI prism combination. In mTBI, the mean VEP amplitude increased significantly in nearly all subjects (∼90%) with BNO alone. In contrast, in VN, it decreased significantly with BNO alone in all subjects (100%), as compared to the other test conditions. These objective findings were consistent with improvements in visual impressions and sensorimotor tasks in the group with mTBI. Latency remained within normal limits under all test conditions in both groups. Only the BNO condition demonstrated significant, but opposite and consistent, directional effects on the VEP amplitude in both groups. The BNO-VEP test condition may be used clinically for the objectively-based, differential diagnosis of persons suspected of having mTBI and VMS from the VNs.

Facilitated assessment of tissue loss following traumatic brain injury

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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.

Early predictors of outcome after mild traumatic brain injury (UPFRONT) : An observational cohort study

NARCIS (Netherlands)

van der Naalt, J.; Timmerman, M.E.; de Koning, M.E.; van der Horn, H.J.; Scheenen, M.E.; Jacobs, B.; Hageman, G.; Yilmaz, T.; Roks, G.; Spikman, J.M.

Background: Mild traumatic brain injury (mTBI) accounts for most cases of TBI, and many patients show incomplete long-term functional recovery. We aimed to create a prognostic model for functional outcome by combining demographics, injury severity, and psychological factors to identify patients at

The synthetic NCAM-derived peptide, FGL, modulates the transcriptional response to traumatic brain injury

DEFF Research Database (Denmark)

Pedersen, Martin Volmer; Helweg-Larsen, Rehannah Borup; Nielsen, Finn Cilius

2008-01-01

Cerebral responses to traumatic brain injury (TBI) include up- and downregulation of a vast number of proteins involved in endogenous inflammatory responses and defense mechanisms developing postinjury. The present study analyzed the global gene expression profile in response to cryo-induced TBI...... at various time-points postlesion (6 h, 1 day and 4 days). The effects of injury, treatment, and injury-treatment interaction were observed. TBI alone rendered a large number of genes affected. Analysis of lesion and treatment interactions resulted in a clear effect of the interaction between injury and FGL......-treatment compared to injury and placebo-treatment. Genes affected by TBI alone included inflammation markers, protein kinases, ion channel members and growth factors. Genes encoding regulators of apoptosis, signal transduction and metabolism were altered by the interaction between FGL-treatment and TBI. FGL...

Family adaptation 18 months after traumatic brain injury in early childhood.

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Stancin, Terry; Wade, Shari L; Walz, Nicolay C; Yeates, Keith Owen; Taylor, H Gerry

2010-05-01

The purpose of this study was to examine family adaptation to a traumatic brain injury (TBI) in young children during the first 18-month postinjury, when compared with children who had an orthopedic injury. A concurrent cohort/prospective research design was used with repeated assessments of children aged 3 to 6 years with TBI or orthopedic injury requiring hospitalization and their families. Shortly after injury and at 6-, 12-, and 18-month postinjury, parents of 99 children with TBI (20 severe, 64 moderate, 15 mild) and 117 with orthopedic injury completed standardized assessments of family functioning, parental distress and coping, injury-related burden, and noninjury-related parent stressors and resources. Mixed models analyses examined group differences in parental burden and distress adjusted for race and social demographic factors. Both moderate and severe TBI were associated with higher levels of injury-related stress than orthopedic injury, with stress levels diminishing over time in all groups. Severe TBI was also associated with greater psychological distress on the Brief Symptom Inventory but not with more depressive symptoms. Family functioning and social resources moderated the relationship of TBI severity to injury-related burden and caregiver distress, respectively. Lower child adaptive skills were associated with poorer family outcome but group differences remained even when controlling for this effect. Severe TBI in young children has adverse consequences for parents and families during the first 18-month postinjury. The consequences lessen over time for many families and vary as a function of social resources.

Mean cortical curvature reflects cytoarchitecture restructuring in mild traumatic brain injury

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Jace B. King

2016-01-01

Full Text Available In the United States alone, the number of persons living with the enduring consequences of traumatic brain injuries is estimated to be between 3.2 and 5 million. This number does not include individuals serving in the United States military or seeking care at Veterans Affairs hospitals. The importance of understanding the neurobiological consequences of mild traumatic brain injury (mTBI has increased with the return of veterans from conflicts overseas, many of who have suffered this type of brain injury. However, identifying the neuroanatomical regions most affected by mTBI continues to prove challenging. The aim of this study was to assess the use of mean cortical curvature as a potential indicator of progressive tissue loss in a cross-sectional sample of 54 veterans with mTBI compared to 31 controls evaluated with MRI. It was hypothesized that mean cortical curvature would be increased in veterans with mTBI, relative to controls, due in part to cortical restructuring related to tissue volume loss. Mean cortical curvature was assessed in 60 bilateral regions (31 sulcal, 29 gyral. Of the 120 regions investigated, nearly 50% demonstrated significantly increased mean cortical curvature in mTBI relative to controls with 25% remaining significant following multiple comparison correction (all, pFDR < .05. These differences were most prominent in deep gray matter regions of the cortex. Additionally, significant relationships were found between mean cortical curvature and gray and white matter volumes (all, p < .05. These findings suggest potentially unique patterns of atrophy by region and indicate that changes in brain microstructure due to mTBI are sensitive to measures of mean curvature.

Secondary injury in traumatic brain injury patients - A prospective ...

African Journals Online (AJOL)

Objective. Secondary insults of hypotension and hypoxia significantly impact on outcome in patients with traumatic brain injury (TBI). More than 4 hours' delay in evacuation of intracranial haematomas has been demonstrated to have an additional impact on outcome. The objective of this study was to document the ...

Diffusion Tensor Imaging of Incentive Effects in Prospective Memory after Pediatric Traumatic Brain Injury

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Wilde, Elisabeth A.; Bigler, Erin D.; Chu, Zili; Yallampalli, Ragini; Oni, Margaret B.; Wu, Trevor C.; Ramos, Marco A.; Pedroza, Claudia; Vásquez, Ana C.; Hunter, Jill V.; Levin, Harvey S.

2011-01-01

Abstract Few studies exist investigating the brain-behavior relations of event-based prospective memory (EB-PM) impairments following traumatic brain injury (TBI). To address this, children with moderate-to-severe TBI performed an EB-PM test with two motivational enhancement conditions and underwent concurrent diffusion tensor imaging (DTI) at 3 months post-injury. Children with orthopedic injuries (OI; n = 37) or moderate-to-severe TBI (n = 40) were contrasted. Significant group differences were found for fractional anisotropy (FA) and apparent diffusion coefficient for orbitofrontal white matter (WM), cingulum bundles, and uncinate fasciculi. The FA of these WM structures in children with TBI significantly correlated with EB-PM performance in the high, but not the low motivation condition. Regression analyses within the TBI group indicated that the FA of the left cingulum bundle (p = 0.003), left orbitofrontal WM (p motivation condition. We infer that the cingulum bundles, orbitofrontal WM, and uncinate fasciculi are important WM structures mediating motivation-based EB-PM responses following moderate-to-severe TBI in children. PMID:21250917

Fisetin alleviates oxidative stress after traumatic brain injury via the Nrf2-ARE pathway.

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Zhang, Li; Wang, Handong; Zhou, Yali; Zhu, Yihao; Fei, Maoxin

2018-05-22

Fisetin, a natural flavonoid, has neuroprotection properties in many brain injury models. However, its role in traumatic brain injury (TBI) has not been fully explained. In the present study, we aimed to explore the neuroprotective effects of fisetin in a mouse model of TBI. We found that fisetin improved neurological function, reduced cerebral edema, attenuated brain lesion and ameliorated blood-brain barrier (BBB) disruption after TBI. Moreover, the up-regulation of malondialdehyde (MDA) and the activity of glutathione peroxidase (GPx) were reversed by fisetin treatment. Furthermore, administration of fisetin suppressed neuron cell death and apoptosis, increased the expression of B-cell lymphoma 2 (Bcl-2), while decreased the expression of Bcl-2-associated X protein (Bax) and caspase-3 after TBI. In addition, fisetin activated the nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway following TBI. However, fisetin only failed to suppress oxidative stress in Nrf2 -/- mice. In conclusion, our data provided the first evidence that fisetin played a critical role in neuroprotection after TBI partly through the activation of the Nrf2-ARE pathway. Copyright © 2018 Elsevier Ltd. All rights reserved.

Hyperbaric oxygen preconditioning protects against traumatic brain injury at high altitude.

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Hu, S L; Hu, R; Li, F; Liu, Z; Xia, Y Z; Cui, G Y; Feng, H

2008-01-01

Recent studies have shown that preconditioning with hyperbaric oxygen (HBO) can reduce ischemic and hemorrhagic brain injury. We investigated effects of HBO preconditioning on traumatic brain injury (TBI) at high altitude and examined the role of matrix metalloproteinase-9 (MMP-9) in such protection. Rats were randomly divided into 3 groups: HBO preconditioning group (HBOP; n = 13), high-altitude group (HA; n = 13), and high-altitude sham operation group (HASO; n = 13). All groups were subjected to head trauma by weight-drop device, except for HASO group. HBOP rats received 5 sessions of HBO preconditioning (2.5 ATA, 100% oxygen, 1 h daily) and then were kept in hypobaric chamber at 0.6 ATA (to simulate pressure at 4000m altitude) for 3 days before operation. HA rats received control pretreatment (1 ATA, room air, 1 h daily), then followed the same procedures as HBOP group. HASO rats were subjected to skull opening only without brain injury. Twenty-four hours after TBI, 7 rats from each group were examined for neurological function and brain water content; 6 rats from each group were killed for analysis by H&E staining and immunohistochemistry. Neurological outcome in HBOP group (0.71 +/- 0.49) was better than HA group (1.57 +/- 0.53; p < 0.05). Preconditioning with HBO significantly reduced percentage of brain water content (86.24 +/- 0.52 vs. 84.60 +/- 0.37; p < 0.01). Brain morphology and structure seen by light microscopy was diminished in HA group, while fewer pathological injuries occurred in HBOP group. Compared to HA group, pretreatment with HBO significantly reduced the number of MMP-9-positive cells (92.25 +/- 8.85 vs. 74.42 +/- 6.27; p < 0.01). HBO preconditioning attenuates TBI in rats at high altitude. Decline in MMP-9 expression may contribute to HBO preconditioning-induced protection of brain tissue against TBI.

Use of brain electrical activity for the identification of hematomas in mild traumatic brain injury.

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Hanley, Daniel F; Chabot, Robert; Mould, W Andrew; Morgan, Timothy; Naunheim, Rosanne; Sheth, Kevin N; Chiang, William; Prichep, Leslie S

2013-12-15

This study investigates the potential clinical utility in the emergency department (ED) of an index of brain electrical activity to identify intracranial hematomas. The relationship between this index and depth, size, and type of hematoma was explored. Ten minutes of brain electrical activity was recorded from a limited montage in 38 adult patients with traumatic hematomas (CT scan positive) and 38 mild head injured controls (CT scan negative) in the ED. The volume of blood and distance from recording electrodes were measured by blinded independent experts. Brain electrical activity data were submitted to a classification algorithm independently developed traumatic brain injury (TBI) index to identify the probability of a CT+traumatic event. There was no significant relationship between the TBI-Index and type of hematoma, or distance of the bleed from recording sites. A significant correlation was found between TBI-Index and blood volume. The sensitivity to hematomas was 100%, positive predictive value was 74.5%, and positive likelihood ratio was 2.92. The TBI-Index, derived from brain electrical activity, demonstrates high accuracy for identification of traumatic hematomas. Further, this was not influenced by distance of the bleed from the recording electrodes, blood volume, or type of hematoma. Distance and volume limitations noted with other methods, (such as that based on near-infrared spectroscopy) were not found, thus suggesting the TBI-Index to be a potentially important adjunct to acute assessment of head injury. Because of the life-threatening risk of undetected hematomas (false negatives), specificity was permitted to be lower, 66%, in exchange for extremely high sensitivity.

Substance Use and Mild Traumatic Brain Injury Risk Reduction and Prevention: A Novel Model for Treatment

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Jennifer H. Olson-Madden

2012-01-01

Full Text Available Traumatic brain injury (TBI and substance use disorders (SUDs frequently co-occur. Individuals with histories of alcohol or other drug use are at greater risk for sustaining TBI, and individuals with TBI frequently misuse substances before and after injury. Further, a growing body of literature supports the relationship between comorbid histories of mild TBI (mTBI and SUDs and negative outcomes. Alcohol and other drug use are strongly associated with risk taking. Disinhibition, impaired executive function, and/or impulsivity as a result of mTBI also contribute to an individual’s proclivity towards risk-taking. Risk-taking behavior may therefore, be a direct result of SUD and/or history of mTBI, and risky behaviors may predispose individuals for subsequent injury or continued use of substances. Based on these findings, evaluation of risk-taking behavior associated with the co-occurrence of SUD and mTBI should be a standard clinical practice. Interventions aimed at reducing risky behavior among members of this population may assist in decreasing negative outcomes. A novel intervention (Substance Use and Traumatic Brain Injury Risk Reduction and Prevention (STRRP for reducing and preventing risky behaviors among individuals with co-occurring mTBI and SUD is presented. Areas for further research are discussed.

Development of an Ontology for Rehabilitation: Traumatic Brain Injury

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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…

Impaired Pituitary Axes Following Traumatic Brain Injury

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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.

Brain functional connectivity and cognition in mild traumatic brain injury

International Nuclear Information System (INIS)

Xiong, K.L.; Zhang, Y.L.; Chen, H.; Zhang, J.N.; Zhang, Y.; Qiu, M.G.

2016-01-01

The aim of this study was to analyze brain functional connectivity and its relationship to cognition in patients with mild traumatic brain injury (mTBI). Twenty-five patients with mTBI and 25 healthy control subjects were studied using resting-state functional MRI (rs-fMRI). Amplitudes of low-frequency fluctuations (ALFFs) and functional connectivity (FC) were calculated and correlated with cognition. Compared with the normal control group, the mTBI patients showed a significant decrease in working memory index (WMI) and processing speed index (PSI), as well as significantly decreased ALFFs in the cingulate gyrus, the middle frontal gyrus and superior frontal gyrus. In contrast, the mTBI patients' ALFFs in the left middle occipital gyrus, the left precuneus, and lingual gyrus increased. Additionally, FC significantly decreased in the thalamus, caudate nucleus, and right hippocampus in the mTBI patients. Statistical analysis further showed a significant positive correlation between the ALFF in the cingulate gyrus and the WMI (R 2 = 0.423, P < 0.05) and a significant positive correlation between the FC in the left thalamus and left middle frontal gyrus and the WMI (R 2 = 0.381, P < 0.05). rs-fMRI can reveal the functional state of the brain in patients with mTBI. This finding differed from observations of the normal control group and was significantly associated with clinical cognitive dysfunction. Therefore, rs-fMRI offers an objective imaging modality for treatment planning and prognosis assessment in patients with mTBI. (orig.)

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

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Mary Wurzelmann

2017-01-01

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

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

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Wurzelmann, Mary; Romeika, Jennifer; Sun, Dong

2017-01-01

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

Multi-modal MRI of mild traumatic brain injury

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Ponnada A. Narayana

2015-01-01

Full Text Available Multi-modal magnetic resonance imaging (MRI that included high resolution structural imaging, diffusion tensor imaging (DTI, magnetization transfer ratio (MTR imaging, and magnetic resonance spectroscopic imaging (MRSI were performed in mild traumatic brain injury (mTBI patients with negative computed tomographic scans and in an orthopedic-injured (OI group without concomitant injury to the brain. The OI group served as a comparison group for mTBI. MRI scans were performed both in the acute phase of injury (~24 h and at follow-up (~90 days. DTI data was analyzed using tract based spatial statistics (TBSS. Global and regional atrophies were calculated using tensor-based morphometry (TBM. MTR values were calculated using the standard method. MRSI was analyzed using LC Model. At the initial scan, the mean diffusivity (MD was significantly higher in the mTBI cohort relative to the comparison group in several white matter (WM regions that included internal capsule, external capsule, superior corona radiata, anterior corona radiata, posterior corona radiata, inferior fronto-occipital fasciculus, inferior longitudinal fasciculus, forceps major and forceps minor of the corpus callosum, superior longitudinal fasciculus, and corticospinal tract in the right hemisphere. TBSS analysis failed to detect significant differences in any DTI measures between the initial and follow-up scans either in the mTBI or OI group. No significant differences were found in MRSI, MTR or morphometry between the mTBI and OI cohorts either at the initial or follow-up scans with or without family wise error (FWE correction. Our study suggests that a number of WM tracts are affected in mTBI in the acute phase of injury and that these changes disappear by 90 days. This study also suggests that none of the MRI-modalities used in this study, with the exception of DTI, is sensitive in detecting changes in the acute phase of mTBI.

Characteristics of Firearm Brain Injury Survivors in the Traumatic Brain Injury Model Systems (TBIMS) National Database: A Comparison of Assault and Self-Inflicted Injury Survivors.

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Bertisch, Hilary; Krellman, Jason W; Bergquist, Thomas F; Dreer, Laura E; Ellois, Valerie; Bushnik, Tamara

2017-11-01

To characterize and compare subgroups of survivors with assault-related versus self-inflicted traumatic brain injuries (TBIs) via firearms at the time of inpatient rehabilitation and at 1-, 2-, and 5-year follow-up. Secondary analysis of data from the Traumatic Brain Injury Model Systems National Database (TBIMS NDB), a multicenter, longitudinal cohort study. Retrospective analyses of a subset of individuals enrolled in the TBIMS NDB. Individuals 16 years and older (N=399; 310 via assault, 89 via self-inflicted injury) with a primary diagnosis of TBI caused by firearm injury enrolled in the TBIMS NDB. Not applicable. Disability Rating Scale, Glasgow Outcome Scale-Extended, sociodemographic variables (sex, age, race, marital status), injury-related/acute care information (posttraumatic amnesia, loss of consciousness, time from injury to acute hospital discharge), and mental health variables (substance use history, psychiatric hospitalizations, suicide history, incarcerations). Individuals who survived TBI secondary to a firearm injury differed by injury mechanism (assault vs self-inflicted) on critical demographic, injury-related/acute care, and mental health variables at inpatient rehabilitation and across long-term recovery. Groups differed in terms of geographic area, age, ethnicity, education, marital status, admission Glasgow Coma Scale score, and alcohol abuse, suicide attempts, and psychiatric hospitalizations at various time points. These findings have implications for prevention (eg, mental health programming and access to firearms in targeted areas) and for rehabilitation planning (eg, by incorporating training with coping strategies and implementation of addictions-related services) for firearm-related TBI, based on subtype of injury. Copyright © 2016 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.

Neurobehavioral Effects of Levetiracetam in Patients with Traumatic Brain Injury

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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.

The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease.

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Sundman, Mark H; Chen, Nan-Kuei; Subbian, Vignesh; Chou, Ying-Hui

2017-11-01

As head injuries and their sequelae have become an increasingly salient matter of public health, experts in the field have made great progress elucidating the biological processes occurring within the brain at the moment of injury and throughout the recovery thereafter. Given the extraordinary rate at which our collective knowledge of neurotrauma has grown, new insights may be revealed by examining the existing literature across disciplines with a new perspective. This article will aim to expand the scope of this rapidly evolving field of research beyond the confines of the central nervous system (CNS). Specifically, we will examine the extent to which the bidirectional influence of the gut-brain axis modulates the complex biological processes occurring at the time of traumatic brain injury (TBI) and over the days, months, and years that follow. In addition to local enteric signals originating in the gut, it is well accepted that gastrointestinal (GI) physiology is highly regulated by innervation from the CNS. Conversely, emerging data suggests that the function and health of the CNS is modulated by the interaction between 1) neurotransmitters, immune signaling, hormones, and neuropeptides produced in the gut, 2) the composition of the gut microbiota, and 3) integrity of the intestinal wall serving as a barrier to the external environment. Specific to TBI, existing pre-clinical data indicates that head injuries can cause structural and functional damage to the GI tract, but research directly investigating the neuronal consequences of this intestinal damage is lacking. Despite this void, the proposed mechanisms emanating from a damaged gut are closely implicated in the inflammatory processes known to promote neuropathology in the brain following TBI, which suggests the gut-brain axis may be a therapeutic target to reduce the risk of Chronic Traumatic Encephalopathy and other neurodegenerative diseases following TBI. To better appreciate how various peripheral

Sensory cortex underpinnings of traumatic brain injury deficits.

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Dasuni S Alwis

Full Text Available Traumatic brain injury (TBI can result in persistent sensorimotor and cognitive deficits including long-term altered sensory processing. The few animal models of sensory cortical processing effects of TBI have been limited to examination of effects immediately after TBI and only in some layers of cortex. We have now used the rat whisker tactile system and the cortex processing whisker-derived input to provide a highly detailed description of TBI-induced long-term changes in neuronal responses across the entire columnar network in primary sensory cortex. Brain injury (n=19 was induced using an impact acceleration method and sham controls received surgery only (n=15. Animals were tested in a range of sensorimotor behaviour tasks prior to and up to 6 weeks post-injury when there were still significant sensorimotor behaviour deficits. At 8-10 weeks post-trauma, in terminal experiments, extracellular recordings were obtained from barrel cortex neurons in response to whisker motion, including motion that mimicked whisker motion observed in awake animals undertaking different tasks. In cortex, there were lamina-specific neuronal response alterations that appeared to reflect local circuit changes. Hyper-excitation was found only in supragranular layers involved in intra-areal processing and long-range integration, and only for stimulation with complex, naturalistic whisker motion patterns and not for stimulation with simple trapezoidal whisker motion. Thus TBI induces long-term directional changes in integrative sensory cortical layers that depend on the complexity of the incoming sensory information. The nature of these changes allow predictions as to what types of sensory processes may be affected in TBI and contribute to post-trauma sensorimotor deficits.

Relationship of mechanical impact magnitude to neurologic dysfunction severity in a rat traumatic brain injury model.

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Tsung-Hsun Hsieh

Full Text Available Traumatic brain injury (TBI is a major brain injury type commonly caused by traffic accidents, falls, violence, or sports injuries. To obtain mechanistic insights about TBI, experimental animal models such as weight-drop-induced TBI in rats have been developed to mimic closed-head injury in humans. However, the relationship between the mechanical impact level and neurological severity following weight-drop-induced TBI remains uncertain. In this study, we comprehensively investigated the relationship between physical impact and graded severity at various weight-drop heights.The acceleration, impact force, and displacement during the impact were accurately measured using an accelerometer, a pressure sensor, and a high-speed camera, respectively. In addition, the longitudinal changes in neurological deficits and balance function were investigated at 1, 4, and 7 days post TBI lesion. The inflammatory expression markers tested by Western blot analysis, including glial fibrillary acidic protein, beta-amyloid precursor protein, and bone marrow tyrosine kinase gene in chromosome X, in the frontal cortex, hippocampus, and corpus callosum were investigated at 1 and 7 days post-lesion.Gradations in impact pressure produced progressive degrees of injury severity in the neurological score and balance function. Western blot analysis demonstrated that all inflammatory expression markers were increased at 1 and 7 days post-impact injury when compared to the sham control rats. The severity of neurologic dysfunction and induction in inflammatory markers strongly correlated with the graded mechanical impact levels.We conclude that the weight-drop-induced TBI model can produce graded brain injury and induction of neurobehavioral deficits and may have translational relevance to developing therapeutic strategies for TBI.

Adult sports-related traumatic brain injury in United States trauma centers.

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Winkler, Ethan A; Yue, John K; Burke, John F; Chan, Andrew K; Dhall, Sanjay S; Berger, Mitchel S; Manley, Geoffrey T; Tarapore, Phiroz E

2016-04-01

OBJECTIVE Sports-related traumatic brain injury (TBI) is an important public health concern estimated to affect 300,000 to 3.8 million people annually in the United States. Although injuries to professional athletes dominate the media, this group represents only a small proportion of the overall population. Here, the authors characterize the demographics of sports-related TBI in adults from a community-based trauma population and identify predictors of prolonged hospitalization and increased morbidity and mortality rates. METHODS Utilizing the National Sample Program of the National Trauma Data Bank (NTDB), the authors retrospectively analyzed sports-related TBI data from adults (age ≥ 18 years) across 5 sporting categories-fall or interpersonal contact (FIC), roller sports, skiing/snowboarding, equestrian sports, and aquatic sports. Multivariable regression analysis was used to identify predictors of prolonged hospital length of stay (LOS), medical complications, inpatient mortality rates, and hospital discharge disposition. Statistical significance was assessed at α sports-related TBIs were documented in the NTDB, which represented 18,310 incidents nationally. Equestrian sports were the greatest contributors to sports-related TBI (45.2%). Mild TBI represented nearly 86% of injuries overall. Mean (± SEM) LOSs in the hospital or intensive care unit (ICU) were 4.25 ± 0.09 days and 1.60 ± 0.06 days, respectively. The mortality rate was 3.0% across all patients, but was statistically higher in TBI from roller sports (4.1%) and aquatic sports (7.7%). Age, hypotension on admission to the emergency department (ED), and the severity of head and extracranial injuries were statistically significant predictors of prolonged hospital and ICU LOSs, medical complications, failure to discharge to home, and death. Traumatic brain injury during aquatic sports was similarly associated with prolonged ICU and hospital LOSs, medical complications, and failure to be discharged to

Clinical and diagnostic approach to patients with hypopituitarism due to traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and ischemic stroke (IS).

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Karamouzis, Ioannis; Pagano, Loredana; Prodam, Flavia; Mele, Chiara; Zavattaro, Marco; Busti, Arianna; Marzullo, Paolo; Aimaretti, Gianluca

2016-06-01

The hypothalamic-pituitary dysfunction attributable to traumatic brain injury (TBI), aneurysmal subarachnoid hemorrhage (SAH), and ischemic stroke (IS) has been lately highlighted. The diagnosis of TBI-induced-hypopituitarism, defined as a deficient secretion of one or more pituitary hormones, is made similarly to the diagnosis of classical hypopituitarism because of hypothalamic/pituitary diseases. Hypopituitarism is believed to contribute to TBI-associated morbidity and to functional and cognitive final outcome, and quality-of-life impairment. Each pituitary hormone must be tested separately, since there is a variable pattern of hormone deficiency among patients with TBI-induced-hypopituitarism. Similarly, the SAH and IS may lead to pituitary dysfunction although the literature in this field is limited. The drive to diagnose hypopituitarism is the suspect that the secretion of one/more pituitary hormone may be subnormal. This suspicion can be based upon the knowledge that the patient has an appropriate clinical context in which hypopituitarism can be present, or a symptom known as caused by hypopituitarism. Hypopituitarism should be diagnosed as a combination of low peripheral and inappropriately normal/low pituitary hormones although their basal evaluation may be not distinctive due to pulsatile, circadian, or situational secretion of some hormones. Evaluation of the somatotroph and corticotroph axes require dynamic stimulation test (ITT for both axes, GHRH + arginine test for somatotroph axis) in order to clearly separate normal from deficient responses.

Brain lesion correlates of fatigue in individuals with traumatic brain injury.

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Schönberger, Michael; Reutens, David; Beare, Richard; O'Sullivan, Richard; Rajaratnam, Shantha M W; Ponsford, Jennie

2017-10-01

The purpose of this study was to investigate the neurological correlates of both subjective fatigue as well as objective fatigability in individuals with traumatic brain injury (TBI). The study has a cross-sectional design. Participants (N = 53) with TBI (77% male, mean age at injury 38 years, mean time since injury 1.8 years) underwent a structural magnetic resonance imaging (MRI) scan and completed the Fatigue Severity Scale (FSS), while a subsample (N = 36) was also tested with a vigilance task. While subjective fatigue (FSS) was not related to measures of brain lesions, multilevel analyses showed that a change in the participants' decision time was significantly predicted by grey matter (GM) lesions in the right frontal lobe. The time-dependent development of the participants' error rate was predicted by total brain white matter (WM) lesion volumes, as well as right temporal GM and WM lesion volumes. These findings could be explained by decreased functional connectivity of attentional networks, which results in accelerated exhaustion during cognitive task performance. The disparate nature of objectively measurable fatigability on the one hand and the subjective experience of fatigue on the other needs further investigation.

Children and youth with 'unspecified injury to the head': implications for traumatic brain injury research and surveillance.

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Chan, Vincy; Mann, Robert E; Pole, Jason D; Colantonio, Angela

2015-01-01

The case definition for traumatic brain injury (TBI) often includes 'unspecified injury to the head' diagnostic codes. However, research has shown that the inclusion of these codes leads to false positives. As such, it is important to determine the degree to which inclusion of these codes affect the overall numbers and profiles of the TBI population. The objective of this paper was to profile and compare the demographic and clinical characteristics, intention and mechanism of injury, and discharge disposition of hospitalized children and youth aged 19 years and under using (1) an inclusive TBI case definition that included 'unspecified injury to the head' diagnostic codes, (2) a restricted TBI case definition that excluded 'unspecified injury to the head 'diagnostic codes, and (3) the 'unspecified injury to the head' only case definition. The National Ambulatory Care Reporting System and the Discharge Abstract Database from Ontario, Canada, were used to identify cases between fiscal years 2003/04 and 2009/10. The rate of TBI episodes of care using the inclusive case definition for TBI (2,667.2 per 100,000) was 1.65 times higher than that of the restricted case definition (1,613.3 per 100,000). 'Unspecified injury to the head' diagnostic codes made up of 39.5 % of all cases identified with the inclusive case definition. Exclusion of 'unspecified injury to the head' diagnostic code in the TBI case definition resulted in a significantly higher proportion of patients in the intensive care units (p definition of TBI for the children and youth population is important, as it has implications for the numbers used for policy, resource allocation, prevention, and planning of healthcare services. This paper can inform future work on reaching consensus on the diagnostic codes for defining TBI in children and youth.

What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment

Directory of Open Access Journals (Sweden)

Cesar Reis

2015-05-01

Full Text Available Traumatic brain injury (TBI, defined as an alteration in brain functions caused by an external force, is responsible for high morbidity and mortality around the world. It is important to identify and treat TBI victims as early as possible. Tracking and monitoring TBI with neuroimaging technologies, including functional magnetic resonance imaging (fMRI, diffusion tensor imaging (DTI, positron emission tomography (PET, and high definition fiber tracking (HDFT show increasing sensitivity and specificity. Classical electrophysiological monitoring, together with newly established brain-on-chip, cerebral microdialysis techniques, both benefit TBI. First generation molecular biomarkers, based on genomic and proteomic changes following TBI, have proven effective and economical. It is conceivable that TBI-specific biomarkers will be developed with the combination of systems biology and bioinformation strategies. Advances in treatment of TBI include stem cell-based and nanotechnology-based therapy, physical and pharmaceutical interventions and also new use in TBI for approved drugs which all present favorable promise in preventing and reversing TBI.

What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment

Science.gov (United States)

Reis, Cesar; Wang, Yuechun; Akyol, Onat; Ho, Wing Mann; Applegate II, Richard; Stier, Gary; Martin, Robert; Zhang, John H.

2015-01-01

Traumatic brain injury (TBI), defined as an alteration in brain functions caused by an external force, is responsible for high morbidity and mortality around the world. It is important to identify and treat TBI victims as early as possible. Tracking and monitoring TBI with neuroimaging technologies, including functional magnetic resonance imaging (fMRI), diffusion tensor imaging (DTI), positron emission tomography (PET), and high definition fiber tracking (HDFT) show increasing sensitivity and specificity. Classical electrophysiological monitoring, together with newly established brain-on-chip, cerebral microdialysis techniques, both benefit TBI. First generation molecular biomarkers, based on genomic and proteomic changes following TBI, have proven effective and economical. It is conceivable that TBI-specific biomarkers will be developed with the combination of systems biology and bioinformation strategies. Advances in treatment of TBI include stem cell-based and nanotechnology-based therapy, physical and pharmaceutical interventions and also new use in TBI for approved drugs which all present favorable promise in preventing and reversing TBI. PMID:26016501

Family Adaptation 18 Months After Traumatic Brain Injury in Early Childhood

Science.gov (United States)

Stancin, Terry; Wade, Shari L.; Walz, Nicolay C.; Yeates, Keith Owen; Taylor, H. Gerry

2014-01-01

Objective The purpose of this study was to examine family adaptation to a traumatic brain injury (TBI) in young children during the first 18-month postinjury, when compared with children who had an orthopedic injury. Methods A concurrent cohort/prospective research design was used with repeated assessments of children aged 3 to 6 years with TBI or orthopedic injury requiring hospitalization and their families. Shortly after injury and at 6-, 12-, and 18-month postinjury, parents of 99 children with TBI (20 severe, 64 moderate, 15 mild) and 117 with orthopedic injury completed standardized assessments of family functioning, parental distress and coping, injury-related burden, and noninjury-related parent stressors and resources. Mixed models analyses examined group differences in parental burden and distress adjusted for race and social demographic factors. Results Both moderate and severe TBI were associated with higher levels of injury-related stress than orthopedic injury, with stress levels diminishing over time in all groups. Severe TBI was also associated with greater psychological distress on the Brief Symptom Inventory but not with more depressive symptoms. Family functioning and social resources moderated the relationship of TBI severity to injury-related burden and caregiver distress, respectively. Lower child adaptive skills were associated with poorer family outcome but group differences remained even when controlling for this effect. Conclusions Severe TBI in young children has adverse consequences for parents and families during the first 18-month postinjury. The consequences lessen over time for many families and vary as a function of social resources. PMID:20431399

Patient Effort in Traumatic Brain Injury Inpatient Rehabilitation: Course and Associations With Age, Brain Injury Severity, and Time Postinjury.

Science.gov (United States)

Seel, Ronald T; Corrigan, John D; Dijkers, Marcel P; Barrett, Ryan S; Bogner, Jennifer; Smout, Randall J; Garmoe, William; Horn, Susan D

2015-08-01

To describe patients' level of effort in occupational, physical, and speech therapy sessions during traumatic brain injury (TBI) inpatient rehabilitation and to evaluate how age, injury severity, cognitive impairment, and time are associated with effort. Prospective, multicenter, longitudinal cohort study. Acute TBI rehabilitation programs. Patients (N=1946) receiving 138,555 therapy sessions. Not applicable. Effort in rehabilitation sessions rated on the Rehabilitation Intensity of Therapy Scale, FIM, Comprehensive Severity Index brain injury severity score, posttraumatic amnesia (PTA), and Agitated Behavior Scale (ABS). The Rehabilitation Intensity of Therapy Scale effort ratings in individual therapy sessions closely conformed to a normative distribution for all 3 disciplines. Mean Rehabilitation Intensity of Therapy Scale ratings for patients' therapy sessions were higher in the discharge week than in the admission week (Prehabilitation, differences in effort ratings (Prehabilitation admission, days from admission, and daily ratings of PTA and ABS score were predictors of level of effort (Prehabilitation setting using the Rehabilitation Intensity of Therapy Scale. Patients who sustain TBI show varying levels of effort in rehabilitation therapy sessions, with effort tending to increase over the stay. PTA and agitated behavior are primary risk factors that substantially reduce patient effort in therapies. Copyright © 2015 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.

The Potential of Stem Cells in Treatment of Traumatic Brain Injury.

Science.gov (United States)

Weston, Nicole M; Sun, Dong

2018-01-25

Traumatic brain injury (TBI) is a global public health concern, with limited treatment options available. Despite improving survival rate after TBI, treatment is lacking for brain functional recovery and structural repair in clinic. Recent studies have suggested that the mature brain harbors neural stem cells which have regenerative capacity following brain insults. Much progress has been made in preclinical TBI model studies in understanding the behaviors, functions, and regulatory mechanisms of neural stem cells in the injured brain. Different strategies targeting these cell population have been assessed in TBI models. In parallel, cell transplantation strategy using a wide range of stem cells has been explored for TBI treatment in pre-clinical studies and some in clinical trials. This review summarized strategies which have been explored to enhance endogenous neural stem cell-mediated regeneration and recent development in cell transplantation studies for post-TBI brain repair. Thus far, neural regeneration through neural stem cells either by modulating endogenous neural stem cells or by stem cell transplantation has attracted much attention. It is highly speculated that targeting neural stem cells could be a potential strategy to repair and regenerate the injured brain. Neuroprotection and neuroregeneration are major aspects for TBI therapeutic development. With technique advancement, it is hoped that stem cell-based therapy targeting neuroregeneration will be able to translate to clinic in not so far future.

Fatigue in the first year after traumatic brain injury: course, relationship with injury severity, and correlates.

Science.gov (United States)

Beaulieu-Bonneau, Simon; Ouellet, Marie-Christine

2017-10-01

The objectives of this study were to document the evolution of fatigue in the first year after traumatic brain injury (TBI), and to explore correlates of fatigue. Participants were 210 adults who were hospitalised following a TBI. They completed questionnaires 4, 8, and 12 months post-injury, including the Multidimensional Fatigue Inventory (MFI). Participants with severe TBI presented greater mental and physical fatigue, and reduced activity compared to participants with moderate TBI. For all MFI subscales except reduced motivation, the general pattern was a reduction of fatigue levels over time after mild TBI, an increase of fatigue after severe TBI, and stable fatigue after moderate TBI. Fatigue was significantly associated with depression, insomnia, cognitive difficulties, and pain at 4 months; the same variables and work status at 8 months; and depression, insomnia, cognitive difficulties, and work status at 12 months. These findings suggest that injury severity could have an impact on the course of fatigue in the first year post-TBI. Depression, insomnia, and cognitive difficulties remain strong correlates of fatigue, while for pain and work status the association with fatigue evolves over time. This could influence the development of intervention strategies for fatigue, implemented at specific times for each severity subgroup.

Factors affecting increased risk for substance use disorders following traumatic brain injury: What we can learn from animal models.

Science.gov (United States)

Merkel, Steven F; Cannella, Lee Anne; Razmpour, Roshanak; Lutton, Evan; Raghupathi, Ramesh; Rawls, Scott M; Ramirez, Servio H

2017-06-01

Recent studies have helped identify multiple factors affecting increased risk for substance use disorders (SUDs) following traumatic brain injury (TBI). These factors include age at the time of injury, repetitive injury and TBI severity, neurocircuits, neurotransmitter systems, neuroinflammation, and sex differences. This review will address each of these factors by discussing 1) the clinical and preclinical data identifying patient populations at greatest risk for SUDs post-TBI, 2) TBI-related neuropathology in discrete brain regions heavily implicated in SUDs, and 3) the effects of TBI on molecular mechanisms that may drive substance abuse behavior, like dopaminergic and glutamatergic transmission or neuroimmune signaling in mesolimbic regions of the brain. Although these studies have laid the groundwork for identifying factors that affect risk of SUDs post-TBI, additional studies are required. Notably, preclinical models have been shown to recapitulate many of the behavioral, cellular, and neurochemical features of SUDs and TBI. Therefore, these models are well suited for answering important questions that remain in future investigations. Copyright © 2017 Elsevier Ltd. All rights reserved.

Self-esteem in children after traumatic brain injury: an exploratory study.

Science.gov (United States)

Hawley, Carol A

2012-01-01

Children with a traumatic brain injury (TBI) often have difficulties in adjusting to their injury and altered abilities, and may be at risk of low self-esteem and loss of confidence. However, few studies have examined self-esteem in this client group. The current study measured the self-esteem of a group of children who were, on average, two years post-TBI and compared this to their performance on other psychometric measures. Participants were 96 children with TBI and 31 peer controls, their parents and teachers. Self-esteem was measured using the Coopersmith Self-esteem Inventory (CSEI). CSEI scores were compared with performance on Wechsler Intelligence Scales (WISC-III), Hospital Anxiety and Depression Scale (HADS); Children's Memory Scale (CMS), Vineland Adaptive Behaviour Scales (VABS) and Parental Stress Index (PSI). Self-esteem was highly correlated with IQ; HADS anxiety and depression; and parental stress (pChildren with TBI had significantly lower self-esteem than controls and population norms (p=0.015). Many children with TBI demonstrate low self-esteem and this is closely linked with anxiety and depression. This may hamper academic performance and could lead to further psychosocial problems. It is recommended that self-esteem is routinely assessed after brain injury and rehabilitation strategies implemented to promote a sense of self-worth.

A systems biology strategy to identify molecular mechanisms of action and protein indicators of traumatic brain injury.

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Yu, Chenggang; Boutté, Angela; Yu, Xueping; Dutta, Bhaskar; Feala, Jacob D; Schmid, Kara; Dave, Jitendra; Tawa, Gregory J; Wallqvist, Anders; Reifman, Jaques

2015-02-01

The multifactorial nature of traumatic brain injury (TBI), especially the complex secondary tissue injury involving intertwined networks of molecular pathways that mediate cellular behavior, has confounded attempts to elucidate the pathology underlying the progression of TBI. Here, systems biology strategies are exploited to identify novel molecular mechanisms and protein indicators of brain injury. To this end, we performed a meta-analysis of four distinct high-throughput gene expression studies involving different animal models of TBI. By using canonical pathways and a large human protein-interaction network as a scaffold, we separately overlaid the gene expression data from each study to identify molecular signatures that were conserved across the different studies. At 24 hr after injury, the significantly activated molecular signatures were nonspecific to TBI, whereas the significantly suppressed molecular signatures were specific to the nervous system. In particular, we identified a suppressed subnetwork consisting of 58 highly interacting, coregulated proteins associated with synaptic function. We selected three proteins from this subnetwork, postsynaptic density protein 95, nitric oxide synthase 1, and disrupted in schizophrenia 1, and hypothesized that their abundance would be significantly reduced after TBI. In a penetrating ballistic-like brain injury rat model of severe TBI, Western blot analysis confirmed our hypothesis. In addition, our analysis recovered 12 previously identified protein biomarkers of TBI. The results suggest that systems biology may provide an efficient, high-yield approach to generate testable hypotheses that can be experimentally validated to identify novel mechanisms of action and molecular indicators of TBI. © 2014 The Authors. Journal of Neuroscience Research Published by Wiley Periodicals, Inc.

Telomere length and advanced diffusion MRI as biomarkers for repetitive mild traumatic brain injury in adolescent rats

Directory of Open Access Journals (Sweden)

David K. Wright

Full Text Available Mild traumatic brain injuries (mTBI are of worldwide concern in adolescents of both sexes, and repeated mTBI (RmTBI may have serious long-term neurological consequences. As such, the study of RmTBI and discovery of objective biomarkers that can help guide medical decisions is an important undertaking. Diffusion-weighted MRI (DWI, which provides markers of axonal injury, and telomere length (TL are two clinically relevant biomarkers that have been implicated in a number of neurological conditions, and may also be affected by RmTBI. Therefore, this study utilized the lateral impact injury model of RmTBI to investigate changes in diffusion MRI and TL, and how these changes relate to each other. Adolescent male and female rats received either three mTBIs or three sham injuries. The first injury was given on postnatal day 30 (P30, with the repeated injuries separated by four days each. Seven days after the final injury, a sample of ear tissue was collected for TL analysis. Rats were then euthanized and whole brains were collected and fixated for MRI analyses that included diffusion and high-resolution structural sequences. Compared to the sham-injured group, RmTBI rats had significantly shorter TL at seven days post-injury. Analysis of advanced DWI measures found that RmTBI rats had abnormalities in the corpus callosum and cortex at seven days post-injury. Notably, many of the DWI changes were correlated with TL. These findings demonstrate that TL and DWI measurements are changed by RmTBI and may represent clinically applicable biomarkers for this. Keywords: Biomarker, Concussion, Track weighted imaging, Animal model, Diffusion tensor imaging, MRI

Late intellectual and academic outcomes following traumatic brain injury sustained during early childhood.

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Ewing-Cobbs, Linda; Prasad, Mary R; Kramer, Larry; Cox, Charles S; Baumgartner, James; Fletcher, Stephen; Mendez, Donna; Barnes, Marcia; Zhang, Xiaoling; Swank, Paul

2006-10-01

Although long-term neurological outcomes after traumatic brain injury (TBI) sustained early in life are generally unfavorable, the effect of TBI on the development of academic competencies is unknown. The present study characterizes intelligence quotient (IQ) and academic outcomes an average of 5.7 years after injury in children who sustained moderate to severe TBI prior to 6 years of age. Twenty-three children who suffered inflicted or noninflicted TBI between the ages of 4 and 71 months were enrolled in a prospective, longitudinal cohort study. Their mean age at injury was 21 months; their mean age at assessment was 89 months. The authors used general linear modeling approaches to compare IQ and standardized academic achievement test scores from the TBI group and a community comparison group (21 children). Children who sustained early TBI scored significantly lower than children in the comparison group on intelligence tests and in the reading, mathematical, and language domains of achievement tests. Forty-eight percent of the TBI group had IQs below the 10th percentile. During the approximately 5-year follow-up period, longitudinal IQ testing revealed continuing deficits and no recovery of function. Both IQ and academic achievement test scores were significantly related to the number of intracranial lesions and the lowest postresuscitation Glasgow Coma Scale score but not to age at the time of injury. Nearly 50% of the TBI group failed a school grade and/or required placement in self-contained special education classrooms; the odds of unfavorable academic performance were 18 times higher for the TBI group than the comparison group. Traumatic brain injury sustained early in life has significant and persistent consequences for the development of intellectual and academic functions and deleterious effects on academic performance.

Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System

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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,...

secondary injury in traumatic brain injury patients - a prospective study

African Journals Online (AJOL)

Objective. Secondary insults of hypotension and hypoxia significantly impact on outcome in patients with traumatic brain injury (TBI). More than 4 hours' delay in evacuation of intracranial haematomas has been demonstrated to have an additional impact on outcome. The objective of this study was to document the ...

Procedural discourse performance in adults with severe traumatic brain injury at 3 and 6 months post injury.

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Stubbs, Elin; Togher, Leanne; Kenny, Belinda; Fromm, Davida; Forbes, Margaret; MacWhinney, Brian; McDonald, Skye; Tate, Robyn; Turkstra, Lyn; Power, Emma

2018-01-01

There is limited research on communicative recovery during the early stages after a severe traumatic brain injury (TBI) in adults. In the current study 43 people with severe TBI described a simple procedure at 3 and 6 months post injury and this was compared to the description provided by 37 healthy speakers. Linguistic productivity and the presence of macrostructural discourse elements were analysed. No change occurred in productivity in the TBI group between the two time points. There was increased use of relevant information (macrostructure) over time for the TBI group, reflecting improvement. People with TBI differed from controls in speech rate and in two out of three macrostructural categories at both time points, indicating difficulties even after 12 weeks of recovery. Overall, the quality, rather than the quantity of discourse was disordered for participants with TBI. Findings indicate that procedural discourse is sensitive to discourse deficits of people with TBI and can be used to map recovery during the sub-acute phase.

Differential Effects of Voluntary and Forced Exercise on Stress Responses after Traumatic Brain Injury

OpenAIRE

Griesbach, Grace S.; Tio, Delia L.; Vincelli, Jennifer; McArthur, David L.; Taylor, Anna N.

2012-01-01

Voluntary exercise increases levels of brain-derived neurotrophic factor (BDNF) after traumatic brain injury (TBI) when it occurs during a delayed time window. In contrast, acute post-TBI exercise does not increase BDNF. It is well known that increases in glucocorticoids suppress levels of BDNF. Moreover, recent work from our laboratory showed that there is a heightened stress response after fluid percussion injury (FPI). In order to determine if a heightened stress response is also observed ...

An evaluation of electropalatograpby in the treatment of dysarthria following paediatric traumatic brain injury: A case study

OpenAIRE

Occomore, L.

2006-01-01

Introduction: Dysarthria is a motor speech disorder commonly associated with Traumatic Brain Injury (TBI). TBI is a substantial cause of acquired brain injury in the paediatric population, with dysarthria being a common, and often persistent, consequence of such injuries, affecting a child's ability to participate fully in a variety of functional contexts. A current lack of literature studying the efficacy of using objective, instrumental techniques in the treatment of this client group forms...

Acute alcohol intoxication in patients with mild traumatic brain injury : Characteristics, recovery, and outcome

NARCIS (Netherlands)

Scheenen, Myrthe E.; de Koning, Myrthe E.; van der Horn, Harm J.; Roks, C.M.A.A.; Yilmaz, Tansel; van der Naalt, Joukje; Spikman, Jacoba M.

2016-01-01

A substantial number of patients (30% to 50%) sustains a mild traumatic brain injury (mTBI) while they are under the influence of alcohol. An acute alcohol intoxication (AAI) at the time of injury has been subject of research in severe TBI, but little is known about the relation between AAI and

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

NARCIS (Netherlands)

Scheenen, Myrthe E.; de Koning, Myrthe E.; van der Horn, Harm; Roks, Gerwin; Yilmaz, Tansel; van der Naalt, Joukje; Spikman, Jacoba M.

2016-01-01

A substantial number of patients (30% to 50%) sustains a mild traumatic brain injury (mTBI) while they are under the influence of alcohol. An acute alcohol intoxication (AAI) at the time of injury has been subject of research in severe TBI, but little is known about the relation between AAI and

Mechanisms of dendritic spine remodeling in a rat model of traumatic brain injury.

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Campbell, John N; Low, Brian; Kurz, Jonathan E; Patel, Sagar S; Young, Matt T; Churn, Severn B

2012-01-20

Traumatic brain injury (TBI), a leading cause of death and disability in the United States, causes potentially preventable damage in part through the dysregulation of neural calcium levels. Calcium dysregulation could affect the activity of the calcium-sensitive phosphatase calcineurin (CaN), with serious implications for neural function. The present study used both an in vitro enzymatic assay and Western blot analyses to characterize the effects of lateral fluid percussion injury on CaN activity and CaN-dependent signaling in the rat forebrain. TBI resulted in an acute alteration of CaN phosphatase activity and long-lasting alterations of its downstream effector, cofilin, an actin-depolymerizing protein. These changes occurred bilaterally in the neocortex and hippocampus, appeared to persist for hours after injury, and coincided with synapse degeneration, as suggested by a loss of the excitatory post-synaptic protein PSD-95. Interestingly, the effect of TBI on cofilin in some brain regions was blocked by a single bolus of the CaN inhibitor FK506, given 1 h post-TBI. Overall, these findings suggest a loss of synapse stability in both hemispheres of the laterally-injured brain, and offer evidence for region-specific, CaN-dependent mechanisms.

Aetiology and treatment outcome of severe traumatic brain injuries ...

African Journals Online (AJOL)

Background: Severe traumatic brain injury (TBI) is a major challenge to the patient, the relatives, the care givers, and the society in general. The primary and secondary injuries, and the high metabolism are formidable stages of the injury, each capable of taking the life of the patient. The objectives were to determine the ...

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 fr...

Brain injury in a forensic psychiatry population.

Science.gov (United States)

Colantonio, A; Stamenova, V; Abramowitz, C; Clarke, D; Christensen, B

2007-12-01

The prevalence and profile of adults with a history of traumatic brain injury (TBI) has not been studied in large North American forensic mental health populations. This study investigated how adults with a documented history of TBI differed with the non-TBI forensic population with respect to demographics, psychiatric diagnoses and history of offences. A retrospective chart review of all consecutive admissions to a forensic psychiatry programme in Toronto, Canada was conducted. Information on history of TBI, psychiatric diagnoses, living environments and types of criminal offences were obtained from medical records. History of TBI was ascertained in 23% of 394 eligible patient records. Compared to those without a documented history of TBI, persons with this history were less likely to be diagnosed with schizophrenia but more likely to have alcohol/substance abuse disorder. There were also differences observed with respect to offence profiles. This study provides evidence to support routine screening for a history of TBI in forensic psychiatry.

Factors affecting mortality in severe traumatic brain injury in adults at ...

African Journals Online (AJOL)

Objective: To assess factors contributing to mortality of adult patients admitted to intensive care units for severe traumatic brain injury (TBI). Patients and methods: This is a retrospective, descriptive and analytical study. Included in the study were all adults patients admitted for severe TBI. From the hospital records, ...

Leveraging Game Consoles for the Delivery of TBI Rehabilitation

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Super, Taryn; Mastaglio, Thomas; Shen, Yuzhong; Walker, Robert

2011-01-01

Military personnel are at a greater risk for traumatic brain injury (TBI) than the civilian population. In addition, the increase in exposure to explosives, i.e. , improvised explosive devices, in the Afghanistan and Iraq wars, along with more effective body armor, has resulted in far more surviving casualties suffering from TBI than in previous wars. This effort presents the results of a feasibility study and early prototype of a brain injury rehabilitation delivery system (BIRDS). BIRDS is designed to provide medical personnel treating TBI with a capability to prescribe game activities for patients to execute using a commercially available game console, either in a clinical setting or in their homes. These therapeutic activities will contribute to recovery or remediation of the patients' cognitive dysfunctions. Solutions such as this that provide new applications for existing platforms have significant potential to address the growing incidence of TBI today.

Symptomatic heterotopic ossification after very severe traumatic brain injury in 114 patients: incidence and risk factors

DEFF Research Database (Denmark)

Simonsen, Louise Lau; Sonne-Holm, Stig; Krasheninnikoff, Michael

2007-01-01

The incidence of heterotopic ossification (HO) among patients with traumatic brain injury (TBI) varies in the literature from 11 to 73.3%. The aim of this study was to determine the incidence of HO among patients with very severe TBI treated in a new established intensive rehabilitation Brain...... Injury Unit and to list some of the risk-predicting features. The study comprised an approximately complete, consecutive series of 114 adult patients from a well-defined geographical area, and with a posttraumatic amnesia period of at least 28 days, i.e. very severe TBI. Demographic and functional data...... as well as data about trauma severity and hospital stay of these patients have been registered prospectively in a database (Danish National Head Injury database) at the Brain Injury Unit where the sub acute rehabilitation took place. The present study was based retrospectively on this database, combined...

The role of Tc-99m HMPAO brain perfusion SPECT in the psychiatric disability evaluation of patients with chronic traumatic brain injury

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So, Young [Nuclear Medicne, Seoul National Univ., Seoul (Korea, Republic of); Lee, Kang Wook; Lee, Sun Woo; Ghi, Lek Sung; Song, Chang June [College of Medicine, Chungnam National Univ., Taejon (Korea, Republic of)

2002-08-01

We studied whether brain perfusion SPECT is useful in the psychiatric disability evaluation of patients with chronic traumatic brain injury (TBI). Sixty-nine patients (M:F=58:11, age 39 {+-} 14 years) who underwent Tc-99m HMPAO brain SPECT, brain MRI and neuropsychological (NP) tests during hospitalization in psychiatric wards for the psychiatric disability evaluation were included; the severity of injury was mild in 31, moderate in 17 and severe in 21. SPECT, MRI, NP tests were performed 6 {approx} 61 months (mean 23 months) post-injury. Diagnostic accuracy of SPECT and MRI to show hypoperfusion or abnormal signal intensity in patients with cognitive impairment represented by NP test results were compared. Forty-two patients were considered to have cognitive impairment on NP tests and 27 not. Brain SPECT showed 71% sensitivity and 85% specificity, while brain MRI showed 62% sensitivity and 93% specificity (p>0.05, McNemar test). SPECT found more cortical lesions and MRI was superior in detecting white matter lesions. sensitivity and specificity of 31 mild TBI patients were 45%, 90% for SPECT and 27%, 100% for MRI (p>0.05, McNemar test). Among 41 patients with normal brain MRI, SEPCT showed 63% sensitivity (50% for mild TBI) and 88% specificity (85% for malingerers). Brain SPECT has a supplementary role to neuropsychological tests in the psychiatric disability evaluation of chronic TBI patients by detecting more cortical lesions than MRI.

The role of Tc-99m HMPAO brain perfusion SPECT in the psychiatric disability evaluation of patients with chronic traumatic brain injury

International Nuclear Information System (INIS)

So, Young; Lee, Kang Wook; Lee, Sun Woo; Ghi, Lek Sung; Song, Chang June

2002-01-01

We studied whether brain perfusion SPECT is useful in the psychiatric disability evaluation of patients with chronic traumatic brain injury (TBI). Sixty-nine patients (M:F=58:11, age 39 ± 14 years) who underwent Tc-99m HMPAO brain SPECT, brain MRI and neuropsychological (NP) tests during hospitalization in psychiatric wards for the psychiatric disability evaluation were included; the severity of injury was mild in 31, moderate in 17 and severe in 21. SPECT, MRI, NP tests were performed 6 ∼ 61 months (mean 23 months) post-injury. Diagnostic accuracy of SPECT and MRI to show hypoperfusion or abnormal signal intensity in patients with cognitive impairment represented by NP test results were compared. Forty-two patients were considered to have cognitive impairment on NP tests and 27 not. Brain SPECT showed 71% sensitivity and 85% specificity, while brain MRI showed 62% sensitivity and 93% specificity (p>0.05, McNemar test). SPECT found more cortical lesions and MRI was superior in detecting white matter lesions. sensitivity and specificity of 31 mild TBI patients were 45%, 90% for SPECT and 27%, 100% for MRI (p>0.05, McNemar test). Among 41 patients with normal brain MRI, SEPCT showed 63% sensitivity (50% for mild TBI) and 88% specificity (85% for malingerers). Brain SPECT has a supplementary role to neuropsychological tests in the psychiatric disability evaluation of chronic TBI patients by detecting more cortical lesions than MRI

Neutrophil depletion reduces edema formation and tissue loss following traumatic brain injury in mice

Directory of Open Access Journals (Sweden)

Kenne Ellinor

2012-01-01

Full Text Available Abstract Background Brain edema as a result of secondary injury following traumatic brain injury (TBI is a major clinical concern. Neutrophils are known to cause increased vascular permeability leading to edema formation in peripheral tissue, but their role in the pathology following TBI remains unclear. Methods In this study we used controlled cortical impact (CCI as a model for TBI and investigated the role of neutrophils in the response to injury. The outcome of mice that were depleted of neutrophils using an anti-Gr-1 antibody was compared to that in mice with intact neutrophil count. The effect of neutrophil depletion on blood-brain barrier function was assessed by Evan's blue dye extravasation, and analysis of brain water content was used as a measurement of brain edema formation (24 and 48 hours after CCI. Lesion volume was measured 7 and 14 days after CCI. Immunohistochemistry was used to assess cell death, using a marker for cleaved caspase-3 at 24 hours after injury, and microglial/macrophage activation 7 days after CCI. Data were analyzed using Mann-Whitney test for non-parametric data. Results Neutrophil depletion did not significantly affect Evan's blue extravasation at any time-point after CCI. However, neutrophil-depleted mice exhibited a decreased water content both at 24 and 48 hours after CCI indicating reduced edema formation. Furthermore, brain tissue loss was attenuated in neutropenic mice at 7 and 14 days after injury. Additionally, these mice had a significantly reduced number of activated microglia/macrophages 7 days after CCI, and of cleaved caspase-3 positive cells 24 h after injury. Conclusion Our results suggest that neutrophils are involved in the edema formation, but not the extravasation of large proteins, as well as contributing to cell death and tissue loss following TBI in mice.

Late-onset social anxiety disorder following traumatic brain injury.

Science.gov (United States)

Chaves, Cristiano; Trzesniak, Clarissa; Derenusson, Guilherme Nogueira; Araújo, David; Wichert-Ana, Lauro; Machado-de-Sousa, João Paulo; Carlotti, Carlos Gilberto; Nardi, Antonio E; Zuardi, Antônio W; de S Crippa, José Alexandre; Hallak, Jaime E C

2012-01-01

Neuropsychiatric sequelae are the predominant long-term disability after traumatic brain injury (TBI). This study reports a case of late-onset social anxiety disorder (SAD) following TBI. A patient that was spontaneous and extroverted up to 18-years-old started to exhibit significant social anxiety symptoms. These symptoms became progressively worse and he sought treatment at age 21. He had a previous history of traumatic brain injury (TBI) at age 17. Neuroimaging investigations (CT, SPECT and MRI) showed a bony protuberance on the left frontal bone, with mass effect on the left frontal lobe. He had no neurological signs or symptoms. The patient underwent neurosurgery with gross total resection of the lesion and the pathological examination was compatible with intradiploic haematoma. Psychiatric symptoms may be the only findings in the initial manifestation of slowly growing extra-axial space-occupying lesions that compress the frontal lobe from the outside. Focal neurological symptoms may occur only when the lesion becomes large. This case report underscores the need for careful exclusion of general medical conditions and TBI history in cases of late-onset SAD and may also contribute to the elucidation of the neurobiology of this disorder.

Anti-high mobility group box-1 antibody therapy for traumatic brain injury.

Science.gov (United States)

Okuma, Yu; Liu, Keyue; Wake, Hidenori; Zhang, Jiyong; Maruo, Tomoko; Date, Isao; Yoshino, Tadashi; Ohtsuka, Aiji; Otani, Naoki; Tomura, Satoshi; Shima, Katsuji; Yamamoto, Yasuhiko; Yamamoto, Hiroshi; Takahashi, Hideo K; Mori, Shuji; Nishibori, Masahiro

2012-09-01

High mobility group box-1 (HMGB1) plays an important role in triggering inflammatory responses in many types of diseases. In this study, we examined the involvement of HMGB1 in traumatic brain injury (TBI) and evaluated the ability of intravenously administered neutralizing anti-HMGB1 monoclonal antibody (mAb) to attenuate brain injury. Traumatic brain injury was induced in rats or mice by fluid percussion. Anti-HMGB1 mAb or control mAb was administered intravenously after TBI. Anti-HMGB1 mAb remarkably inhibited fluid percussion-induced brain edema in rats, as detected by T2-weighted magnetic resonance imaging; this was associated with inhibition of HMGB1 translocation, protection of blood-brain barrier (BBB) integrity, suppression of inflammatory molecule expression, and improvement of motor function. In contrast, intravenous injection of recombinant HMGB1 dose-dependently produced the opposite effects. Experiments using receptor for advanced glycation end product (RAGE)(-/-) , toll-like receptor-4 (TLR4)(-/-) , and TLR2(-/-) mice suggested the involvement of RAGE as the predominant receptor for HMGB1. Anti-HMGB1 mAb may provide a novel and effective therapy for TBI by protecting against BBB disruption and reducing the inflammatory responses induced by HMGB1. Copyright © 2012 American Neurological Association.

Clinical evidence of inflammation driving secondary brain injury: A systematic review

Science.gov (United States)

Hinson, Holly E.; Rowell, Susan; Schreiber, Martin

2015-01-01

Background Despite advances in both prevention and treatment, traumatic brain injury (TBI) remains one of the most burdensome diseases; 2% of the US population currently lives with disabilities resulting from TBI. Recent advances in the understanding of inflammation and its impact on the pathophysiology of trauma have increased the interest in inflammation as a possible mediator in TBI outcome. Objectives The goal of this systematic review is to address the question: “What is the evidence in humans that inflammation is linked to secondary brain injury?” As the experimental evidence has been well described elsewhere, this review will focus on the clinical evidence for inflammation as a mechanism of secondary brain injury. Data Sources Medline database (1996-Week 1 June 2014), Pubmed and Google Scholar databases were queried for relevant studies. Study Eligibility Criteria Studies were eligible if participants were adults and/or children who sustained moderate or severe TBI in the acute phase of injury, published in English. Studies published in the last decade (since 2004) were preferentially included. Trials could be observational or interventional in nature. Appraisal and Synthesis Methods To address the quality of the studies retrieved, we applied the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) criteria to assess the limitations of the included studies. Results Trauma initiates local central nervous system as well as systemic immune activation. Numerous observational studies describe elevation of pro-inflammatory cytokines that are associated with important clinical variables including neurologic outcome and mortality. A small number of clinical trials have included immunomodulating strategies, but no intervention to date has proven effective in improving outcomes after TBI. Limitations Inclusion of studies not initially retrieved by the search terms may have biased our results. Additionally, some reports may have been

Neuroprotective Effects of Platonin, a Therapeutic Immunomodulating Medicine, on Traumatic Brain Injury in Mice after Controlled Cortical Impact

Directory of Open Access Journals (Sweden)

Ting-Lin Yen

2018-04-01

Full Text Available Traumatic brain injury (TBI is one of the leading causes of mortality worldwide and leads to persistent cognitive, sensory, motor dysfunction, and emotional disorders. TBI-caused primary injury results in structural damage to brain tissues. Following the primary injury, secondary injuries which are accompanied by neuroinflammation, microglial activation, and additional cell death subsequently occur. Platonin, a cyanine photosensitizing dye, has been used to treat trauma, ulcers, and some types of acute inflammation. In the present study, the neuroprotective effects of platonin against TBI were explored in a controlled cortical impact (CCI injury model in mice. Treatment with platonin (200 µg/kg significantly reduced the neurological severity score, general locomotor activity, and anxiety-related behavior, and improved the rotarod performance of CCI-injured mice. In addition, platonin reduced lesion volumes, the expression of cleaved caspase-3, and microglial activation in TBI-insulted brains. Platonin also suppressed messenger (mRNA levels of caspase-3, caspase-1, cyclooxygenase-2, tumor necrosis factor-α, interleukin-6, and interleukin-1β. On the other hand, free radical production after TBI was obviously attenuated in platonin-treated mice. Treatment with platonin exhibited prominent neuroprotective properties against TBI in a CCI mouse model through its anti-inflammatory, anti-apoptotic, and anti-free radical capabilities. This evidence collectively indicates that platonin may be a potential therapeutic medicine for use with TBIs.

Parenting style is related to executive dysfunction after brain injury in children.

Science.gov (United States)

Potter, Jennifer L; Wade, Shari L; Walz, Nicolay C; Cassedy, Amy; Stevens, M Hank; Yeates, Keith O; Taylor, H Gerry

2011-11-01

The goal of this study was to examine how parenting style (authoritarian, authoritative, permissive) and family functioning are related to behavioral aspects of executive function following traumatic brain injury (TBI) in young children. Participants included 75 children with TBI and 97 children with orthopedic injuries (OI), ages 3-7 years at injury. Pre-injury parenting behavior and family functioning were assessed shortly after injury, and postinjury executive functions were assessed using the Behavior Rating Inventory of Executive Functioning (BRIEF; Gioia & Isquith, 2004) at 6, 12, and 18 months postinjury. Mixed model analyses, using pre-injury executive functioning (assessed by the BRIEF at baseline) as a covariate, examined the relationship of parenting style and family characteristics to executive functioning in children with moderate and severe TBI compared to OI. Among children with moderate TBI, higher levels of authoritarian parenting were associated with greater executive difficulties at 12 and 18 months following injury. Permissive and authoritative parenting styles were not significantly associated with postinjury executive skills. Finally, fewer family resources predicted more executive deficits across all of the groups, regardless of injury type. These findings provide additional evidence regarding the role of the social and familial environment in emerging behavior problems following childhood TBI.

Parenting Style Is Related to Executive Dysfunction After Brain Injury in Children

Science.gov (United States)

Potter, Jennifer L.; Wade, Shari L.; Walz, Nicolay C.; Cassedy, Amy; Yeates, Keith O.; Stevens, M. Hank; Taylor, H. Gerry

2013-01-01

Objective The goal of this study was to examine how parenting style (authoritarian, authoritative, permissive) and family functioning are related to behavioral aspects of executive function following traumatic brain injury (TBI) in young children. Method Participants included 75 children with TBI and 97 children with orthopedic injuries (OI), ages 3–7 years at injury. Pre-injury parenting behavior and family functioning were assessed shortly after injury, and postinjury executive functions were assessed using the Behavior Rating Inventory of Executive Functioning (BRIEF; Gioia & Isquith, 2004) at 6, 12, and 18 months postinjury. Mixed model analyses, using pre-injury executive functioning (assessed by the BRIEF at baseline) as a covariate, examined the relationship of parenting style and family characteristics to executive functioning in children with moderate and severe TBI compared to OI. Results Among children with moderate TBI, higher levels of authoritarian parenting were associated with greater executive difficulties at 12 and 18 months following injury. Permissive and authoritative parenting styles were not significantly associated with postinjury executive skills. Finally, fewer family resources predicted more executive deficits across all of the groups, regardless of injury type. Conclusion These findings provide additional evidence regarding the role of the social and familial environment in emerging behavior problems following childhood TBI. PMID:21928918

Mental Health in Women With Traumatic Brain Injury: A Systematic Review on Depression and Hope

Science.gov (United States)

OYESANYA, TOLU O.; WARD, EARLISE C.

2017-01-01

The prevalence of traumatic brain injury (TBI) in women has recently increased from 25% to 40%. Current literature inadequately captures challenges women face after injury, including depression. The limited focus on depression is problematic as rates of depression are increasing simultaneously with rates of TBI. A disabling symptom of depression is lack of hope; thus, depression, comorbid with TBI, leads to disability among women. Unfortunately, depression and hope among women with TBI has yet to be systematically examined. The purpose of this systematic review is to examine and synthesize current literature focusing on women with TBI, comorbid with depression, and hope. PMID:25635844

Still Making Music: How Students with Traumatic Brain Injury Can Continue with Musical Activities

Science.gov (United States)

Bennington, Patrick M.

2017-01-01

Traumatic brain injury (TBI) is common in the United States. All age groups are at risk for TBI, but there is a larger occurrence among school-age children and young adults. No matter the severity of a student's injury, he or she can benefit from music education, whether listening to music, singing, or performing on an instrument. Students can…

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

Science.gov (United States)

Ilie, Gabriela; Boak, Angela; Mann, Robert E; Adlaf, Edward M; Hamilton, Hayley; Asbridge, Mark; Rehm, Jürgen; Cusimano, Michael D

2015-01-01

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 mixed with

Differential effects of fresh frozen plasma and normal saline on secondary brain damage in a large animal model of polytrauma, hemorrhage and traumatic brain injury

DEFF Research Database (Denmark)

Hwabejire, John O; Imam, Ayesha M; Jin, Guang

2013-01-01

We have previously shown that the extent of traumatic brain injury (TBI) in large animal models can be reduced with early infusion of fresh frozen plasma (FFP), but the precise mechanisms remain unclear. In this study, we investigated whether resuscitation with FFP or normal saline differed in th...... in their effects on cerebral metabolism and excitotoxic secondary brain injury in a model of polytrauma, TBI, and hemorrhagic shock....

Differences in Marital Satisfaction, Coping and Social Support following a Traumatic Brain Injury

LENUS (Irish Health Repository)

Carroll, Aine Dr.

2009-01-01

Objective: Adverse cognitive, emotional and behavioural sequelae of Traumatic Brain Injury (TBI) are commonly noted by family members. These sequelae can adversely impact on marital and family relationships. The aim of this study is to examine marital and relationship satisfaction following a TBI amongst patients and partners. Design: A questionnaire based postal survey was used to investigate relationship and marital satisfaction. Participants: Thirty four participants (14 male; 20 female), ranging in age from 25-68 years ( = 44 years, SD 11 years), took part in this study. Sixteen had sustained a TBI and eighteen were partners of patients with TBI. Participants with TBI who were inpatients at the National Rehabilitation Hospital (NRH) and their partners were invited to participate in the study. Outcome Measures: The Marital Satisfaction Questionnaire (MSI-R) was used to examine marital and relationship satisfaction. Results: Both patients and partners reported relationship difficulties following brain injury (z = -3.078, p < .05 patients; z = 2.699, p < .05 partners). Conclusion: This study highlights the significant impact of TBI on relationships for both the TBI survivor and their partners. Implications for interventions in neuropsychological rehabilitation are discussed.

Changes in brain-behavior relationships following a 3-month pilot cognitive intervention program for adults with traumatic brain injury

OpenAIRE

S. Porter; I.J. Torres; W. Panenka; Z. Rajwani; D. Fawcett; A. Hyder; N. Virji-Babul

2017-01-01

Facilitating functional recovery following brain injury is a key goal of neurorehabilitation. Direct, objective measures of changes in the brain are critical to understanding how and when meaningful changes occur, however, assessing neuroplasticity using brain based results remains a significant challenge. Little is known about the underlying changes in functional brain networks that correlate with cognitive outcomes in traumatic brain injury (TBI). The purpose of this pilot study was to asse...

Chest Injuries Associated with Head Injury

African Journals Online (AJOL)

Traumatic brain injury (TBI) is a common cause of mortality and severe morbidity. Although there have been significant advances in management, associated severe injuries, in particular chest injuries, remain a major challenge. Extracranial injuries, especially chest injuries increase mortality in patients with TBI in both short.

Transcranial vibro-acoustography can detect traumatic brain injury, in-vivo: Preliminary studies.

Science.gov (United States)

Suarez, Martin W; Dever, David D; Gu, Xiaohan; Ray Illian, P; McClintic, Abbi M; Mehic, Edin; Mourad, Pierre D

2015-08-01

Vibro-acoustography (VA) uses two or more beams of confocal ultrasound to generate local vibrations within their target tissue through induction of a time-dependent radiation force whose frequency equals that of the difference of the applied frequencies. While VA has proven effective for assaying the mechanical properties of clinically relevant tissue such as breast lesions and tissue calcifications, its application to brain remains unexplored. Here we investigate the ability of VA to detect acute and focal traumatic brain injury (TBI) in-vivo through the use of transcranially delivered high-frequency (2 MHz) diagnostic focused ultrasound to rat brain capable of generating measurable low-frequency (200-270 kHz) acoustic emissions from outside of the brain. We applied VA to acute sham-control and TBI model rats (sham N=6; TBI N=6) and observed that acoustic emissions, captured away from the site of TBI, had lower amplitudes for TBI as compared to sham-TBI animals. The sensitivity of VA to acute brain damage at frequencies currently transmittable across human skulls, as demonstrated in this preliminary study, supports the possibility that the VA methodology may one day serve as a technique for detecting TBI. Copyright © 2015. Published by Elsevier B.V.

Friendship Quality and Psychosocial Outcomes among Children with Traumatic Brain Injury

Science.gov (United States)

Heverly-Fitt, Sara; Wimsatt, Maureen A.; Menzer, Melissa M.; Rubin, Kenneth H.; Dennis, Maureen; Taylor, Gerry; Stancin, Terry; Gerhardt, Cynthia A.; Vannatta, Kathryn; Bigler, Erin D.; Yeates, Keith Owen

2014-01-01

This study examined differences in friendship quality between children with traumatic brain injury (TBI) and orthopedic injury (OI) and behavioral outcomes for children from both groups. Participants were 41 children with TBI and 43 children with OI (M age = 10.4). Data were collected using peer- and teacher-reported measures of participants’ social adjustment and parent-reported measures of children’s post-injury behaviors. Participants and their mutually nominated best friends also completed a measure of the quality of their friendships. Children with TBI reported significantly more support and satisfaction in their friendships than children with OI. Children with TBI and their mutual best friend were more similar in their reports of friendship quality compared to children with OI and their mutual best friends. Additionally, for children with TBI who were rejected by peers, friendship support buffered against maladaptive psychosocial outcomes, and predicted skills related to social competence. Friendship satisfaction was related to higher teacher ratings of social skills for the TBI group only. Positive and supportive friendships play an important role for children with TBI, especially for those not accepted by peers. Such friendships may protect children with TBI who are rejected against maladaptive psychosocial outcomes, and promote skills related to social competence. PMID:24840021

Fitness to drive after traumatic brain injury

NARCIS (Netherlands)

Brouwer, WH; Withaar, FK

This paper deals with the issue of fitness to drive in patients suffering from traumatic brain injury (TBI). Guidelines for assessment are proposed and three types of studies are reviewed: studies about impairments of attention and information processing, studies of driving competence, and driver

A review of mild traumatic brain injury diagnostics: current perspectives, limitations, and emerging technology.

Science.gov (United States)

Cook, Glen A; Hawley, Jason S

2014-10-01

Mild traumatic brain injury (mTBI) or concussion is a common battlefield and in-garrison injury caused by transmission of mechanical forces to the head. The energy transferred in such events can cause structural and/or functional changes in the brain that manifest as focal neurological, cognitive, or behavioral dysfunction. Current diagnostic criteria for mTBI are highly limited, variable, and based on subjective self-report. The subjective nature of the symptoms, both in quantity and quality, together with their large overlap in other physical and behavioral maladies, limit the clinician's ability to accurately diagnose, treat, and make prognostic decisions after such injuries. These diagnostic challenges are magnified in an operational environment as well. The Department of Defense has invested significant resources into improving the diagnostic tools and accuracy for mTBI. This focus has been to supplement the clinician's examination with technology that is better able to objectify brain dysfunction after mTBI. Through this review, we discuss the current state of three promising technologies--soluble protein biomarkers, advanced neuroimaging, and quantitative electroencephalography--that are of particular interest within military medicine. Reprint & Copyright © 2014 Association of Military Surgeons of the U.S.

Maternal and Paternal Distress and Coping Over Time Following Pediatric Traumatic Brain Injury.

Science.gov (United States)

Narad, Megan E; Yeates, Keith O; Taylor, H Gerry; Stancin, Terry; Wade, Shari L

2017-04-01

Examine differences in maternal and paternal coping and distress following traumatic brain injury (TBI) and orthopedic injuries (OI). Concurrent cohort/prospective design with five assessments between 1 and an average of 7 years after injury of children aged 3-6 years hospitalized for TBI ( n  = 87) or OI ( n  = 119). Mixed models analyses were used to examine hypotheses. Overall, fathers reported greater depression and general distress than mothers 18 months after injury, but not at long-term follow-up. Active and acceptance coping were unrelated to parental sex, injury factors, or time since injury. A group × rater × time interaction was noted for Denial coping. Following severe TBI, fathers reported greater denial at 18 months, whereas mothers reported greater denial at the long-term follow-up. Denial coping did not differ between mothers and fathers following OI and moderate TBI. Parental response to early TBI is complex and may warrant clinical intervention even years after injury. © The Author 2016. Published by Oxford University Press on behalf of the Society of Pediatric Psychology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com

GFAP and S100B in the acute phase of mild traumatic brain injury

NARCIS (Netherlands)

Metting, Z.; Wilczak, N.; Rodiger, L. A.; Schaaf, J. M.; van der Naalt, J.

Objective: The biomarkers glial fibrillary acid protein (GFAP) and S100B are increasingly used as prognostic tools in severe traumatic brain injury (TBI). Data for mild TBI are scarce. This study aims to analyze the predictive value of GFAP and S100B for outcome in mild TBI and the relation with

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...

Prognosis in moderate and severe traumatic brain injury: External validation of the IMPACT models and the role of extracranial injuries

NARCIS (Netherlands)

Lingsma, Hester; Andriessen, Teuntje M. J. C.; Haitsema, Iain; Horn, Janneke; van der Naalt, Joukje; Franschman, Gaby; Maas, Andrew I. R.; Vos, Pieter E.; Steyerberg, Ewout W.

2013-01-01

BACKGROUND: Several prognostic models to predict outcome in traumatic brain injury (TBI) have been developed, but few are externally validated. We aimed to validate the International Mission on Prognosis and Analysis of Clinical Trials in TBI (IMPACT) prognostic models in a recent unselected patient

Hypopituitarism in pediatric survivors of inflicted traumatic brain injury.

Science.gov (United States)

Auble, Bethany A; Bollepalli, Sureka; Makoroff, Kathi; Weis, Tammy; Khoury, Jane; Colliers, Tracy; Rose, Susan R

2014-02-15

Endocrine dysfunction is common after accidental traumatic brain injury (TBI). Prevalence of endocrine dysfunction after inflicted traumatic brain injury (iTBI) is not known. The aim of this study was to examine endocrinopathy in children after moderate-to-severe iTBI. Children with previous iTBI (n=14) were evaluated for growth/endocrine dysfunction, including anthropometric measurements and hormonal evaluation (nocturnal growth hormone [GH], thyrotropin surge, morning and low-dose adrenocorticotropin stimulated cortisol, insulin-like growth factor 1, IGF-binding protein 3, free thyroxine, prolactin [PRL], and serum/urine osmolality). Analysis used Fisher's exact test and Wilcoxon's rank-sum test, as appropriate. Eighty-six percent of subjects had endocrine dysfunction with at least one abnormality, whereas 50% had two or more abnormalities, significantly increased compared to an estimated 2.5% with endocrine abnormality in the general population (p<0.001). Elevated prolactin was common (64%), followed by abnormal thyroid function (33%), short stature (29%), and low GH peak (17%). High prolactin was common in subjects with other endocrine abnormalities. Two were treated with thyroid hormone and 2 may require GH therapy. In conclusion, children with a history of iTBI show high risk for endocrine dysfunction, including elevated PRL and growth abnormalities. This effect of iTBI has not been well described in the literature. Larger, multi-center, prospective studies would provide more data to determine the extent of endocrine dysfunction in iTBI. We recommend that any child with a history of iTBI be followed closely for growth velocity and pubertal changes. If growth velocity is slow, PRL level and a full endocrine evaluation should be performed.

Expressive writing in people with traumatic brain injury and learning disability.

Science.gov (United States)

Wheeler, Lisa; Nickerson, Sherry; Long, Kayla; Silver, Rebecca

2014-01-01

There is a dearth of systematic studies of expressive writing disorder (EWD) in persons with Traumatic Brain Injury (TBI). It is unclear if TBI survivors' written expression differs significantly from that experienced by persons with learning disabilities. It is also unclear which cognitive or neuropsychological variables predict problems with expressive writing (EW) or the EWD. This study investigated the EW skill, and the EWD in adults with mild traumatic brain injuries (TBI) relative to those with learning disabilities (LD). It also determined which of several cognitive variables predicted EW and EWD. Principle Component Analysis (PCA) of writing samples from 28 LD participants and 28 TBI survivors revealed four components of expressive writing skills: Reading Ease, Sentence Fluency, Grammar and Spelling, and Paragraph Fluency. There were no significant differences between the LD and TBI groups on any of the expressive writing components. Several neuropsychological variables predicted skills of written expression. The best predictors included measures of spatial perception, verbal IQ, working memory, and visual memory. TBI survivors and persons with LD do not differ markedly in terms of expressive writing skill. Measures of spatial perception, visual memory, verbal intelligence, and working memory predict writing skill in both groups. Several therapeutic interventions are suggested that are specifically designed to improve deficits in expressive writing skills in individuals with TBI and LD.

Traumatic brain injury: caregivers' problems and needs.

Science.gov (United States)

Hassan, S T S; Khaw, W F; Rosna, A R; Husna, J

2011-01-01

Traumatic brain injury (TBI) is an increasingly major world health problem. This short review using the most pertinent articles on TBI caregiving problems and needs highlights the pressing issues. Articles focusing on both TBI-caregivers' problems and needs are rarely found, especially for developing countries. Most TBI-caregiving is done by family members, whose altered lives portend burden and stresses which add to the overwhelming demand of caring for the TBI-survivor. Lack of information, financial inadequacy, anxiety, distress, coping deficits, poor adaptability, inadequate knowledge and skills, and a poor support system comprise the major problems. Dysfunctional communication between caregivers and care-receivers has been little researched. The major needs are focused on health and rehabilitation information, financial advice and assistance, emotional and social support, and positive psychological encouragement. In time, health information needs may be met, but not emotional support. Information on TBI caregiving problems and unmet needs is critical to all relevant healthcare stakeholders.

Dietary Docosahexaenoic Acid Improves Cognitive Function, Tissue Sparing, and Magnetic Resonance Imaging Indices of Edema and White Matter Injury in the Immature Rat after Traumatic Brain Injury.

Science.gov (United States)

Schober, Michelle E; Requena, Daniela F; Abdullah, Osama M; Casper, T Charles; Beachy, Joanna; Malleske, Daniel; Pauly, James R

2016-02-15

Traumatic brain injury (TBI) is the leading cause of acquired neurologic disability in children. Specific therapies to treat acute TBI are lacking. Cognitive impairment from TBI may be blunted by decreasing inflammation and oxidative damage after injury. Docosahexaenoic acid (DHA) decreases cognitive impairment, oxidative stress, and white matter injury in adult rats after TBI. Effects of DHA on cognitive outcome, oxidative stress, and white matter injury in the developing rat after experimental TBI are unknown. We hypothesized that DHA would decrease early inflammatory markers and oxidative stress, and improve cognitive, imaging and histologic outcomes in rat pups after controlled cortical impact (CCI). CCI or sham surgery was delivered to 17 d old male rat pups exposed to DHA or standard diet for the duration of the experiments. DHA was introduced into the dam diet the day before CCI to allow timely DHA delivery to the pre-weanling pups. Inflammatory cytokines and nitrates/nitrites were measured in the injured brains at post-injury Day (PID) 1 and PID2. Morris water maze (MWM) testing was performed at PID41-PID47. T2-weighted and diffusion tensor imaging studies were obtained at PID12 and PID28. Tissue sparing was calculated histologically at PID3 and PID50. DHA did not adversely affect rat survival or weight gain. DHA acutely decreased oxidative stress and increased anti-inflammatory interleukin 10 in CCI brains. DHA improved MWM performance and lesion volume late after injury. At PID12, DHA decreased T2-imaging measures of cerebral edema and decreased radial diffusivity, an index of white matter injury. DHA improved short- and long-term neurologic outcomes after CCI in the rat pup. Given its favorable safety profile, DHA is a promising candidate therapy for pediatric TBI. Further studies are needed to explore neuroprotective mechanisms of DHA after developmental TBI.

The impact of female reproductive function on outcomes after traumatic brain injury.

Science.gov (United States)

Ripley, David L; Harrison-Felix, Cindy; Sendroy-Terrill, Melissa; Cusick, Christopher P; Dannels-McClure, Amy; Morey, Clare

2008-06-01

To determine the impact of traumatic brain injury (TBI) on female menstrual and reproductive functioning and to examine the relationships between severity of injury, duration of amenorrhea, and TBI outcomes. Retrospective cohort survey. Telephone interview. Women (N=30; age range, 18-45y), between 1 and 3 years postinjury, who had completed inpatient rehabilitation for TBI. Not applicable. Data collected included menstrual and reproductive functioning pre- and postinjury, demographic, and injury characteristics. Outcome measures included the Glasgow Outcome Scale-Extended (GOS-E), the Mayo-Portland Adaptability Inventory-4 (MPAI-4), and the Medical Outcome Study 12-Item Short-Form Health Survey, Version 2 (SF-12v2). The median duration of amenorrhea was 61 days (range, 20-344d). Many subjects' menstrual function changed after TBI, reporting a significant increase in skipped menses postinjury (PMPAI-4 participation subscale (P=.05) after controlling for age, injury severity, and time postinjury. The severity of TBI was predictive of duration of amenorrhea and a shorter duration of amenorrhea was predictive of better ratings of global outcome, community participation, and health-related quality of life postinjury.

Parental distress, parenting practices, and child adaptive outcomes following traumatic brain injury.

Science.gov (United States)

Micklewright, Jackie L; King, Tricia Z; O'Toole, Kathleen; Henrich, Chris; Floyd, Frank J

2012-03-01

Moderate and severe pediatric traumatic brain injuries (TBI) are associated with significant familial distress and child adaptive sequelae. Our aim was to examine the relationship between parental psychological distress, parenting practices (authoritarian, permissive, authoritative), and child adaptive functioning 12-36 months following TBI or orthopedic injury (OI). Injury type was hypothesized to moderate the relationship between parental distress and child adaptive functioning, demonstrating a significantly stronger relationship in the TBI relative to OI group. Authoritarian parenting practices were hypothesized to mediate relationship between parental distress and child adaptive functioning across groups. Groups (TBI n = 21, OI n = 23) did not differ significantly on age at injury, time since injury, sex, race, or SES. Parents completed the Brief Symptom Inventory, Parenting Practices Questionnaire, and Vineland-II. Moderation and mediation hypotheses were tested using hierarchical multiple regression and a bootstrapping approach, respectively. Results supported moderation and revealed that higher parental psychological distress was associated with lower child adaptive functioning in the TBI group only. Mediation results indicated that higher parental distress was associated with authoritarian parenting practices and lower adaptive functioning across groups. Results suggest that parenting practices are an important area of focus for studies attempting to elucidate the relationship between parent and child functioning following TBI.

The Neuropsychology of Traumatic Brain Injury: Looking Back, Peering Ahead.

Science.gov (United States)

Yeates, Keith Owen; Levin, Harvey S; Ponsford, Jennie

2017-10-01

The past 50 years have been a period of exciting progress in neuropsychological research on traumatic brain injury (TBI). Neuropsychologists and neuropsychological testing have played a critical role in these advances. This study looks back at three major scientific advances in research on TBI that have been critical in pushing the field forward over the past several decades: The advent of modern neuroimaging; the recognition of the importance of non-injury factors in determining recovery from TBI; and the growth of cognitive rehabilitation. Thanks to these advances, we now have a better understanding of the pathophysiology of TBI and how recovery from the injury is also shaped by pre-injury, comorbid, and contextual factors, and we also have increasing evidence that active interventions, including cognitive rehabilitation, can help to promote better outcomes. The study also peers ahead to discern two important directions that seem destined to influence research on TBI over the next 50 years: the development of large, multi-site observational studies and randomized controlled trials, bolstered by international research consortia and the adoption of common data elements; and attempts to translate research into health care and health policy by the application of rigorous methods drawn from implementation science. Future research shaped by these trends should provide critical evidence regarding the outcomes of TBI and its treatment, and should help to disseminate and implement the knowledge gained from research to the betterment of the quality of life of persons with TBI. (JINS, 2017, 23, 806-817).

Emotional recognition from dynamic facial, vocal and musical expressions following traumatic brain injury.

Science.gov (United States)

Drapeau, Joanie; Gosselin, Nathalie; Peretz, Isabelle; McKerral, Michelle

2017-01-01

To assess emotion recognition from dynamic facial, vocal and musical expressions in sub-groups of adults with traumatic brain injuries (TBI) of different severities and identify possible common underlying mechanisms across domains. Forty-one adults participated in this study: 10 with moderate-severe TBI, nine with complicated mild TBI, 11 with uncomplicated mild TBI and 11 healthy controls, who were administered experimental (emotional recognition, valence-arousal) and control tasks (emotional and structural discrimination) for each domain. Recognition of fearful faces was significantly impaired in moderate-severe and in complicated mild TBI sub-groups, as compared to those with uncomplicated mild TBI and controls. Effect sizes were medium-large. Participants with lower GCS scores performed more poorly when recognizing fearful dynamic facial expressions. Emotion recognition from auditory domains was preserved following TBI, irrespective of severity. All groups performed equally on control tasks, indicating no perceptual disorders. Although emotional recognition from vocal and musical expressions was preserved, no correlation was found across auditory domains. This preliminary study may contribute to improving comprehension of emotional recognition following TBI. Future studies of larger samples could usefully include measures of functional impacts of recognition deficits for fearful facial expressions. These could help refine interventions for emotional recognition following a brain injury.

Pathological Fingerprints, Systems Biology and Biomarkers of Blast Brain Injury

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2010-06-01

changes after blast injury. J. Trauma 56, 393–403. Murthy, J.M., Chopra, J.S., and Gulati, D.R. (1979). Subdural hematoma in an adult following a blast...neuronal damage), diffuse brain injury, and subdural hemorrhage. It is still controversial whether primary blast forces directly damage the brain, and if...emboli, leading to infarction (Guy et al., 2000a; Guy et al., 2000b). The most common types of TBI are diffuse axonal injury, contusion, and subdural

Music-Based Cognitive Remediation Therapy for Patients with Traumatic Brain Injury

OpenAIRE

Hegde, Shantala

2014-01-01

Traumatic brain injury (TBI) is one of the common causes of disability in physical, psychological, and social domains of functioning leading to poor quality of life. TBI leads to impairment in sensory, motor, language, and emotional processing, and also in cognitive functions such as attention, information processing, executive functions, and memory. Cognitive impairment plays a central role in functional recovery in TBI. Innovative methods such as music therapy to alleviate cognitive impairm...

Examination of corticothalamic fiber projections in United States service members with mild traumatic brain injury

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Rashid, Faisal M.; Dennis, Emily L.; Villalon-Reina, Julio E.; Jin, Yan; Lewis, Jeffrey D.; York, Gerald E.; Thompson, Paul M.; Tate, David F.

2017-11-01

Mild traumatic brain injury (mTBI) is characterized clinically by a closed head injury involving differential or rotational movement of the brain inside the skull. Over 3 million mTBIs occur annually in the United States alone. Many of the individuals who sustain an mTBI go on to recover fully, but around 20% experience persistent symptoms. These symptoms often last for many weeks to several months. The thalamus, a structure known to serve as a global networking or relay system for the rest of the brain, may play a critical role in neurorehabiliation and its integrity and connectivity after injury may also affect cognitive outcomes. To examine the thalamus, conventional tractography methods to map corticothalamic pathways with diffusion-weighted MRI (DWI) lead to sparse reconstructions that may contain false positive fibers that are anatomically inaccurate. Using a specialized method to zero in on corticothalamic pathways with greater robustness, we noninvasively examined corticothalamic fiber projections using DWI, in 68 service members. We found significantly lower fractional anisotropy (FA), a measure of white matter microstructural integrity, in pathways projecting to the left pre- and postcentral gyri - consistent with sensorimotor deficits often found post-mTBI. Mapping of neural circuitry in mTBI may help to further our understanding of mechanisms underlying recovery post-TBI.

Traumatic brain injury: future assessment tools and treatment prospects

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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

[International multicenter studies of treatment of severe traumatic brain injury].

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Talypov, A E; Kordonsky, A Yu; Krylov, V V

2016-01-01

Despite the introduction of new diagnostic and therapeutic methods, traumatic brain injury (TBI) remains one of the leading cause of death and disability worldwide. Standards and recommendations on conservative and surgical treatment of TBI patients should be based on concepts and methods with proven efficacy. The authors present a review of studies of the treatment and surgery of severe TBI: DECRA, RESCUEicp, STITCH(TRAUMA), CRASH, CRASH-2, CAPTAIN, NABIS: H ll, Eurotherm 3235. Important recommendations of the international group IMPACT are considered.

Inhibitory Effect on Cerebral Inflammatory Response following Traumatic Brain Injury in Rats: A Potential Neuroprotective Mechanism of N-Acetylcysteine

Directory of Open Access Journals (Sweden)

Gang Chen

2008-01-01

Full Text Available Although N-acetylcysteine (NAC has been shown to be neuroprotective for traumatic brain injury (TBI, the mechanisms for this beneficial effect are still poorly understood. Cerebral inflammation plays an important role in the pathogenesis of secondary brain injury after TBI. However, it has not been investigated whether NAC modulates TBI-induced cerebral inflammatory response. In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-κB and inflammatory proteins such as interleukin-1β (IL-1β, tumor necrosis factor-α (TNF-α, interleukin-6 (IL-6, and intercellular adhesion molecule-1 (ICAM-1 after TBI. As a result, we found that NF-κB, proinflammatory cytokines, and ICAM-1 were increased in all injured animals. In animals given NAC post-TBI, NF-κB, IL-1β, TNF-α, and ICAM-1 were decreased in comparison to vehicle-treated animals. Measures of IL-6 showed no change after NAC treatment. NAC administration reduced brain edema, BBB permeability, and apoptotic index in the injured brain. The results suggest that post-TBI NAC administration may attenuate inflammatory response in the injured rat brain, and this may be one mechanism by which NAC ameliorates secondary brain damage following TBI.