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Sample records for traumatic brain edema

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

    Science.gov (United States)

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

    2016-10-01

    Traumatic brain injury is a heterogeneous disorder resulting from an external force applied to the head. The development of cerebral edema plays a central role in the evolution of injury following brain trauma and is closely associated with neurologic outcomes. Recent advances in the understanding of the molecular and cellular pathways contributing to the posttraumatic development of cerebral edema have led to the identification of multiple prospective therapeutic targets. The authors summarize the pathogenic mechanisms underlying cerebral edema and highlight the molecular pathways that may be therapeutically targeted to mitigate cerebral edema and associated sequelae following traumatic brain injury. Copyright © 2016 Elsevier Inc. All rights reserved.

  2. Sulfonylurea Receptor-1: A Novel Biomarker for Cerebral Edema in Severe Traumatic Brain Injury.

    Science.gov (United States)

    Jha, Ruchira M; Puccio, Ava M; Chou, Sherry Hsiang-Yi; Chang, Chung-Chou H; Wallisch, Jessica S; Molyneaux, Bradley J; Zusman, Benjamin E; Shutter, Lori A; Poloyac, Samuel M; Janesko-Feldman, Keri L; Okonkwo, David O; Kochanek, Patrick M

    2017-03-01

    Cerebral edema is a key poor prognosticator in traumatic brain injury. There are no biomarkers identifying patients at-risk, or guiding mechanistically-precise therapies. Sulfonylurea receptor-1-transient receptor potential cation channel M4 is upregulated only after brain injury, causing edema in animal studies. We hypothesized that sulfonylurea receptor-1 is measurable in human cerebrospinal fluid after severe traumatic brain injury and is an informative biomarker of edema and outcome. A total of 119 cerebrospinal fluid samples were collected from 28 severe traumatic brain injury patients. Samples were retrieved at 12, 24, 48, 72 hours and before external ventricular drain removal. Fifteen control samples were obtained from patients with normal pressure hydrocephalus. Sulfonylurea receptor- 1 was quantified by enzyme-linked immunosorbent assay. Outcomes included CT edema, intracranial pressure measurements, therapies targeting edema, and 3-month Glasgow Outcome Scale score. Sulfonylurea receptor-1 was present in all severe traumatic brain injury patients (mean = 3.54 ± 3.39 ng/mL, peak = 7.13 ± 6.09 ng/mL) but undetectable in all controls (p edema (4.96 ± 1.13 ng/mL vs 2.10 ± 0.34 ng/mL; p = 0.023). There was a temporal delay between peak sulfonylurea receptor-1 and peak intracranial pressure in 91.7% of patients with intracranial hypertension. There was no association between mean/peak sulfonylurea receptor-1 and mean/peak intracranial pressure, proportion of intracranial pressure greater than 20 mm Hg, use of edema-directed therapies, decompressive craniotomy, or 3-month Glasgow Outcome Scale. However, decreasing sulfonylurea receptor-1 trajectories between 48 and 72 hours were significantly associated with improved cerebral edema and clinical outcome. Area under the multivariate model receiver operating characteristic curve was 0.881. This is the first report quantifying human cerebrospinal fluid sulfonylurea receptor-1. Sulfonylurea receptor-1 was

  3. Regional differences in cerebral edema after traumatic brain injury identified by impedance analysis.

    Science.gov (United States)

    Harting, Matthew T; Smith, Carter T; Radhakrishnan, Ravi S; Aroom, Kevin R; Dash, Pramod K; Gill, Brijesh; Cox, Charles S

    2010-03-01

    Cerebral edema is a common and potentially devastating sequel of traumatic brain injury. We developed and validated a system capable of tissue impedance analysis, which was found to correlate with cerebral edema. Constant sinusoidal current (50 microA), at frequencies from 500 to 5000 Hz, was applied across a bipolar electrode unit superficially placed in a rat brain after traumatic brain injury. Rats were randomized to three groups: severe controlled cortical injury (CCI), mild CCI, or sham injury. At 60 h post-CCI, cerebral voltage and phase angle were measured at each frequency at the site of injury, at the penumbral region, at the ipsilateral frontal region, and in the contralateral hemisphere. Impedance measurements were also obtained in vivo. The electrical properties of varied injuries and specified locations were compared using a repeated measures analysis of variance (RMANOVA), were correlated with regional tissue water percentage using regression analyses, and were combined to generate polar coordinates. The measured voltage was significantly different at the site of injury (Pimpedance measurements correlated with measured tissue water percentage at the site of injury (R2=0.69; Pimpedance areas unique to normal, mild edema, and severe edema measurements in the rat brain. Electrical measurements and tissue water percentages quantified regional and severity differences in rat brain edema after CCI. Impedance was inversely proportional to the tissue water percentage. Thus, impedance measurement can be used to quantify severity of cerebral edema in real time at specific sites. Copyright (c) 2010 Elsevier Inc. All rights reserved.

  4. Does Vasopressin Exacerbate Cerebral Edema in Patients with Severe Traumatic Brain Injury?

    Science.gov (United States)

    Allen, Casey J; Subhawong, Ty K; Hanna, Mena M; Chelala, Lydia; Bullock, M Ross; Schulman, Carl I; Proctor, Kenneth G

    2018-01-01

    Arginine vasopressin (AVP) is often used as an alternative pressor to catecholamines (CATs). However, unlike CATs, AVP is a powerful antidiuretic that could promote edema. We tested the hypothesis that AVP promoted cerebral edema and/or increased requirements for osmotherapy, relative to those who received CATs, for cerebral perfusion pressure (CPP) management after traumatic brain injury (TBI). This is a retrospective review of 286 consecutive TBI patients with intracranial pressure monitoring at a single institution from September 2008 to January 2015. Cerebral edema was quantitated using CT attenuation in prespecified areas of gray and white matter. To maintain CPP >60 mm Hg, 205 patients required no vasopressors, 41 received a single CAT, 12 received AVP, and 28 required both. Those who required no pressors were generally less injured; required less hyperosmolar therapy and less total fluid; and had lower plasma Na, lower intracranial pressure, less edema, and lower mortality (all P Edema; daily mean, minimum, and maximum Na levels; and mortality were similar with AVP versus CATs, but the daily requirement of mannitol and 3 per cent NaCl were reduced by 45 and 35 per cent (both P cerebral edema compared with CATs.

  5. Reduction of cerebral edema after traumatic brain injury using an osmotic transport device.

    Science.gov (United States)

    McBride, Devin W; Szu, Jenny I; Hale, Chris; Hsu, Mike S; Rodgers, Victor G J; Binder, Devin K

    2014-12-01

    Traumatic brain injury (TBI) is significant, from a public health standpoint, because it is a major cause of the morbidity and mortality of young people. Cerebral edema after a TBI, if untreated, can lead to devastating damage of the remaining tissue. The current therapies of severe TBI (sTBI), as outlined by the Brain Trauma Foundation, are often ineffective, thus a new method for the treatment of sTBI is necessary. Herein, the reduction of cerebral edema, after TBI, using an osmotic transport device (OTD) was evaluated. Controlled cortical impact (CCI) was performed on adult female CD-1 mice, and cerebral edema was allowed to form for 3 h, followed by 2 h of treatment. The treatment groups were craniectomy only, craniectomy with a hydrogel, OTD without bovine serum albumin (BSA), and OTD. After CCI, brain water content was significantly higher for animals treated with a craniectomy only, craniectomy with a hydrogel, and OTD without BSA, compared to that of control animals. However, when TBI animals were treated with an OTD, brain water content was not significantly higher than that of controls. Further, brain water content of TBI animals treated with an OTD was significantly reduced, compared to that of untreated TBI animals, TBI animals treated with a craniectomy and a hydrogel, and TBI animals treated with an OTD without BSA. Here, we demonstrate the successful reduction of cerebral edema, as determined by brain water content, after TBI using an OTD. These results demonstrate proof of principle for direct water extraction from edematous brain tissue by direct osmotherapy using an OTD.

  6. Near-infrared spectroscopy technique to evaluate the effects of drugs in treating traumatic brain edema

    International Nuclear Information System (INIS)

    Xie, J; Qian, Z; Li, W; Hu, G; Yang, T

    2011-01-01

    The aim of this study was to evaluate the effects of several drugs in treating traumatic brain edema (TBE) following traumatic brain injury (TBI) using near-infrared spectroscopy (NIRs) technology. Rats with TBE models were given hypertonic saline (HS), mannitol and mannitol+HS respectively for different groups. Light scattering properties of rat's local cortex was measured by NIRs within the wavelength range from 700 to 850 nm. TBE models were built in rats' left brains. The scattering properties of the right and left target corresponding to the position of normal and TBE tissue were measured and recorded in vivo and real-time by a bifurcated needle probe. The brain water contents (BWC) were measured by the wet and dry weight method after injury and treatment hours 1, 6, 24, 72 and 120. A marked linear relationship was observed between reduced scattering coefficient (μ s ') and BWC. By recording μ s ' of rats' brains, the entire progressions of effects of several drugs were observed. The result may suggest that the NIRs techniques have a potential for assessing effects in vivo and real-time on treatment of the brain injury.

  7. Rhubarb attenuates cerebral edema via inhibition of the extracellular signal-regulated kinase pathway following traumatic brain injury in rats.

    Science.gov (United States)

    Yang, Zhaoyu; Fan, Rong; Sun, Peng; Cui, Hanjin; Peng, Weijun; Luo, Jiekun; Zhang, Chunhu; Xiong, Xingui; Huang, Wei; Liu, Wei

    2018-01-01

    Rhubarb is a traditional Chinese medicine for treating traumatic brain injury (TBI). The purpose of this study is to elucidate the potential mechanism of rhubarb by suppressing extracellular signal-regulated kinase (ERK) to ameliorate brain edema. Sprague-Dawley rats were separated into four groups at random. One group received 3 g/kg rhubarb, and another group received 12 g/kg rhubarb, and the vehicle group and sham group were administered the same dose of saline solution. The blood-brain barrier disruption and edema were detected by Evans blue extravasation and water content, respectively. ERK, Matrix metalloproteinase 9 (MMP-9), and zonula occluden-1 (ZO-1) in the damaged tissue were measured by western blot analysis and quantitative real-time polymerase chain reaction. Rhubarb attenuated the brain edema after TBI, especially at the dose of 12 g/kg. Rhubarb significantly suppressed ERK, down-regulated MMP-9, and up-regulated ZO-1. Rhubarb might be a prospective therapeutic regimen to decrease edema in TBI. Rhubarb alleviates the edema by restraining the ERK signaling pathway. Our results contribute to the validation of the traditional use of rhubarb in the treatment of TBI and its mechanism. The aim of this study was to explore the potential mechanism of rhubarb by suppressing extracellular signal-regulated kinase to ameliorate brain edema. Results: Rhubarb ameliorates edema caused by traumatic brain injury by inhibiting the ERK/Matrix metalloproteinase 9/zonula occluden-1 signaling pathway. Abbreviations used: TBI: Traumatic brain injury, ERK: Extracellular signal-regulated kinase pathway, MMP-9: Matrix metalloproteinase 9, ZO-1: Zonula occluden-1, BBB: Blood-brain barrier, PCR: Polymerase chain reaction, TCM: Traditional Chinese medicine, MAPKs: Mitogen-activated protein kinases, CCI: Controlled cortical impact, DL: Rhubarb 3 g/kg in distilled water, DH: Rhubarb 12 g/kg in distilled water, EB: Evans blue, IOD: Integral optical density, MEK: Mitogen

  8. Astaxanthin alleviates cerebral edema by modulating NKCC1 and AQP4 expression after traumatic brain injury in mice.

    Science.gov (United States)

    Zhang, Mingkun; Cui, Zhenwen; Cui, Hua; Cao, Yang; Zhong, Chunlong; Wang, Yong

    2016-08-31

    Astaxanthin is a carotenoid pigment that possesses potent antioxidative, anti-inflammatory, antitumor, and immunomodulatory activities. Previous studies have demonstrated that astaxanthin displays potential neuroprotective properties for the treatment of central nervous system diseases, such as ischemic brain injury and subarachnoid hemorrhage. This study explored whether astaxanthin is neuroprotective and ameliorates neurological deficits following traumatic brain injury (TBI). Our results showed that, following CCI, treatment with astaxanthin compared to vehicle ameliorated neurologic dysfunctions after day 3 and alleviated cerebral edema and Evans blue extravasation at 24 h (p cerebral edema and that NKCC1 contributes to the upregulation of AQP4 after TBI.

  9. Quantitative analysis of computed tomography images and early detection of cerebral edema for pediatric traumatic brain injury patients: retrospective study.

    Science.gov (United States)

    Kim, Hakseung; Kim, Gwang-dong; Yoon, Byung C; Kim, Keewon; Kim, Byung-Jo; Choi, Young Hun; Czosnyka, Marek; Oh, Byung-Mo; Kim, Dong-Joo

    2014-10-22

    The purpose of this study was to identify whether the distribution of Hounsfield Unit (HU) values across the intracranial area in computed tomography (CT) images can be used as an effective diagnostic tool for determining the severity of cerebral edema in pediatric traumatic brain injury (TBI) patients. CT images, medical records and radiology reports on 70 pediatric patients were collected. Based on radiology reports and the Marshall classification, the patients were grouped as mild edema patients (n=37) or severe edema patients (n=33). Automated quantitative analysis using unenhanced CT images was applied to eliminate artifacts and identify the difference in HU value distribution across the intracranial area between these groups. The proportion of pixels with HU=17 to 24 was highly correlated with the existence of severe cerebral edema (Pcerebral edema from mild TBI patients. A significant difference between deceased patients and surviving patients in terms of the HU distribution came from the proportion of pixels with HU=19 to HU=23 (Pcerebral area of a non-enhanced CT image can be an effective basis for evaluating the severity of cerebral edema. Based on this result, we propose a novel approach for the early detection of severe cerebral edema.

  10. [Therapeutic bloodletting at Jing-well points combine hypothermia attenuated acute cerebral edema after traumatic brain injury in rats].

    Science.gov (United States)

    Miao, Xiao-mei; Cheng, Shi-xiang; Yang, Zhen; Zhang, Sai; Han, Wan-jun; Tu, Yue; Sun, Hong-tao

    2015-05-01

    To investigate the influence of therapeutic bloodletting at Jing-well points and hypothermia on acute cerebral edema after traumatic brain injury (TBI) in rats. Seventy-five SD rats were randomly divided into sham-operation group (Sham), TBI group (TBI), bloodletting group (BL), mild-induced hypothermia group (MIH), and bloodletting plus MIH group (BL + MIH) (n = 15). The model of TBI was established by electric controlled cortical impactor (eCCI). The rats of BL group were bloodletting at Jing-well points immediately after injury, twice daily. While the MIH group was settled on a hypothermia blanket promptly after TBI for 6 hours, so that the temperature dropped to 32 degrees. Each of measurement was performed after 48 hours. Magnetic resonance imaging (MRI) was used to evaluate the dynamic impairment of cerebral edema after TBI (n = 3). In addition, mNSS score, measurements of wet and dry brain weight, and Evans Blue assay were performed to investigate the neurologic deficit, cerebral water content (n = 8), and blood-brain barrier permeability (BBB), (n = 4), respectively. MRI analysis showed that the cerebral edema, hematoma and midline shifting of rats in TBI group was more serious than other treatment group. Meanwhile compared with TBI group, the mNSS scores of every treatment group were meaningfully lower (all P cerebral edema and BBB dysfunction and exert neuroprotective effects after TBI. The results suggest that the combination of BL and MIH is more effective than other treatment being used alone.

  11. Early heparin administration after traumatic brain injury: Prolonged cognitive recovery associated with reduced cerebral edema and neutrophil sequestration.

    Science.gov (United States)

    Nagata, Katsuhiro; Browne, Kevin D; Suto, Yujin; Kumasaka, Kenichiro; Cognetti, John; Johnson, Victoria E; Marks, Joshua; Smith, Douglas H; Pascual, Jose L

    2017-09-01

    Early administration of unfractionated heparin (UFH) after traumatic brain injury (TBI) reduces early in vivo circulating leukocytes (LEUs) in peri-injury penumbral brain tissue, enhancing cognitive recovery 2 days after injury. It remains unclear how long this effect lasts and if this is related to persistently accumulating LEUs in penumbral brain tissue. We hypothesized that UFH reduces LEU brain tissue sequestration resulting in prolonged cognitive recovery. CD1 male mice underwent either TBI by controlled cortical impact (CCI) or sham craniotomy. Unfractionated heparin (75 or 225 U/kg) or vehicle was repeatedly administered after TBI. Neurologic function (Garcia Neurological Test [maximum score = 18]) and body weight loss ratios were evaluated at 24 hours to 96 hours after TBI. Brain and lung wet-to-dry ratios, hemoglobin levels, and brain LEU sequestration (Ly6G immunohistochemistry) were evaluated 96 hours postmortem. Analysis of variance with Bonferroni correction determined significance (p cerebral edema to uninjured levels (77.4 ± 0.6%, p = 0.04 vs. CCI). Only UFH225 (10.6 ± 1.2 g/dL) resulted in lower hemoglobin than in uninjured animals (13.0 ± 1.2 g/dL, p edema in injured brain for up to 4 days. This is associated with persistent improved cognitive recovery, but only when low-dose UFH is given. Early administration of UFH following TBI may blunt LEU-related cerebral swelling and slow progression of secondary brain injury.

  12. Inhibition of Myosin light-chain kinase attenuates cerebral edema after traumatic brain injury in postnatal mice.

    Science.gov (United States)

    Rossi, Janet L; Todd, Tracey; Bazan, Nicolas G; Belayev, Ludmila

    2013-10-01

    Traumatic brain injury (TBI) in children less than 8 years of age leads to decline in intelligence and executive functioning. Neurological outcomes after TBI correlate to development of cerebral edema, which affect survival rates after TBI. It has been shown that myosin light-chain kinase (MLCK) increases cerebral edema and that pretreatment with an MLCK inhibitor (ML-7) reduces cerebral edema. The aim of this study was to determine whether inhibition of MLCK after TBI in postnatal day 24 (PND-24) mice would prevent breakdown of the blood-brain barrier (BBB) and development of cerebral edema and improve neurological outcome. We used a closed head injury model of TBI. ML-7 or saline treatment was administered at 4 h and every 24 h until sacrifice or 5 days after TBI. Mice were sacrificed at 24 h, 48 h, and 72 h and 7 days after impact. Mice treated with ML-7 after TBI had decreased levels of MLCK-expressing cells (20.7±4.8 vs. 149.3±40.6), less albumin extravasation (28.3±11.2 vs. 116.2±60.7 mm(2)) into surrounding parenchymal tissue, less Evans Blue extravasation (339±314 vs. 4017±560 ng/g), and showed a significant difference in wet/dry weight ratio (1.9±0.07 vs. 2.2±0.05 g), compared to saline-treated groups. Treatment with ML-7 also resulted in preserved neurological function measured by the wire hang test (57 vs. 21 sec) and two-object novel recognition test (old vs. new, 10.5 touches). We concluded that inhibition of MLCK reduces cerebral edema and preserves neurological function in PND-24 mice.

  13. Activation of P2X7 promotes cerebral edema and neurological injury after traumatic brain injury in mice.

    Science.gov (United States)

    Kimbler, Donald E; Shields, Jessica; Yanasak, Nathan; Vender, John R; Dhandapani, Krishnan M

    2012-01-01

    Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP) and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches to alleviate increased ICP remain controversial and medical therapies are lacking due in part to the absence of viable drug targets. In the present study, genetic inhibition (P2X7-/- mice) of the purinergic P2x7 receptor attenuated the expression of the pro-inflammatory cytokine, interleukin-1β (IL-1β) and reduced cerebral edema following controlled cortical impact, as compared to wild-type mice. Similarly, brilliant blue G (BBG), a clinically non-toxic P2X7 inhibitor, inhibited IL-1β expression, limited edemic development, and improved neurobehavioral outcomes after TBI. The beneficial effects of BBG followed either prophylactic administration via the drinking water for one week prior to injury or via an intravenous bolus administration up to four hours after TBI, suggesting a clinically-implementable therapeutic window. Notably, P2X7 localized within astrocytic end feet and administration of BBG decreased the expression of glial fibrillary acidic protein (GFAP), a reactive astrocyte marker, and attenuated the expression of aquaporin-4 (AQP4), an astrocytic water channel that promotes cellular edema. Together, these data implicate P2X7 as a novel therapeutic target to prevent secondary neurological injury after TBI, a finding that warrants further investigation.

  14. Activation of P2X7 promotes cerebral edema and neurological injury after traumatic brain injury in mice.

    Directory of Open Access Journals (Sweden)

    Donald E Kimbler

    Full Text Available Traumatic brain injury (TBI is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches to alleviate increased ICP remain controversial and medical therapies are lacking due in part to the absence of viable drug targets. In the present study, genetic inhibition (P2X7-/- mice of the purinergic P2x7 receptor attenuated the expression of the pro-inflammatory cytokine, interleukin-1β (IL-1β and reduced cerebral edema following controlled cortical impact, as compared to wild-type mice. Similarly, brilliant blue G (BBG, a clinically non-toxic P2X7 inhibitor, inhibited IL-1β expression, limited edemic development, and improved neurobehavioral outcomes after TBI. The beneficial effects of BBG followed either prophylactic administration via the drinking water for one week prior to injury or via an intravenous bolus administration up to four hours after TBI, suggesting a clinically-implementable therapeutic window. Notably, P2X7 localized within astrocytic end feet and administration of BBG decreased the expression of glial fibrillary acidic protein (GFAP, a reactive astrocyte marker, and attenuated the expression of aquaporin-4 (AQP4, an astrocytic water channel that promotes cellular edema. Together, these data implicate P2X7 as a novel therapeutic target to prevent secondary neurological injury after TBI, a finding that warrants further investigation.

  15. Reduction of Cerebral Edema via an Osmotic Transport Device Improves Functional Outcome after Traumatic Brain Injury in Mice.

    Science.gov (United States)

    McBride, Devin W; Donovan, Virginia; Hsu, Mike S; Obenaus, Andre; Rodgers, V G J; Binder, Devin K

    2016-01-01

    Traumatic brain injury (TBI), the foremost cause of morbidity and mortality in persons under 45 years of age worldwide, leads to about 200,000 victims requiring hospitalization and approximately 52,000 deaths per year in the United States. TBI is characterized by cerebral edema leading to raised intracranial pressure, brain herniation, and subsequent death. Current therapies for TBI treatment are often ineffective, thus novel therapies are needed. Recent studies have shown that an osmotic transport device (OTD) is capable of reducing brain water content and improving survival in mice with severe cerebral edema. Here we compare the effects of a craniectomy and an OTD plus craniectomy on neurological function in mice after TBI. Animals treated with a craniectomy plus an OTD had significantly better neurological function 2 days after TBI compared with those treated with craniectomy only. This study suggests that an OTD for severe brain swelling may improve patient functional outcome. Future studies include a more comprehensive neurological examination, including long-term memory tests.

  16. Purinergic 2Y1 receptor stimulation decreases cerebral edema and reactive gliosis in a traumatic brain injury model.

    Science.gov (United States)

    Talley Watts, Lora; Sprague, Shane; Zheng, Wei; Garling, R Justin; Jimenez, David; Digicaylioglu, Murat; Lechleiter, James

    2013-01-01

    Traumatic brain injury (TBI) is the leading cause of death and disability in children and young adults. Neuroprotective agents that may promote repair or counteract damage after injury do not currently exist. We recently reported that stimulation of the purinergic receptor subtype P2Y(1)R using 2-methylthioladenosine 5' diphosphate (2MeSADP) significantly reduced cytotoxic edema induced by photothrombosis. Here, we tested whether P2Y(1)R stimulation was neuroprotective after TBI. A controlled closed head injury model was established for mice using a pneumatic impact device. Brains were harvested at 1, 3, or 7 days post-injury and assayed for morphological changes by immunocytochemistry, Western blot analysis, and wet/dry weight. Cerebral edema and expression of both aquaporin type 4 and glial fibrillary acidic protein were increased at all time points examined. Immunocytochemical measurements in both cortical and hippocampal slices also revealed significant neuronal swelling and reactive gliosis. Treatment of mice with 2MeSADP (100 μM) or MRS2365 (100 μM) 30 min after trauma significantly reduced all post-injury symptoms of TBI including edema, neuronal swelling, reactive gliosis, and AQ4 expression. The neuroprotective effect was lost in IP(3)R2-/- mice treated with 2MeSADP. Immunocytochemical labeling of brain slices confirmed that P2Y(1)R expression was defined to cortical and hippocampal astrocytes, but not neurons. Taken together, the data show that stimulation of astrocytic P2Y(1)Rs significantly reduces brain injury after acute trauma and is mediated by the IP(3)-signaling pathway. We suggest that enhancing astrocyte mitochondrial metabolism offers a promising neuroprotective strategy for a broad range of brain injuries.

  17. High mobility group box protein-1 promotes cerebral edema after traumatic brain injury via activation of toll-like receptor 4.

    Science.gov (United States)

    Laird, Melissa D; Shields, Jessica S; Sukumari-Ramesh, Sangeetha; Kimbler, Donald E; Fessler, R David; Shakir, Basheer; Youssef, Patrick; Yanasak, Nathan; Vender, John R; Dhandapani, Krishnan M

    2014-01-01

    Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Cerebral edema, a life-threatening medical complication, contributes to elevated intracranial pressure (ICP) and a poor clinical prognosis after TBI. Unfortunately, treatment options to reduce post-traumatic edema remain suboptimal, due in part, to a dearth of viable therapeutic targets. Herein, we tested the hypothesis that cerebral innate immune responses contribute to edema development after TBI. Our results demonstrate that high-mobility group box protein 1 (HMGB1) was released from necrotic neurons via a NR2B-mediated mechanism. HMGB1 was clinically associated with elevated ICP in patients and functionally promoted cerebral edema after TBI in mice. The detrimental effects of HMGB1 were mediated, at least in part, via activation of microglial toll-like receptor 4 (TLR4) and the subsequent expression of the astrocytic water channel, aquaporin-4 (AQP4). Genetic or pharmacological (VGX-1027) TLR4 inhibition attenuated the neuroinflammatory response and limited post-traumatic edema with a delayed, clinically implementable therapeutic window. Human and rodent tissue culture studies further defined the cellular mechanisms demonstrating neuronal HMGB1 initiates the microglial release of interleukin-6 (IL-6) in a TLR4 dependent mechanism. In turn, microglial IL-6 increased the astrocytic expression of AQP4. Taken together, these data implicate microglia as key mediators of post-traumatic brain edema and suggest HMGB1-TLR4 signaling promotes neurovascular dysfunction after TBI. Copyright © 2013 Wiley Periodicals, Inc.

  18. Osmotherapy in brain edema

    DEFF Research Database (Denmark)

    Grände, Per-Olof; Romner, Bertil

    2012-01-01

    Despite the fact that it has been used since the 1960s in diseases associated with brain edema and has been investigated in >150 publications on head injury, very little has been published on the outcome of osmotherapy. We can only speculate whether osmotherapy improves outcome, has no effect......, osmotherapy can be negative for outcome, which may explain why we lack scientific support for its use. These drawbacks, and the fact that the most recent Cochrane meta-analyses of osmotherapy in brain edema and stroke could not find any beneficial effects on outcome, make routine use of osmotherapy in brain...... edema doubtful. Nevertheless, the use of osmotherapy as a temporary measure may be justified to acutely prevent brain stem compression until other measures, such as evacuation of space-occupying lesions or decompressive craniotomy, can be performed. This article is the Con part in a Pro-Con debate...

  19. Interferon-Stimulated Gene 15 Upregulation Precedes the Development of Blood-Brain Barrier Disruption and Cerebral Edema after Traumatic Brain Injury in Young Mice.

    Science.gov (United States)

    Rossi, Janet L; Todd, Tracey; Daniels, Zachary; Bazan, Nicolas G; Belayev, Ludmila

    2015-07-15

    Recent studies show that myosin light chain kinase (MLCK) plays a pivotal role in development of cerebral edema, a known complication following traumatic brain injury (TBI) in children and a contributing factor to worsened neurologic recovery. Interferon-stimulated gene 15 (ISG15) is upregulated after cerebral ischemia and is neuroprotective. The significant role of ISG15 after TBI has not been studied. Postnatal Day (PND) 21 and PND24 mice were subjected to lateral closed-skull injury with impact depth of 2.0 or 2.25 mm. Behavior was examined at 7 d using two-object novel recognition and Wire Hang tests. Mice were sacrificed at 6 h, 12 h, 24 h, 48 h, 72 h, and 7 d. ISG15 and MLCK were analyzed by Western blot and immunohistochemistry, blood-brain barrier (BBB) disruption with Evans Blue (EB), and cerebral edema with wet/dry weights. EB extravasation and edema peaked at 72 h in both ages. PND21 mice had more severe neurological deficits, compared with PND24 mice. PND24 mice showed peak ISG15 expression at 6 h, and PND21 mice at 72 h. MLCK peaked in both age groups at 12 h and co-localized with ISG15 on immunohistochemistry and co-immunoprecipitation. These studies provide evidence, ISG15 is elevated following TBI in mice, preceding MLCK elevation, development of BBB disruption, and cerebral edema.

  20. Delayed Administration of BQ788, an ETB Antagonist, after Experimental Traumatic Brain Injury Promotes Recovery of Blood-Brain Barrier Function and a Reduction of Cerebral Edema in Mice.

    Science.gov (United States)

    Michinaga, Shotaro; Kimura, Akimasa; Hatanaka, Shunichi; Minami, Shizuho; Asano, Arisa; Ikushima, Yuki; Matsui, Shingo; Toriyama, Yoshiya; Fujii, Manami; Koyama, Yutaka

    2018-03-20

    Traumatic brain injury (TBI) is induced by immediate physical disruption of brain tissue, and causes death and disability. Studies on experimental TBI animal models show that disruption of the blood-brain barrier (BBB) underlies brain edema and neuroinflammation during the delayed phase of TBI. In neurological disorders, endothelin-1 (ET-1) is involved in BBB dysfunction and brain edema. In this study, the effect of ET antagonists on BBB dysfunction and brain edema were examined in a mouse focal TBI model using lateral fluid percussion injury (FPI). ET-1 and ET B receptors were increased at 2-7 days after FPI, which was accompanied by extravasation of Evans blue (EB) and brain edema. Repeated intracerebroventricular administration of BQ788 (15 nmol/day), an ET B antagonist, from 2 days after FPI promoted recovery of EB extravasation and brain edema, while FR 139317, an ET A antagonist, had no effect. Delayed intravenous administration of BQ788 also promoted recovery from FPI-induced EB extravasation and brain edema. While FPI caused decreases in claudin-5, occludin, and zonula occludens-1 proteins, BQ788 reversed FPI-induced reductions of them. Immunohistochemical observation of the cerebrum after FPI showed that ET B receptors are predominantly expressed in glial fibrillary acidic protein (GFAP)-positive astrocytes. BQ788 reduced FPI-induced increases in GFAP-positive astrocytes. GFAP-positive astrocytes produced vascular endothelial growth factor-A (VEGF-A) and matrix metalloproteinase-9 (MMP9). FPI-induced increases in VEGF-A and MMP-9 production were reversed by BQ788. These results suggest that ET B receptor antagonism during the delayed phase of focal TBI promotes recovery of BBB function and reduction of brain edema.

  1. Enoxaparin ameliorates post-traumatic brain injury edema and neurologic recovery, reducing cerebral leukocyte endothelial interactions and vessel permeability in vivo.

    Science.gov (United States)

    Li, Shengjie; Marks, Joshua A; Eisenstadt, Rachel; Kumasaka, Kenichiro; Samadi, Davoud; Johnson, Victoria E; Holena, Daniel N; Allen, Steven R; Browne, Kevin D; Smith, Douglas H; Pascual, Jose L

    2015-07-01

    Traumatic brain injury (TBI) confers a high risk of venous thrombosis, but early prevention with heparinoids is often withheld, fearing cerebral hematoma expansion. Yet, studies have shown heparinoids not only to be safe but also to limit brain edema and contusion size after TBI. Human TBI data also suggest faster radiologic and clinical neurologic recovery with earlier heparinoid administration. We hypothesized that enoxaparin (ENX) after TBI blunts in vivo leukocyte (LEU) mobilization to injured brain and cerebral edema, while improving neurologic recovery without increasing the size of the cerebral hemorrhagic contusion. CD1 male mice underwent either TBI by controlled cortical impact (CCI, 1-mm depth, 6 m/s) or sham craniotomy. ENX (1 mg/kg) or vehicle (VEH, 0.9% saline, 1 mL/kg) was administered at 2, 8, 14, 23, and 32 hours after TBI. At 48 hours, intravital microscopy was used to visualize live LEUs interacting with endothelium and microvascular leakage of fluorescein isothiocyanate-albumin. Neurologic function (Neurological Severity Score, NSS), activated clotting time, hemorrhagic contusion size, as well as brain and lung wet-to-dry ratios were evaluated post mortem. Analysis of variance with Bonferroni correction was used for statistical comparisons between groups. Compared with VEH, ENX significantly reduced in vivo LEU rolling on endothelium (72.7 ± 28.3 LEU/100 μm/min vs. 30.6 ± 18.3 LEU/100 μm/min, p = 0.02) and cerebrovascular albumin leakage (34.5% ± 8.1% vs. 23.8% ± 5.5%, p = 0.047). CCI significantly increased ipsilateral cerebral hemisphere edema, but ENX treatment reduced post-CCI edema to near control levels (81.5% ± 1.5% vs. 77.6% ± 0.6%, p edema. ENX may also accelerate neurologic recovery without increasing cerebral contusion size. Further study in humans is necessary to determine safety, appropriate dosage, and timing of ENX administration early after TBI.

  2. Decompressive surgery for severe brain edema.

    Science.gov (United States)

    Diedler, Jennifer; Sykora, Marek; Blatow, Maria; Jüttler, Eric; Unterberg, Andreas; Hacke, Werner

    2009-01-01

    Decompressive surgery has since long been a promising therapeutic approach for patients with acute severe brain injury at risk to develop severe brain edema. The underlying rationale of removing part of the cranium is to create space for the expanding brain to prevent secondary damage to vital brain tissue. However, until recently, randomized controlled trials that demonstrate the efficacy of decompressive surgery or benefit for outcome were missing. This has changed since the results of 3 randomized trials on hemicraniectomy in malignant infarction of the middle cerebral artery have been published in 2007. In this article, the current evidence for decompressive surgery in the treatment of cerebral ischemia, intracranial hemorrhage, traumatic brain injury, inflammatory diseases, or severe metabolic derangements is reviewed. Although there is increasing evidence for the efficacy of decompressive surgery in reducing intracranial pressure and even mortality, a critical point remains the definition of good or acceptable outcome.

  3. Glibenclamide produces region-dependent effects on cerebral edema in a combined injury model of traumatic brain injury and hemorrhagic shock in mice.

    Science.gov (United States)

    Jha, Ruchira; Molyneaux, Bradley J; Jackson, Travis C; Wallisch, Jessica; Park, Seo-Young; Poloyac, Samuel M; Vagni, Vincent A; Janesko-Feldman, Keri L; Hoshitsuki, Keito; Minnigh, Margaret Beth; Kochanek, Patrick M

    2018-03-08

    Cerebral edema is critical to morbidity/mortality in TBI and is worsened by hypotension. Glibenclamide may reduce cerebral edema by inhibiting sulfonylurea receptor-1 (Sur1); its effect on diffuse cerebral edema exacerbated by hypotension/resuscitation is unknown. We aimed to determine if glibenclamide improves pericontusional and/or diffuse edema in controlled cortical impact (CCI, 5m/s, 1 mm-depth)+hemorrhagic shock (HS, 35 minutes), and compare its effects in CCI alone. C57/BL6 mice were divided into 5 groups (n=10/group): naïve, CCI+vehicle, CCI+glibenclamide, CCI+HS+vehicle, and CCI+HS+glibenclamide. Intravenous glibenclamide (10min post-injury) was followed by a subcutaneous infusion for 24h. Brain edema in injured and contralateral hemispheres was subsequently quantified (wet-dry weight). This protocol was also followed for 72h in CCI+HS (n=9/group). Ipsilateral (I) edema was greater in CCI+HS (I%BW=80.4% vehicle vs 78.3% naïve, pedema also developed in CCI alone (I%BW= 80.2% vehicle vs 78.3% naïve, pcerebral edema (C%BW=78.3%) with no difference vs naïve. By 72h, contralateral cerebral edema had resolved (C%BW=78.5±0.09% vehicle vs 78.3±0.05% naïve). Glibenclamide decreases 24h contralateral cerebral edema in CCI+HS. This beneficial effect merits additional exploration in the important setting of TBI with polytrauma, shock, and resuscitation. Contralateral edema did not develop in CCI alone. Surprisingly, 24h of glibenclamide treatment failed to decrease ipsilateral edema in either model. Inter-species dosing differences vs prior studies may play an important role in these findings. Mechanisms underlying brain edema may differ regionally, with pericontusional/osmolar swelling refractory to glibenclamide but diffuse edema (via Sur1) from combined injury and/or resuscitation responsive to this therapy. TBI phenotype may mandate precision medicine approaches to treat brain edema.

  4. Dynamics of cerebral edema and the apparent diffusion coefficient of water changes in patients with severe traumatic brain injury. A prospective MRI study

    International Nuclear Information System (INIS)

    Pasco, Anne; Minassian, Aram Ter; Chapon, Catherine; Lemaire, Laurent; Benoit, Jean-Pierre; Jeune, Jean-Jacques Le; Franconi, Florence; Darabi, Dana; Caron, Christine

    2006-01-01

    The distinction between intracellular (ICE) and extracellular edema (ECE) has a crucial prognostic and therapeutic importance in patients with severe traumatic brain injury (STBI). Indeed, ICE usually leads to cellular death, and maintenance of a cerebral perfusion pressure (CPP) above 70 mmHg is still under debate since this practice may increase ECE. The purpose of this study was to describe the ECE and ICE kinetics associated with STBI using quantitative diffusion MRI. Twelve patients were prospectively studied. The initial ADC in ICE measured on day 1.3±0.7 is significantly reduced compared to normal-appearing parenchyma (0.51±0.12 * 10 -3 mm 2 /s vs. 0.76±0.03 * 10 -3 mm 2 /s, n=12, P MRI2 =0.40±0.11 * 10 -3 mm 2 /s), ADC values in the extension area at the first MRI were slightly, but not significantly reduced compared to normal parenchyma (0.69±0.05 * 10 -3 mm 2 /s, P=0.29). Normalization occurred equally by day 14. ADC in ECE (1.34±0.22 * 10 -3 mm 2 /s) was elevated and stable with time under CPP therapy. Therefore, ECE is not worsened by CCP therapy, and ICE appears more relevant than ECE in STBI. (orig.)

  5. Dynamics of cerebral edema and the apparent diffusion coefficient of water changes in patients with severe traumatic brain injury. A prospective MRI study

    Energy Technology Data Exchange (ETDEWEB)

    Pasco, Anne [Larrey Hospital, Angers University, Department of Radiology, Cedex (France); Inserm, Angers (France); Angers University, Angers (France); Minassian, Aram Ter [Larrey Hospital, Angers University, Department of Anaesthesiology, Cedex (France); Chapon, Catherine; Lemaire, Laurent; Benoit, Jean-Pierre; Jeune, Jean-Jacques Le [Inserm, Angers (France); Angers University, Angers (France); Franconi, Florence [Angers University, SCAS, Angers (France); Darabi, Dana; Caron, Christine [Larrey Hospital, Angers University, Department of Radiology, Cedex (France)

    2006-07-15

    The distinction between intracellular (ICE) and extracellular edema (ECE) has a crucial prognostic and therapeutic importance in patients with severe traumatic brain injury (STBI). Indeed, ICE usually leads to cellular death, and maintenance of a cerebral perfusion pressure (CPP) above 70 mmHg is still under debate since this practice may increase ECE. The purpose of this study was to describe the ECE and ICE kinetics associated with STBI using quantitative diffusion MRI. Twelve patients were prospectively studied. The initial ADC in ICE measured on day 1.3{+-}0.7 is significantly reduced compared to normal-appearing parenchyma (0.51{+-}0.12 * 10{sup -3} mm{sup 2}/s vs. 0.76{+-}0.03 * 10{sup -3} mm{sup 2}/s, n=12, P<0.0001) and reaches normality on MRI 3 performed on day 14.2{+-}3.3. In patients presenting an extension of ICE on MRI 2 performed on day 6.7{+-}1.4 (ADC{sub MRI2}=0.40{+-}0.11 * 10{sup -3} mm{sup 2}/s), ADC values in the extension area at the first MRI were slightly, but not significantly reduced compared to normal parenchyma (0.69{+-}0.05 * 10{sup -3} mm{sup 2}/s, P=0.29). Normalization occurred equally by day 14. ADC in ECE (1.34{+-}0.22 * 10{sup -3} mm{sup 2}/s) was elevated and stable with time under CPP therapy. Therefore, ECE is not worsened by CCP therapy, and ICE appears more relevant than ECE in STBI. (orig.)

  6. Traumatic Brain Injury

    Science.gov (United States)

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

  7. Brain edema associated with unruptured brain arteriovenous malformations

    International Nuclear Information System (INIS)

    Kim, Bum-soo; Sarma, Dipanka; Lee, Seon-Kyu; ter Brugge, Karel G.

    2009-01-01

    Brain edema in unruptured brain arteriovenous malformations (AVMs) is rare; this study examines (1) its frequency and clinical presentation, (2) imaging findings with emphasis on venous drainage abnormalities, and (3) implications of these findings on natural history and management. Presentation and imaging features of all unruptured brain AVMs were prospectively collected in our brain AVM database. Neurological findings, size, location, venous drainage pattern, presence of venous thrombosis, ectasia, or stenosis, and brain edema were specifically recorded. Treatment details of all patients with brain edema and their clinical and imaging follow-up were reviewed. Finally, a comparison was made between patients with and without edema. Brain edema was found in 13/329 unruptured brain AVMs (3.9%). Neurological deficit (46.2%), venous thrombosis (38.5%), venous ectasia (84.6%), stenosis (38.5%), and contrast stagnation in the draining veins (84.6%) were more frequent in patients with brain edema than without edema. Eight patients with brain edema received specific treatment (embolization = 5, surgery = 2, radiosurgery = 1). Clinical features correlated well with change in degree of edema in six. Three of five embolized patients were stable or showed improvement after the procedure. On follow-up, however, intracranial hemorrhage developed in three. Brain edema in unruptured brain AVMs is rare, 3.9% in this series. Venous outflow abnormalities are frequently associated and appear to contribute to the development of edema. Progressive nonhemorrhagic symptoms are also associated, with a possible increased risk of hemorrhage. Palliative embolization arrests the nonhemorrhagic symptoms in selected patients, although it may not have an effect on hemorrhagic risk. (orig.)

  8. Peritumoral brain edema in angiomatous supratentorial meningiomas

    DEFF Research Database (Denmark)

    Nassehi, Damoun; Sørensen, Lars Peter; Dyrbye, Henrik

    2013-01-01

    The aim of this work was to study the vascular endothelial growth factor A (VEGF-A) pathway and peritumoral brain edema (PTBE) through comparison of non-angiomatous and angiomatous meningiomas. Meningiomas are common intracranial tumors, which often have PTBE. VEGF-A is an integral part of PTBE...

  9. Pathogenesis of Brain Edema and Investigation into Anti-Edema Drugs

    Directory of Open Access Journals (Sweden)

    Shotaro Michinaga

    2015-04-01

    Full Text Available Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head trauma. In the edematous brain, excess accumulation of extracellular fluid results in elevation of intracranial pressure, leading to impaired nerve function. Despite the seriousness of brain edema, only symptomatic treatments to remove edema fluid are currently available. Thus, the development of novel anti-edema drugs is required. The pathogenesis of brain edema is classified as vasogenic or cytotoxic edema. Vasogenic edema is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB and extravasations of serum proteins, while cytotoxic edema is characterized by cell swelling caused by intracellular accumulation of fluid. Various experimental animal models are often used to investigate mechanisms underlying brain edema. Many soluble factors and functional molecules have been confirmed to induce BBB disruption or cell swelling and drugs targeted to these factors are expected to have anti-edema effects. In this review, we discuss the mechanisms and involvement of factors that induce brain edema formation, and the possibility of anti-edema drugs targeting them.

  10. Effects of dexamethasone on brain edema

    International Nuclear Information System (INIS)

    Takemoto, Motohisa

    1982-01-01

    Experimental cerebral edema was produced on the right parietal lobe of Wistar male rats with a cold metal probe cooled by liquid nitrogen. Twenty hour later, 3 H-dexamethasone was either intramuscularly or intravenously injected into rats, estimated in the brain tissue by the liquid scintillation counting method. Edematous brain generally contained much higher 3 H-activity than the control. Furthermore, I.V. injection showed higher 3 H-activity than I.M injection in edematous and control brains at all times. For examination of the subcellular distribution of 3 H-dexamethasone in edematous brain, 3 H-activity was most strongly detected in the supernatant fraction (63%), followed by the heavy mitochondrial fraction (25.4%) and the nuclear fraction (8.4%). Although edematous brain tissue constantly demonstrated higher 3 H-activity than the control, its supernatant fraction conversely had less activity. As a next step, distribution of 3 H-dexamethasone in the supernatant fraction was studies. The result was that the high molecular weight fraction in the edematous brain showed higher radioactivity than the control. From these findings, unequivocal distribution of dexamethasone in the supernatant fraction of edematous brain tissue could be correlated with its biochemical action for preventing brain edema. (J.P.N.)

  11. Traumatic Brain Injury and Aggression.

    Science.gov (United States)

    Miller, Laurence

    1994-01-01

    Persons who have suffered traumatic injury to the brain may subsequently display aggressive behavior. Three main syndromes of aggression following traumatic brain injury are described: (1) episodic dyscontrol; (2) frontal lobe disinhibition; and (3) exacerbation of premorbid antisociality. The neuropsychological substrates of these syndromes are…

  12. Traumatic Brain Injury - Multiple Languages

    Science.gov (United States)

    ... Supplements Videos & Tools You Are Here: Home → Multiple Languages → All Health Topics → Traumatic Brain Injury URL of this page: https://medlineplus.gov/ ... W XYZ List of All Topics All Traumatic Brain Injury - Multiple Languages To use the sharing features on this page, ...

  13. Cognitive retraining in traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Diya Nangia

    2012-04-01

    Full Text Available Traumatic brain injury (TBI is often associated with cognitive impairments. The psychological sequelae of cognitive deficits and emotional problems contribute significantly to the disability in the patient and to the distress of the family. The study aimed to develop a cognitive retraining programme to enhance cognitive functioning in TBI. 25 years old male presenting with history of left temporal hemorrhagic contusion with cerebral edema underwent 2 months of a cognitive retaining programme, addressing executive functions impairment. A single case experimental design with pre- and post-assessment was adopted to evaluate changes in the patient in response to the intervention. Improvements were found in cognitive functioning, and in symptom reduction and behaviour. The 2 months hospital based cognitive retraining programme was found to be efficacious in ameliorating symptoms and improving cognitive, social and occupational functioning post traumatic brain injury.

  14. Post-traumatic contrast enhancing brain lesion

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Dae Jung; Kim, Hyun Sook; Jeong, Min Sun; Kim, Deok Ryeong; Cho, Young Kwon; Choi, Yun Sun [Eulji Hospital, Eulji University College of Medicine, Seoul (Korea, Republic of)

    2014-10-15

    Only a few studies have been reported on the MR contrast enhancement and the apparent diffusion coefficient (ADC) findings of the post-traumatic lesion of the brain. We report a case of the venous ischemia in the left frontal lobe observed in the MRI obtained one day after the incidence of trauma. Considering the presented slight increase in the ADC, the vasogenic edema was thought to be the major mechanism of the venous ischemia and excitotoxic injury. In spite of a slight increase in the ADC, the hyperintensity in the diffusion weighted imaging and contrast-enhanced areas eventually changed into hemorrhagic lesions.

  15. Isolated brain stem edema in a pediatric patient with head trauma: a case report.

    Science.gov (United States)

    Basarslan, K; Basarslan, F; Karakus, A; Yilmaz, C

    2015-01-01

    Brain stem is the most vital part of our body and is a transitional region of the brain that connects the cerebrum with the spinal cord. Though, being small in size, it is full of indispensible functions such as the breathing, heart beat. Injury to the brain stem has similar effects as a brain injury, but it is more fatal. Use of the Glasgow Coma Score as a prognostic indicator of outcome in patients with head injuries is widely accepted in clinical practice. Traumatic brain stem edema in children is rare, but is associated with poor outcome. The question is that whether it is being aware of computerized tomography appearance of the posterior fossa when initial evaluating pediatric patients with head trauma at emergency clinics. Normal and edematous brain stem without an additional pathology are slightly different and not distinguished easily. On the other hand, brain stem edema should be promptly identified and appropriately treated in a short time.

  16. Traumatic Brain Injury Registry (TBI)

    Data.gov (United States)

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

  17. Telmisartan reduced cerebral edema by inhibiting NLRP3 inflammasome in mice with cold brain injury.

    Science.gov (United States)

    Wei, Xin; Hu, Chen-Chen; Zhang, Ya-Li; Yao, Shang-Long; Mao, Wei-Ke

    2016-08-01

    The aim of this study was to investigate the possible beneficial role of telmisartan in cerebral edema after traumatic brain injury (TBI) and the potential mechanisms related to the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) pyrin domain-containing 3 (NLRP3) inflammasome activation. TBI model was established by cold-induced brain injury. Male C57BL/6 mice were randomly assigned into 3, 6, 12, 24, 48 and 72 h survival groups to investigate cerebral edema development with time and received 0, 5, 10, 20 and 40 mg/kg telmisartan by oral gavage, 1 h prior to TBI to determine the efficient anti-edemic dose. The therapeutic window was identified by post-treating 30 min, 1 h, 2 h and 4 h after TBI. Blood-brain barrier (BBB) integrity, the neurological function and histological injury were assessed, at the same time, the mRNA and protein expression levels of NLRP3 inflammasome, IL-1β and IL-18 concentrations in peri-contused brain tissue were measured 24 h post TBI. The results showed that the traumatic cerebral edema occurred from 6 h, reached the peak at 24 h and recovered to the baseline 72 h after TBI. A single oral dose of 5, 10 and 20 mg/kg telmisartan could reduce cerebral edema. Post-treatment up to 2 h effectively limited the edema development. Furthermore, prophylactic administration of telmisartan markedly inhibited BBB impairment, NLRP3, apoptotic speck-containing protein (ASC) and Caspase-1 activation, as well as IL-1β and IL-18 maturation, subsequently improved the neurological outcomes. In conclusion, telmisartan can reduce traumatic cerebral edema by inhibiting the NLRP3 inflammasome-regulated IL-1β and IL-18 accumulation.

  18. Monte Carlo and phantom study in the brain edema models

    Directory of Open Access Journals (Sweden)

    Yubing Liu

    2017-05-01

    Full Text Available Because the brain edema has a crucial impact on morbidity and mortality, it is important to develop a noninvasive method to monitor the process of the brain edema effectively. When the brain edema occurs, the optical properties of the brain will change. The goal of this study is to access the feasibility and reliability of using noninvasive near-infrared spectroscopy (NIRS monitoring method to measure the brain edema. Specifically, three models, including the water content changes in the cerebrospinal fluid (CSF, gray matter and white matter, were explored. Moreover, these models were numerically simulated by the Monte Carlo studies. Then, the phantom experiments were performed to investigate the light intensity which was measured at different detecting radius on the tissue surface. The results indicated that the light intensity correlated well with the conditions of the brain edema and the detecting radius. Briefly, at the detecting radius of 3.0cm and 4.0cm, the light intensity has a high response to the change of tissue parameters and optical properties. Thus, it is possible to monitor the brain edema noninvasively by NIRS method and the light intensity is a reliable and simple parameter to assess the brain edema.

  19. Drowning stars: Reassessing the role of astrocytes in brain edema

    Science.gov (United States)

    Thrane, Alexander S.; Thrane, Vinita Rangroo; Nedergaard, Maiken

    2014-01-01

    Edema formation frequently complicates brain infarction, tumors and trauma. Despite the significant mortality of this condition, current treatment options are often ineffective or incompletely understood. Recent studies have revealed the existence of a brain-wide paravascular pathway for cerebrospinal (CSF) and interstitial fluid (ISF) exchange. The current review critically examines the contribution of this ‘glymphatic’ system to the main types of brain edema. We propose that in cytotoxic edema, energy depletion enhances glymphatic CSF influx, whilst suppressing ISF efflux. We also argue that paravascular inflammation or ‘paravasculitis’ plays a critical role in vasogenic edema. Finally, recent advances in diagnostic imaging of glymphatic function may hold the key to defining the edema profile of individual patients and thus enable more targeted therapy. PMID:25236348

  20. Critical Care Management of Cerebral Edema in Brain Tumors.

    Science.gov (United States)

    Esquenazi, Yoshua; Lo, Victor P; Lee, Kiwon

    2017-01-01

    Cerebral edema associated with brain tumors is extremely common and can occur in both primary and metastatic tumors. The edema surrounding brain tumors results from leakage of plasma across the vessel wall into the parenchyma secondary to disruption of the blood-brain barrier. The clinical signs of brain tumor edema depend on the location of the tumor as well as the extent of the edema, which often exceeds the mass effect induced by the tumor itself. Uncontrolled cerebral edema may result in increased intracranial pressure and acute herniation syndromes that can result in permanent neurological dysfunction and potentially fatal herniation. Treatment strategies for elevated intracranial pressure consist of general measures, medical interventions, and surgery. Alhough the definitive treatment for the edema may ultimately be surgical resection of the tumor, the impact of the critical care management cannot be underestimated and thus patients must be vigilantly monitored in the intensive care unit. In this review, we discuss the pathology, pathophysiology, and clinical features of patients presenting with cerebral edema. Imaging findings and treatment modalities used in the intensive care unit are also discussed. © The Author(s) 2015.

  1. Traumatic brain injury : from impact to rehabilitation

    NARCIS (Netherlands)

    Halliday, J.; Absalom, A. R.

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

  2. 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...

  3. Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.

    Science.gov (United States)

    Timaru-Kast, Ralph; Luh, Clara; Gotthardt, Philipp; Huang, Changsheng; Schäfer, Michael K; Engelhard, Kristin; Thal, Serge C

    2012-01-01

    After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurologic function, cerebral and systemic inflammation (CD3+ T cell migration, inflammatory cytokine expression in brain and lung, blood differential cell count) were determined. Old animals showed worse neurological function 72 h after CCI and a high mortality rate (19.2%) compared to young (0%). This did not correlate with histopathological damage, as contusion volumes were equal in both age groups. Although a more pronounced brain edema formation was detected in old mice 24 hours after TBI, lack of correlation between brain water content and neurological deficit indicated that brain edema formation is not solely responsible for age-dependent differences in neurological outcome. Brains of old naïve mice were about 8% smaller compared to young naïve brains, suggesting age-related brain atrophy with possible decline in plasticity. Onset of cerebral inflammation started earlier and primarily ipsilateral to damage in old mice, whereas in young mice inflammation was delayed and present in both hemispheres with a characteristic T cell migration pattern. Pulmonary interleukin 1β expression was up-regulated after cerebral injury only in young, not aged mice. The results therefore indicate that old animals are prone to functional deficits and strong ipsilateral cerebral inflammation

  4. Traumatic Brain Injury

    Science.gov (United States)

    ... not always visible on your skin. A skull fracture is when the skull cracks. Sometimes broken bones cut into your brain and cause bleeding or ... brain. They show if there is a skull fracture or bleeding, bruising, or blood ... skating, horse riding, and skiing and snowboarding avoid dangerous sports ...

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

    Directory of Open Access Journals (Sweden)

    Hui Liu

    2012-03-01

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

  6. Edema

    Science.gov (United States)

    ... breathing Chest pain These can be signs of pulmonary edema, which requires prompt treatment. If you've been ... can cause fluid to accumulate in your lungs (pulmonary edema), which can lead to shortness of breath. Cirrhosis. ...

  7. The spreading of focal brain edema induced by ultraviolet irradiation

    International Nuclear Information System (INIS)

    Ferszt, R.; Neu, S.; Cervos-Navarro, J.; Sperner, J.

    1978-01-01

    Focal brain edema limited to one cerebral hemisphere was produced by ultraviolet irradiation of the exposed cortex. Tissue water content was determined by the gravimetric method which allows microsampling. Therefore, the spread of edema around the small necrotic area be mapped more precisely than by determination of dry weight which calls for larger samples. As early as 30 min after irradiation, hyperemia and swelling of the brain are observed under the operating microscope. This correlates with venous stasis, hyperemia, and broadened perivascular spaces around venules and large capillaries accompanied by a marked rise in the specific weigth of the tissue. After 4h an edema front can be observed spreading from the perinerotic zone in which there is a marked rise in endothelial cell vesicular activity. Edema reaches maximum levels in the deep white matter at 48h post irradiation with normalisation of the tissue water content after 96h. The velocity at which the edema front spreads from the cortex to the periventricular area lies in the range of 0.25mm/h. Edema reabsorption coincides with signs of retrograde micropinocytosis in endothelial cells. (orig./AJ) [de

  8. Global cerebral edema and brain metabolism after subarachnoid hemorrhage.

    Science.gov (United States)

    Helbok, Raimund; Ko, Sang-Bae; Schmidt, J Michael; Kurtz, Pedro; Fernandez, Luis; Choi, H Alex; Connolly, E Sander; Lee, Kiwon; Badjatia, Neeraj; Mayer, Stephan A; Claassen, Jan

    2011-06-01

    Global cerebral edema is common among patients with poor-grade subarachnoid hemorrhage and is associated with poor outcome. Currently no targeted therapy exists largely due to an incomplete understanding of the underlying mechanisms. This is a prospective observational study including 39 consecutive patients with poor-grade subarachnoid hemorrhage with multimodal neuromonitoring. Levels of microdialysate lactate-pyruvate ratio, episodes of cerebral metabolic crisis (lactate-pyruvate ratio >40 and brain glucose cerebral perfusion pressure, and transcranial Doppler sonography flow velocities were analyzed. Median age was 54 years (range, 45 to 61 years) and 62% were female. Patients with global cerebral edema on admission (n=24 [62%]) had a higher incidence of metabolic crisis in the first 12 hours of monitoring (n=15 [15% versus 2%], Pcerebral edema. There was no difference in brain tissue oxygen tension or cerebral perfusion pressure between the groups; however, in patients with global cerebral edema, a higher cerebral perfusion pressure was associated with lower lactate-pyruvate ratio (Pcerebral edema is associated with early brain metabolic distress.

  9. Generalised brain edema and brain infarct in ergotamine abuse: Visualization by CT, MR and angiography

    International Nuclear Information System (INIS)

    Toedt, C.; Hoetzinger, H.; Salbeck, R.; Beyer, H.K.

    1989-01-01

    Abuse of ergotamine can release a generalised brain edema and brain infarctions. This can be visualized by CT, MR and angiography. The reason, however, can only be found in the patients history. (orig.) [de

  10. Emerging Therapies in Traumatic Brain Injury

    Science.gov (United States)

    Kochanek, Patrick M.; Jackson, Travis C.; Ferguson, Nikki Miller; Carlson, Shaun W.; Simon, Dennis W.; Brockman, Erik C.; Ji, Jing; Bayir, Hülya; Poloyac, Samuel M.; Wagner, Amy K.; Kline, Anthony E.; Empey, Philip E.; Clark, Robert S.B.; Jackson, Edwin K.; Dixon, C. Edward

    2015-01-01

    Despite decades of basic and clinical research, treatments to improve outcomes after traumatic brain injury (TBI) are limited. However, based on the recent recognition of the prevalence of mild TBI, and its potential link to neurodegenerative disease, many new and exciting secondary injury mechanisms have been identified and several new therapies are being evaluated targeting both classic and novel paradigms. This includes a robust increase in both preclinical and clinical investigations. Using a mechanism-based approach the authors define the targets and emerging therapies for TBI. They address putative new therapies for TBI across both the spectrum of injury severity and the continuum of care, from the field to rehabilitation. They discuss TBI therapy using 11 categories, namely, (1) excitotoxicity and neuronal death, (2) brain edema, (3) mitochondria and oxidative stress, (4) axonal injury, (5) inflammation, (6) ischemia and cerebral blood flow dysregulation, (7) cognitive enhancement, (8) augmentation of endogenous neuroprotection, (9) cellular therapies, (10) combination therapy, and (11) TBI resuscitation. The current golden age of TBI research represents a special opportunity for the development of breakthroughs in the field. PMID:25714870

  11. BPSD following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Renato Anghinah

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

  12. BPSD following traumatic brain injury

    Science.gov (United States)

    Anghinah, Renato; Freire, Fabio Rios; Coelho, Fernanda; Lacerda, Juliana Rhein; Schmidt, Magali Taino; Calado, Vanessa Tomé Gonçalves; Ianof, Jéssica Natuline; Machado, Sergio; Velasques, Bruna; Ribeiro, Pedro; Basile, Luis Fernando Hindi; Paiva, Wellingson Silva; Amorim, Robson Luis

    2013-01-01

    Annually, 700,000 people are hospitalized with brain injury acquired after traumatic brain injury (TBI) in Brazil. OBJECTIVE We aim to review the basic concepts related to TBI, and the most common Behavioral and Psychological Symptoms of Dementia (BPSD) findings in moderate and severe TBI survivors. We also discussed our strategies used to manage such patients in the post-acute period. METHODS Fifteen TBI outpatients followed at the Center for Cognitive Rehabilitation Post-TBI of the Clinicas Hospital of the University of São Paulo were submitted to a neurological, neuropsychological, speech and occupational therapy evaluation, including the Mini-Mental State Examination. Rehabilitation strategies will then be developed, together with the interdisciplinary team, for each patient individually. Where necessary, the pharmacological approach will be adopted. RESULTS Our study will discuss options of pharmacologic treatment choices for cognitive, behavioral, or affective disorders following TBI, providing relevant information related to a structured cognitive rehabilitation service and certainly will offer an alternative for patients and families afflicted by TBI. CONCLUSION Traumatic brain injury can cause a variety of potentially disabling psychiatric symptoms and syndromes. Combined behavioral and pharmacological strategies, in the treatment of a set of highly challenging behavioral problems, appears to be essential for good patient recovery. PMID:29213850

  13. Traumatic Brain Injury: Hope Through Research

    Science.gov (United States)

    ... a traumatic brain injury, marked by difficulty with perception, thinking, remembering, and concentration; during this acute stage, ... of nerve cells in the brain causing strange sensations, emotions, and behavior, or sometimes convulsions, muscle spasms, ...

  14. Traumatic Brain Injury (TBI) in Kids

    Science.gov (United States)

    ... Information Share Facebook Twitter Pinterest Email Print Traumatic Brain Injury (TBI): Condition Information What is TBI? TBI ... external force that affects the functioning of the brain. It can be caused by a bump or ...

  15. Personality Disturbances Associated with Traumatic Brain Injury.

    Science.gov (United States)

    Prigatano, George P.

    1992-01-01

    Reviews personality disturbances associated with traumatic brain injury. Attempts to clarify terms and review empirical findings. Notes that longitudinal prospective studies that use appropriate control groups are needed. Suggests future research may benefit by considering long-term effects of early agitation following traumatic brain injury and…

  16. Unfractionated heparin after TBI reduces in vivo cerebrovascular inflammation, brain edema and accelerates cognitive recovery.

    Science.gov (United States)

    Nagata, Katsuhiro; Kumasaka, Kenichiro; Browne, Kevin D; Li, Shengjie; St-Pierre, Jesse; Cognetti, John; Marks, Joshua; Johnson, Victoria E; Smith, Douglas H; Pascual, Jose L

    2016-12-01

    Severe traumatic brain injury (TBI) may increase the risk of venous thromboembolic complications; however, early prevention with heparinoids is often withheld for its anticoagulant effect. New evidence suggests low molecular weight heparin reduces cerebral edema and improves neurological recovery after stroke and TBI, through blunting of cerebral leukocyte (LEU) recruitment. It remains unknown if unfractionated heparin (UFH) similarly affects brain inflammation and neurological recovery post-TBI. We hypothesized that UFH after TBI reduces cerebral edema by reducing LEU-mediated inflammation and improves neurological recovery. CD1 male mice underwent either TBI by controlled cortical impact (CCI) or sham craniotomy. UFH (75 U/kg or 225 U/kg) or vehicle (VEH, 0.9% saline) was administered 2, 11, 20, 27, and 34 hours after TBI. At 48 hours, pial intravital microscopy through a craniotomy was used to visualize live brain LEUs interacting with endothelium and microvascular fluorescein isothiocyanate-albumin leakage. Neurologic function (Garcia Neurological Test, GNT) and body weight loss ratios were evaluated 24 and 48 hours after TBI. Cerebral and lung wet-to-dry ratios were evaluated post mortem. ANOVA with Bonferroni correction was used to determine significance (p < 0.05). Compared to positive controls (CCI), both UFH doses reduced post-TBI in vivo LEU rolling on endothelium, concurrent cerebrovascular albumin leakage, and ipsilateral cerebral water content after TBI. Additionally, only low dose UFH (75 U/kg) improved GNT at both 24 and 48 hours after TBI. High dose UFH (225 U/kg) significantly increased body weight loss above sham at 48 hours. Differences in lung water content and blood pressure between groups were not significant. UFH after TBI reduces LEU recruitment, microvascular permeability, and brain edema to injured brain. Lower UFH doses concurrently improve neurological recovery whereas higher UFH may worsen functional recovery. Further study is needed to

  17. Central diabetes insipidus in pediatric severe traumatic brain injury.

    Science.gov (United States)

    Alharfi, Ibrahim M; Stewart, Tanya Charyk; Foster, Jennifer; Morrison, Gavin C; Fraser, Douglas D

    2013-02-01

    To determine the occurrence rate of central diabetes insipidus in pediatric patients with severe traumatic brain injury and to describe the clinical, injury, biochemical, imaging, and intervention variables associated with mortality. Retrospective chart and imaging review. Children's Hospital, level 1 trauma center. Severely injured (Injury Severity Score ≥ 12) pediatric trauma patients (>1 month and diabetes insipidus between January 2000 and December 2011. Of 818 severely injured trauma patients, 180 had severe traumatic brain injury with an overall mortality rate of 27.2%. Thirty-two of the severe traumatic brain injury patients developed acute central diabetes insipidus that responded to desamino-8-D-arginine vasopressin and/or vasopressin infusion, providing an occurrence rate of 18%. At the time of central diabetes insipidus diagnosis, median urine output and serum sodium were 6.8 ml/kg/hr (interquartile range = 5-11) and 154 mmol/L (interquartile range = 149-159), respectively. The mortality rate of central diabetes insipidus patients was 87.5%, with 71.4% declared brain dead after central diabetes insipidus diagnosis. Early central diabetes insipidus onset, within the first 2 days of severe traumatic brain injury, was strongly associated with mortality (p diabetes insipidus were more likely to have intracranial pressure monitoring (p = 0.03), have thiopental administered to induce coma (p = 0.04) and have received a decompressive craniectomy for elevated intracranial pressure (p = 0.04). The incidence of central diabetes insipidus in pediatric patients with severe traumatic brain injury is 18%. Mortality was associated with early central diabetes insipidus onset and cerebral edema on head computed tomography. Central diabetes insipidus nonsurvivors were less likely to have received intracranial pressure monitoring, thiopental coma and decompressive craniectomy.

  18. Effects of glycerol administration on experimental brain edema.

    Science.gov (United States)

    Guisado, R; Arieff, A I; Massry, S G

    1976-01-01

    The effects of glycerol on brain water and solute distribution in cerebral edema are not well known. In brail edema induced in dogs by focal freezing, tissue underlying the necrotic lesion had an elevated water content but the remainder of the brain was unaltered. Administration of glycerol to maintain plasma glycerol at about 35 mM dehydrated normal white matter, but water and solute contents of the edematous white matter were not changed. During the initial 3 hours of glycerol infusion, CSF pressure fell, but when the infusion was continued for 6 hours or more, a gradual rise in CSF pressure was observed. In three animals, the final CSF pressure was higher than preinfusion values. At this time, brain water content was significantly less than normal, but both CSF osmolality and glycerol concentration were higher than plasma. The data show that glycerol infusion can decrease intracranial volume towards normal by dehydration of normal, but not damaged, brain tissue. The rebound rise in CSF pressure observed during the continuous administration of glycerol cannot be explained by rehydration of brain tissue but may be related to alterations in CSF dynamics.

  19. Effects of Gender and Estrogen Receptors on Iron-Induced Brain Edema Formation.

    Science.gov (United States)

    Xie, Qing; Xi, Guohua; Keep, Richard F; Hua, Ya

    2016-01-01

    Our previous studies have shown that female mice have less brain edema and better recovery in neurological deficits after intracerebral hemorrhage (ICH) and that 17β-estradiol treatment in male mice markedly reduces ICH-induced brain edema. In this study, we investigated the role of gender and the estrogen receptors (ERs) in iron-induced brain edema. There were three parts in this study: (1) either male or female mice received an injection of 10 μL FeCl2 (1 mM) into the right caudate; (2) females received an intracaudate injection of FeCl2 or saline with 1 μg of ICI 182,780 (antagonists of ERs) or vehicle; and (3) males were treated with the ER regulator tamoxifen (5 mg/kg subcutaneously) or vehicle 1 h after FeCl2 injection. Mice were euthanized 24 h later for brain edema determination. FeCl2 induced lower brain edema in females than in males. Co-injection of ICI 182,780 with FeCl2 aggravated iron-induced brain edema in female mice. ICI 182,780 itself did not induce brain edema at the dose of 1 μg. Tamoxifen treatment reduced FeCl2-induced brain edema in male mice. In conclusion, iron induced less brain edema in female mice than in males. ER modification can affect iron-induced brain edema.

  20. Dysautonomia after severe traumatic brain injury.

    NARCIS (Netherlands)

    Hendricks, H.T.; Heeren, J.H.M.; Vos, P.E.

    2010-01-01

    BACKGROUND: Dysautonomia after traumatic brain injury (TBI) is characterized by episodes of increased heart rate, respiratory rate, temperature, blood pressure, muscle tone, decorticate or decerebrate posturing, and profuse sweating. This study addresses the incidence of dysautonomia after severe

  1. Intraoperative monitoring of brain tissue oxygen and carbon dioxide pressures reveals low oxygenation in peritumoral brain edema

    NARCIS (Netherlands)

    Pennings, Frederik A.; Bouma, Gerrit J.; Kedaria, Mohan; Jansen, Gerard F. A.; Bosch, D. Andries

    2003-01-01

    Brain edema and swelling often complicate surgery for brain tumors. Its pathophysiology is unclear, as is the relationship with brain tissue oxygenation. Our hypothesis was that brain edema around tumor is cytotoxic type caused by impaired local tissue oxygenation due to increased local tissue

  2. Brain Imaging and Behavioral Outcome in Traumatic Brain Injury.

    Science.gov (United States)

    Bigler, Erin D.

    1996-01-01

    This review explores the cellular pathology associated with traumatic brain injury (TBI) and its relation to neurobehavioral outcomes, the relationship of brain imaging findings to underlying pathology, brain imaging techniques, various image analysis procedures and how they relate to neuropsychological testing, and the importance of brain imaging…

  3. Traumatic brain injury-induced sleep disorders

    Directory of Open Access Journals (Sweden)

    Viola-Saltzman M

    2016-02-01

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

  4. Peritumoral brain edema in intracranial meningiomas Edema peritumoral em meningiomas intracranianos

    Directory of Open Access Journals (Sweden)

    Nelson de Azambuja Pereira-Filho

    2010-06-01

    Full Text Available Occurrence of peritumoral brain edema (PBE in meningiomas has been associated with several factors in recent years, although its pathophysiological mechanism has not yet been fully elucidated. The aim of this study was to analyze the correlation between the presence / degree of PBE and factors such as gender, age, size and histological subtype of tumor. We analyzed the MRI images of 74 patients operated on Hospital Beneficência Portuguesa de Porto Alegre for the presence / degree of PBE and data was statistically correlated with the parameters of the patient. PBE was present in 70.1% of patients. Tumors with higher volume had more PBE. Tumors of the olfactory groove showed more PBE than sphenoid wing and parassagittal tumors. Transitional subtype showed more PBE than fibroblastic and meningothelial subtypes.A presença de edema cerebral peritumoral (ECP em meningiomas tem sido associada a diversos fatores nos últimos anos, embora o seu mecanismo fisiopatológico ainda não tenha sido inteiramente elucidado. O objetivo desse estudo foi analisar a correlação entre a presença/grau de ECP e fatores como sexo, idade, volume e subtipo histológico do tumor. Foram analisadas imagens de RM de 74 pacientes operados no Hospital Beneficência Portuguesa de Porto Alegre quanto à presença/grau de ECP e os dados correlacionados estatisticamente com os parâmetros do paciente. ECP estava presente em 70,1% dos pacientes. Tumores com maior volume apresentaram mais ECP. Tumores da goteira olfatória apresentaram mais ECP que os da asa do esfenóide e que os parassagitais. Meningiomas transicionais apresentaram mais ECP que os fibroblásticos e que os meningoteliais.

  5. Is intra-articular pathology associated with MCL edema on MR imaging of the non-traumatic knee?

    Energy Technology Data Exchange (ETDEWEB)

    Blankenbaker, Donna G.; De Smet, Arthur A. [University of Wisconsin Medical School, Division of Musculoskeletal Imaging, Department of Radiology, Madison (United States); Fine, Jason P. [University of Wisconsin, Department of Statistics, Madison (United States); University of Wisconsin, Department of Biostatistics and Informatics, Madison (United States)

    2005-08-01

    Edema surrounding the medial collateral ligament (MCL) is seen on MR imaging in patients with MCL injuries and in patients with radiographic osteoarthritis in the non-traumatic knee. Because we noted MCL edema in patients without prior trauma or osteoarthritis, we studied the association between intra-articular pathology and MCL edema in patients without knee trauma. We evaluated the MR examinations of 247 consecutive patients (121 male, 126 female with a mean age of 44 years) without recent trauma for the presence of edema surrounding the MCL, meniscal and ACL tears, medial meniscal extrusion, medial compartment chondromalacia, and osteoarthritis. The percentages of patients illustrating MCL edema with and without each type of pathology were compared using Fisher's exact test to determine if there was a statistically significant association. We found MCL edema in 60% of 247 patients. MCL edema was present in 67% of patients with medial meniscal tears, 35% with lateral meniscal tears, 100% with meniscal extrusion of 3 mm or more, 78% with femoral chondromalacia, 82% with tibial chondromalacia, and 50% with osteoarthritis. The percentage of patients with edema increased with the severity of the chondromalacia. These associations were all statistically significant (p <0.02). The mean age of those with MCL edema was 49.7 years compared with 34.9 years without MCL edema (p <0.001). Patient gender and ACL tear did not correlate with MCL edema. Nine (4%) of the 247 patients had MCL edema without intra-articular pathology. None of these 9 patients had MCL tenderness or joint laxity on physical examination. We confirmed that MCL edema is associated with osteoarthritis, but is also associated with meniscal tears, meniscal extrusion, and chondromalacia. In addition, MCL edema can be seen in patients without intra-articular pathology, recent trauma or MCL abnormality on physical examination. (orig.)

  6. Association between a quantitative CT scan measure of brain edema and outcome after cardiac arrest.

    Science.gov (United States)

    Metter, Robert B; Rittenberger, Jon C; Guyette, Francis X; Callaway, Clifton W

    2011-09-01

    Cerebral edema is one physical change associated with brain injury and decreased survival after cardiac arrest. Edema appears on computed tomography (CT) scan of the brain as decreased X-ray attenuation by gray matter. This study tested whether the gray matter attenuation to white matter attenuation ratio (GWR) was associated with survival and functional recovery. Subjects were patients hospitalized after cardiac arrest at a single institution between 1/1/2005 and 7/30/2010. Subjects were included if they had non-traumatic cardiac arrest and a non-contrast CT scan within 24h after cardiac arrest. Attenuation (Hounsfield Units) was measured in gray matter (caudate nucleus, putamen, thalamus, and cortex) and in white matter (internal capsule, corpus callosum and centrum semiovale). The GWR was calculated for basal ganglia and cerebrum. Outcomes included survival and functional status at hospital discharge. For 680 patients, 258 CT scans were available, but 18 were excluded because of hemorrhage (10), intravenous contrast (3) or technical artifact (5), leaving 240 CT scans for analysis. Lower GWR values were associated with lower initial Glasgow Coma Scale motor score. Overall survival was 36%, but decreased with decreasing GWR. The average of basal ganglia and cerebrum GWR provided the best discrimination. Only 2/58 subjects with average GWR<1.20 survived and both were treated with hypothermia. The association of GWR with functional outcome was completely explained by mortality when GWR<1.20. Subjects with severe cerebral edema, defined by GWR<1.20, have very low survival with conventional care, including hypothermia. GWR estimates pre-treatment likelihood of survival after cardiac arrest. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

  7. Melatonin alleviates brain and peripheral tissue edema in a neonatal rat model of hypoxic-ischemic brain damage: the involvement of edema related proteins.

    Science.gov (United States)

    Xu, Li-Xiao; Lv, Yuan; Li, Yan-Hong; Ding, Xin; Wang, Ying; Han, Xing; Liu, Ming-Hua; Sun, Bin; Feng, Xing

    2017-03-28

    Previous studies have indicated edema may be involved in the pathophysiology following hypoxic-ischemic encephalopathy (HIE), and melatonin may exhibit neuro-protection against brain insults. However, little is known regarding the mechanisms that involve the protective effects of melatonin in the brain and peripheral tissues after HIE. The present study aimed to examine the effects of melatonin on multiple organs, and the expression of edema related proteins in a neonatal rat model of hypoxic-ischemic brain damage (HIBD). One hundred ninety-two neonatal rats were randomly divided into three subgroups that underwent a sham surgery or HIBD. After the HIBD or sham-injury, the rats received an intraperitoneal injection of melatonin or an equal volume vehicle, respectively. We investigated the effects of melatonin on brain, kidney, and colon edema via histological examination and the expression of edema related proteins, including AQP-4, ZO-1 and occludin, via qPCR and western blot. Our data indicated (1) Melatonin reduced the histological injury in the brain and peripheral organs induced by HIBD as assessed via H-E staining and transmission electron microscopy. (2) Melatonin alleviated the HIBD-induced cerebral edema characterized by increased brain water content. (3) HIBD induced significant changes of edema related proteins, such as AQP-4, ZO-1 and occludin, and these changes were partially reversed by melatonin treatment. These findings provide substantial evidence that melatonin treatment has protective effects on the brain and peripheral organs after HIBD, and the edema related proteins, AQP4, ZO-1, and occludin, may indirectly contribute tothe mechanism of the edema protection by melatonin.

  8. Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema

    DEFF Research Database (Denmark)

    Eefsen, Martin; Jelnes, Peter; Schmidt, Lars E

    2010-01-01

    Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and....../or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. Liver injury and hyperammonemia were induced by +D-galactosamine (GLN) plus lipopolysaccharide (LPS) intraperitoneally...

  9. Perspective on Pediatric Traumatic Brain Injury | Igun | African ...

    African Journals Online (AJOL)

    Background: Traumatic brain injury is an important aspect of paediatric trauma because of its contribution to mortality ant post trauma seqeulae. Management of traumatic brain injury remains a challenge to surgeons, especially in developing countries. This study aims to determine the pattern of traumatic brain injury among ...

  10. Blast-induced Mild Traumatic Brain Injury

    Science.gov (United States)

    2010-01-01

    directly to the brain after craniotomy 154 or 240 kPa Unknown 2.8 or 20 kPa 40 kPa 1 or 10 MPa Redistribution of phosphorylated neurofilament H...m a: 1𔃻) .... !l ~ Blast-induced Mild Traumatic Brain Injury 767 colleagues55 compared neuropsychological test results in a group of primarily...patterns between blast and non-blast-injured subjects, thus providing no support at the neuropsychological level that blast is different. However

  11. Fatigue in adults with traumatic brain injury

    DEFF Research Database (Denmark)

    Mollayeva, Tatyana; Kendzerska, Tetyana; Mollayeva, Shirin

    2013-01-01

    , assess, and critically appraise studies that assessed predictors for fatigue and the consequences of fatigue on at least two separate time points following traumatic brain injury. METHODS/DESIGN: MEDLINE, EMBASE, the Cochrane Database of Systematic Reviews, CINAHL, and PsycINFO will be systematically...

  12. 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

  13. 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

  14. Centralized rehabilitation after servere traumatic brain injury

    DEFF Research Database (Denmark)

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

    2006-01-01

    OBJECTIVES: To present results from the first 3 years of centralized subacute rehabilitation after very severe traumatic brain injury (TBI), and to compare results of centralized versus decentralized rehabilitation. MATERIAL AND METHODS: Prospectively, the most severely injured group of adults fr...

  15. Response of the cerebral vasculature following traumatic brain injury.

    Science.gov (United States)

    Salehi, Arjang; Zhang, John H; Obenaus, Andre

    2017-07-01

    The critical role of the vasculature and its repair in neurological disease states is beginning to emerge particularly for stroke, dementia, epilepsy, Parkinson's disease, tumors and others. However, little attention has been focused on how the cerebral vasculature responds following traumatic brain injury (TBI). TBI often results in significant injury to the vasculature in the brain with subsequent cerebral hypoperfusion, ischemia, hypoxia, hemorrhage, blood-brain barrier disruption and edema. The sequalae that follow TBI result in neurological dysfunction across a host of physiological and psychological domains. Given the importance of restoring vascular function after injury, emerging research has focused on understanding the vascular response after TBI and the key cellular and molecular components of vascular repair. A more complete understanding of vascular repair mechanisms are needed and could lead to development of new vasculogenic therapies, not only for TBI but potentially vascular-related brain injuries. In this review, we delineate the vascular effects of TBI, its temporal response to injury and putative biomarkers for arterial and venous repair in TBI. We highlight several molecular pathways that may play a significant role in vascular repair after brain injury.

  16. Differentiation of brain tumor-related edema based on 3D T1rho imaging.

    Science.gov (United States)

    Villanueva-Meyer, J E; Barajas, R F; Mabray, M C; Chen, W; Shankaranarayanan, A; Koon, P; Barani, I J; Tihan, T; Cha, S

    2017-06-01

    Cerebral edema associated with brain tumors is an important source of morbidity. Its type depends largely on the capillary ultra-structures of the histopathologic subtype of underlying brain tumor. The purpose of our study was to differentiate vasogenic edema associated with brain metastases and infiltrative edema related to diffuse gliomas using quantitative 3D T1 rho (T1ρ) imaging. Preoperative MR examination including whole brain 3D T1ρ imaging was performed in 23 patients with newly diagnosed brain tumors (9 with metastasis, 8 with lower grade glioma, LGG, 6 with glioblastoma, GBM). Mean T1ρ values were measured in regions of peritumoral non-enhancing T2 signal hyperintensity, excluding both enhancing and necrotic or cystic component, and normal-appearing white matter. Mean T1ρ values were significantly elevated in the vasogenic edema surrounding intracranial metastases when compared to the infiltrative edema associated with either LGG or GBM (p=0.02 and <0.01, respectively). No significant difference was noted between T1ρ values of infiltrative edema between LGG and GBM (p=0.84 and 0.96, respectively). Our study demonstrates the feasibility and potential diagnostic role of T1ρ in the quantitative differentiation between edema related to intracranial metastases and gliomas and as a potentially complementary tool to standard MR techniques in further characterizing pathophysiology of vasogenic and infiltrative edema. Copyright © 2017. Published by Elsevier B.V.

  17. Rapamycin alleviates brain edema after focal cerebral ischemia reperfusion in rats.

    Science.gov (United States)

    Guo, Wei; Feng, Guoying; Miao, Yanying; Liu, Guixiang; Xu, Chunsheng

    2014-06-01

    Brain edema is a major consequence of cerebral ischemia reperfusion. However, few effective therapeutic options are available for retarding the brain edema progression after cerebral ischemia. Recently, rapamycin has been shown to produce neuroprotective effects in rats after cerebral ischemia reperfusion. Whether rapamycin could alleviate this brain edema injury is still unclear. In this study, the rat stroke model was induced by a 1-h left transient middle cerebral artery occlusion using an intraluminal filament, followed by 48 h of reperfusion. The effects of rapamycin (250 μg/kg body weight, intraperitoneal; i.p.) on brain edema progression were evaluated. The results showed that rapamycin treatment significantly reduced the infarct volume, the water content of the brain tissue and the Evans blue extravasation through the blood-brain barrier (BBB). Rapamycin treatment could improve histological appearance of the brain tissue, increased the capillary lumen space and maintain the integrity of BBB. Rapamycin also inhibited matrix metalloproteinase 9 (MMP9) and aquaporin 4 (AQP4) expression. These data imply that rapamycin could improve brain edema progression after reperfusion injury through maintaining BBB integrity and inhibiting MMP9 and AQP4 expression. The data of this study provide a new possible approach for improving brain edema after cerebral ischemia reperfusion by administration of rapamycin.

  18. Fluid Intake Related to Brain Edema in Acute Middle Cerebral Artery Infarction.

    Science.gov (United States)

    Dharmasaroja, Pornpatr A

    2016-02-01

    Evidence of the appropriate amount of fluid intake during the first few days after acute stroke was scarce. Concerns were raised in patients with acute malignant middle cerebral infarction, who tended to have malignant brain edema later. The purpose of the study was to evaluate the effect of fluid intake on the occurrence of malignant brain edema in patients with acute middle cerebral artery infarction. Patients with acute middle cerebral artery infarction who had National Institute of Health Stroke Scale (NIHSS) score of at least 15 were included. Baseline characteristics and amount of fluid intake during the first few days were compared in patients with and without malignant brain edema. One hundred ninety-three patients were studied. Mean NIHSS score was 20. Malignant brain edema occurred in 69 patients (36%). Higher amount of fluid intake (>1650 ml or >28 ml/kg/day or >93% of daily maintenance fluid) showed a significant association with malignant brain edema (OR = 13.86, 95% CI 5.11-37.60, p value edema, 39 patients (39/65, 60%) died and only 11% (7/65 patients) had favorable outcome. High amount of fluid intake in the first few days of acute middle cerebral infarction was related to the occurrence of malignant brain edema.

  19. Mathematical model in post-mortem estimation of brain edema using morphometric parameters.

    Science.gov (United States)

    Radojevic, Nemanja; Radnic, Bojana; Vucinic, Jelena; Cukic, Dragana; Lazovic, Ranko; Asanin, Bogdan; Savic, Slobodan

    2017-01-01

    Current autopsy principles for evaluating the existence of brain edema are based on a macroscopic subjective assessment performed by pathologists. The gold standard is a time-consuming histological verification of the presence of the edema. By measuring the diameters of the cranial cavity, as individually determined morphometric parameters, a mathematical model for rapid evaluation of brain edema was created, based on the brain weight measured during the autopsy. A cohort study was performed on 110 subjects, divided into two groups according to the histological presence or absence of (the - deleted from the text) brain edema. In all subjects, the following measures were determined: the volume and the diameters of the cranial cavity (longitudinal and transverse distance and height), the brain volume, and the brain weight. The complex mathematical algorithm revealed a formula for the coefficient ε, which is useful to conclude whether a brain edema is present or not. The average density of non-edematous brain is 0.967 g/ml, while the average density of edematous brain is 1.148 g/ml. The resulting formula for the coefficient ε is (5.79 x longitudinal distance x transverse distance)/brain weight. Coefficient ε can be calculated using measurements of the diameters of the cranial cavity and the brain weight, performed during the autopsy. If the resulting ε is less than 0.9484, it could be stated that there is cerebral edema with a reliability of 98.5%. The method discussed in this paper aims to eliminate the burden of relying on subjective assessments when determining the presence of a brain edema. Copyright © 2016 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.

  20. Peritumoral brain edema in intracranial tumor evaluated by CT perfusion imaging

    International Nuclear Information System (INIS)

    Shi Yuxin; Xu Jianfeng

    2005-01-01

    Objective: To semi-quantitatively evaluate the cerebral perfusion in the peritumoral brain edema of cerebral tumors using CT perfusion imaging. Methods: Twenty-one patients with peritumoral brain edema (including pathologically confirmed meningiomas n=4, metastasis n=10, gliomas n=7) were examined by CT perfusion imaging. The regional cerebral blood flow (rCBF), regional cerebral blood volume (rCBV), and mean transit time (MTT) were calculated for peritumoral brain edema and the contralateralwhite matter. The rCBF and rCBV were compared between peritumoral brain edema and the contralateral white matter. The mean ratios (edema/contralateral white matter) of rCBF and rCBV were compared among the three tumors. Results: The rCBF and rCBV of peritumoral brain edema were significantly lower than those of contralateral white matter in patients with meningiomas and metastasis (rCBF: t=2.92 and 3.82, P 0.05). The mean ratios (edema/contralateralwhite matter) of rCBF and rCBV were not significantly different between meningiomas and metastasis (t=0.23 and 0.73, P>0.05), but both of them were significantly lower than those of gliomas (t=3.05 and 3.37, P<0.01, 0.005). Conclusion: The rCBF and rCBV in peritumoral brain edema were significantly lower than those of contralateral white matter in patients with meningiomas and metastasis, while almost the same with or higher than those of contralateral white matter in patients with gliomas. CT perfusion can provide quantitative information of blood flow in peritumoral brain edema, and is useful in the diagnosis and follow-up of cerebral tumors. (authors)

  1. Alterations in diffusion and perfusion in the pathogenesis of peritumoral brain edema in meningiomas

    International Nuclear Information System (INIS)

    Bitzer, M.; Klose, U.; Naegele, T.; Voigt, K.; Geist-Barth, B.; Schick, F.; Claussen, C.D.; Morgalla, M.

    2002-01-01

    Magnetic resonance perfusion and diffusion studies were undertaken to clarify the significance of ischemia in the pathogenesis of peritumoral brain edema in patients with meningiomas. Included in this study were 26 patients with 27 meningiomas and 5 gliomas. Perfusion-weighted imaging (PWI) was performed using a gradient-echo, echo-planar-imaging (EPI) sequence for calculation of the relative regional cerebral blood volume (rrCBV) and the relative regional cerebral blood flow index (rrCBFi). Furthermore, multi-slice spin-echo EPI sequences were applied in order to obtain anisotropic and isotropic diffusion-weighted imaging (DWI). Apparent diffusion coefficient (ADC) values were then calculated for peritumoral brain parenchyma from tumors, with and without edema, using various diffusion sensitivities. Meningiomas without edema demonstrated a minimal increase of perfusion parameters in the peritumoral brain tissue. In contrast, cases with brain edema had highly significant (p 2 . The DWI showed a significantly larger ADC value within areas of brain edema, compared with the normal white matter (0.74 x 10 -3 vs 1.55 x 10 -3 mm 2 /s; p<0.0001). Increases in EI correlated with increases in ADC values. In 31% of the meningiomas associated with edema, areas with increased signal, probable ischemia, demonstrated significantly lower ADC values, in comparison with the rest of the edematous areas. These areas were confined to tissue immediately adjacent to the tumor. In general, the decrease in rrCBV in brain edema represents a consequence from, rather than a cause of, vasogenic edema. Ischemic alterations can be regarded as secondary, facultative phenomena in the pathogenesis of meningioma-related brain edema. (orig.)

  2. Efficacy and safety of bevacizumab treatment for refractory brain edema: Case report.

    Science.gov (United States)

    Meng, Xiangying; Zhao, Rugang; Shen, Ge; Dong, Dapeng; Ding, Lijuan; Wu, Shikai

    2017-11-01

    This retrospective study investigated the efficacy and safety of bevacizumab treatment for refractory brain edema. Between March 2009 and December 2015, bevacizumab was used to treat 59 cases of brain metastatic patients with refractory brain edema. The median dose of bevacizumab was 4.68 mg/kg (range 2.8-6.52 mg/kg). The clinical-pathological data, the efficacy, and the side effects of bevacizumab were recorded. Magnetic resonance imaging (MRI) was performed before and after bevacizumab treatment. Tumor and edema volumes were measured separately. The clinical symptoms of 50 out of 59 cases (84.74%) improved the day after the bevacizumab treatment, and the edema volumes of 55 (93.22%) cases were reduced after the bevacizumab treatment. The average edema volume was significantly reduced after bevacizumab treatment from 125,583.43 ± 14,093.27 to 71,613.42 ± 9473.42 mm (Mann-Whitney rank test, P bevacizumab for refractory brain edema is 84.74%. Hypertension was the main side effect of the bevacizumab treatment. Bevacizumab is an effective and relatively safe treatment for brain edema.

  3. Prevention and management of brain edema in patients with acute liver failure

    DEFF Research Database (Denmark)

    Wendon, J.; Larsen, Finn Stolze

    2008-01-01

    1. Intracranial pressure is the pressure exerted by the cranial contents on the dural envelope and consists of the partial pressures of the brain, blood, and cerebrospinal fluid. 2. Severe cases of acute liver failure are frequently complicated by brain edema (due to cytotoxic edema) and an incre......1. Intracranial pressure is the pressure exerted by the cranial contents on the dural envelope and consists of the partial pressures of the brain, blood, and cerebrospinal fluid. 2. Severe cases of acute liver failure are frequently complicated by brain edema (due to cytotoxic edema......) and an increase in cerebral blood flow while the cerebrospinal fluid volume remains constant. 3. The development of intracranial hypertension in patients with acute liver failure may be controlled by manipulation of the position, body temperature, plasma tonicity, arterial carbon dioxide tension, and arterial...

  4. Falls and traumatic brain injury among older adults.

    Science.gov (United States)

    Filer, William; Harris, Matthew

    2015-04-01

    This commentary discusses traumatic brain injury (TBI) related to falls among elderly individuals, as well as common TBI sequelae and their treatment. It also discusses the current understanding of TBI-related dementia and chronic traumatic encephalopathy.

  5. Post traumatic Headache and Psychological Health: Mindfulness Training for Mild TraumaticBrain Injury

    Science.gov (United States)

    2015-10-01

    Award Number: W81XWH-10-1-1021 TITLE: Post-traumatic Headache and Psychological Health: Mindfulness Training for Mild Traumatic Brain Injury...traumatic Headache and Psychological Health: Mindfulness Training for Mild Traumatic Brain Injury” 5b. GRANT NUMBER 5c. PROGRAM ELEMENT NUMBER 6. AUTHOR...negative psychological/mood states, and impair overall quality of life. Comorbid anxiety, depression, PTSD and other psychological, psychosocial

  6. Goreisan Prevents Brain Edema after Cerebral Ischemic Stroke by Inhibiting Aquaporin 4 Upregulation in Mice.

    Science.gov (United States)

    Nakano, Takafumi; Nishigami, Chisa; Irie, Keiichi; Shigemori, Yutaka; Sano, Kazunori; Yamashita, Yuta; Myose, Takayuki; Tominaga, Koji; Matsuo, Koichi; Nakamura, Yoshihiko; Ishikura, Hiroyasu; Kamimura, Hidetoshi; Egawa, Takashi; Mishima, Kenichi

    2018-03-01

    Aquaporin 4 (AQP4) is a water-selective transport protein expressed in astrocytes throughout the central nervous system. AQP4 level increases after cerebral ischemia and results in ischemic brain edema. Brain edema markedly influences mortality and motor function by elevating intracranial pressure that leads to secondary brain damage. Therefore, AQP4 is an important target to improve brain edema after cerebral ischemia. The Japanese herbal Kampo medicine, goreisan, is known to inhibit AQP4 activity. Here, we investigated whether goreisan prevents induction of brain edema by cerebral ischemia via AQP4 using 4-hour middle cerebral artery occlusion (4h MCAO) mice. Goreisan was orally administered at a dose of 500 mg/kg twice a day for 5 days before MCAO. AQP4 expression and motor coordination were measured by Western blotting and rotarod test, respectively. Brain water content of 4h MCAO mice was significantly increased at 24 hours after MCAO. Treatment with goreisan significantly decreased both brain water content and AQP4 expression in the ischemic brain at 24 hours after MCAO. In addition, treatment with goreisan alleviated motor coordination deficits at 24 hours after MCAO. The results of this study suggested that goreisan may be a useful new therapeutic option for ischemic brain edema. Copyright © 2018 National Stroke Association. Published by Elsevier Inc. All rights reserved.

  7. Managing traumatic brain injury secondary to explosions

    Directory of Open Access Journals (Sweden)

    Burgess Paula

    2010-01-01

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

  8. Traumatic Brain Injury and Sleep Disorders

    OpenAIRE

    Viola-Saltzman, Mari; Watson, Nathaniel F.

    2012-01-01

    Sleep disturbance is common following traumatic brain injury (TBI), affecting 30–70% of individuals, many occurring after mild injuries. Insomnia, fatigue and sleepiness are the most frequent post-TBI sleep complaints with narcolepsy (with or without cataplexy), sleep apnea (obstructive and/or central), periodic limb movement disorder, and parasomnias occurring less commonly. In addition, depression, anxiety and pain are common TBI co-morbidities with substantial influence on sleep quality. T...

  9. 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,...

  10. Brain edema and blood-brain barrier permeability following quantitative cerebral microembolism

    International Nuclear Information System (INIS)

    Bralet, A.M.; Bdley, A.; Beley, P.; Bralet, J.

    1979-01-01

    Cerebral microemboli were formed in rats by injecting 4000 carbonized microspheres, 50 +- 10 mu in diameter, labelled with 85 Sr, into the internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. The microspheres were mainly distributed in the cerebral hemisphere on the side of the injection. In 61 rats this hemisphere contained 582 +- 20 microspheres against 99 +- 9 in the contralateral hemisphere. Brain edema was assessed by measuring brain content of water, sodium and potassium. Blood-brain barrier (BBB) permeability was determined by brain accumulation of 125 I-albumin. In the ipsilateral hemisphere brain edema and an increase in BBB permeability appeared 6 hours after embolization and progressed up to 48 hours. Twenty-four hours after embolization, significant correlations were observed between the microsphere content of the cerebral hemispheres and (1) increases in water and sodium levels, (2) the decrease in potassium level, (3) the increase in BBB permeability. The study of these correlations should make it possible to ignore the poor reproducibility of embolizations and to analyze with increased accuracy the results of various experiments

  11. Effect of dexmedetomidine on brain edema and neurological outcomes in surgical brain injury in rats.

    Science.gov (United States)

    Benggon, Michael; Chen, Han; Applegate, Richard; Martin, Robert; Zhang, John H

    2012-07-01

    Surgical brain injury (SBI) is damage to functional brain tissue resulting from neurosurgical manipulations such as sharp dissection, electrocautery, retraction, and direct applied pressure. Brain edema is the major contributor to morbidity with inflammation, necrosis, oxidative stress, and apoptosis likely playing smaller roles. Effective therapies for SBI may improve neurological outcomes and postoperative morbidities associated with brain surgery. Previous studies show an adrenergic correlation to blood-brain barrier control. The α-2 receptor agonist dexmedetomidine (DEX) has been shown to improve neurological outcomes in stroke models. We hypothesized that DEX may reduce brain edema and improve neurological outcomes in a rat model of SBI. Male Sprague-Dawley rats (n = 63) weighing 280 to 350 g were randomly assigned to 1 of 4 IP treatment groups: sham IP, vehicle IP, DEX 10 mg/kg, and DEX 30 mg/kg. Treatments were given 30 min before SBI. These treatment groups were repeated to observe the physiologic impact of DEX on mean arterial blood pressure (MAP), heart rate (HR), and blood glucose on SBI naïve animals. Rats were also assigned to 4 postinjury IV treatment groups: sham IV, vehicle IV, DEX 10/5, and DEX 30/15 (DEX group doses were 10 and 30 mg/kg/hr, with 5 and 15 mg/kg initial loading doses, respectively). Initial loading doses began 20 min after SBI, followed by 2 h of infusion. SBI animals were subjected to neurological testing 24 h after brain injury by a blinded observer, promptly killed, and brain water content measured via the dry/wet weight method. All treatment groups showed a significant difference in ipsilateral frontal brain water content and neurological scores when compared with sham animals. However, there was no difference between DEX-treated and vehicle animals. Physiologic monitoring showed treatment with low or high doses of DEX significantly decreased MAP and HR, and briefly increased blood glucose compared with naïve or vehicle

  12. Application of Blood-Brain Barrier Permeability Imaging in Global Cerebral Edema.

    Science.gov (United States)

    Ivanidze, J; Kallas, O N; Gupta, A; Weidman, E; Baradaran, H; Mir, D; Giambrone, A; Segal, A Z; Claassen, J; Sanelli, P C

    2016-09-01

    Blood-brain barrier permeability is not routinely evaluated in the clinical setting. Global cerebral edema occurs after SAH and is associated with BBB disruption. Detection of global cerebral edema using current imaging techniques is challenging. Our purpose was to apply blood-brain barrier permeability imaging in patients with global cerebral edema by using extended CT perfusion. Patients with SAH underwent CTP in the early phase after aneurysmal rupture (days 0-3) and were classified as having global cerebral edema or nonglobal cerebral edema using established noncontrast CT criteria. CTP data were postprocessed into blood-brain barrier permeability quantitative maps of PS (permeability surface-area product), K(trans) (volume transfer constant from blood plasma to extravascular extracellular space), Kep (washout rate constant of the contrast agent from extravascular extracellular space to intravascular space), VE (extravascular extracellular space volume per unit of tissue volume), VP (plasmatic volume per unit of tissue volume), and F (plasma flow) by using Olea Sphere software. Mean values were compared using t tests. Twenty-two patients were included in the analysis. Kep (1.32 versus 1.52, P cerebral edema compared with nonglobal cerebral edema while VE (0.81 versus 0.39, P cerebral edema. Kep is an important indicator of altered blood-brain barrier permeability in patients with decreased blood flow, as Kep is flow-independent. Further study of blood-brain barrier permeability is needed to improve diagnosis and monitoring of global cerebral edema. © 2016 by American Journal of Neuroradiology.

  13. Significance of Primary Tumor Location and Histology for Brain Metastasis Development and Peritumoral Brain Edema in Lung Cancer

    DEFF Research Database (Denmark)

    Fabian, Katalin; Gyulai, Marton; Furak, Jozsef

    2016-01-01

    of peritumoral brain edema (p tumors (p = 0.019), in younger patients (= 50 years) (p = 0.042), and in females (p = 0.016). The time to development of brain metastasis was shorter in central than in peripheral lung cancer (5.3 vs. 9.0 months, p = 0.035). Early brain......Background: Brain metastasis of lung cancer adversely affects overall survival (OS) and quality of life, while peritumoral brain edema is responsible for life-threatening complications. Methods: We retrospectively analyzed the clinicopathological and cerebral radiological data of 575 consecutive...... lung cancer patients with brain metastases. Results: In adenocarcinoma and squamous cell carcinoma, peritumoral brain edema was more pronounced than in small-cell lung cancer (p

  14. Synthesis of 11C-methylated inulin as a radiopharmaceutical for imaging brain edema and pulmonary edema

    International Nuclear Information System (INIS)

    Hara, Toshihiko; Iio, Masaaki; Inagaki, Keizo

    1988-01-01

    11 C-methylated inulin, supposedly useful for imaging of brain edema and pulmonary edema, was prepared using cyclotron produced 11 CO 2 . The synthesis consists of the production of 11 C-methyl iodide and its coupling with inulin alkoxide sodium in dimethylsulfoxide as solvent. 11 C labeled inulin was purified by alcohol precipitation. The radiochemical yield of pure 11 C-inulin was 34% of 11 CO 2 30 min after the end of bombardment. The blood clearance and body distribution of 11 C was observed in rabbits after i.v. injection of 11 C-inulin. The blood clearance curve was composed of a sum of three exponential functions. The gamma camera image showed that the 11 C activity in blood moved quickly to kidneys and urine and a small dose of radioactivity remained persistently in edematous tissues, i.e. the edematous lung tissues produced by oleic acid treatment. (orig.)

  15. Traumatic brain injury and forensic neuropsychology.

    Science.gov (United States)

    Bigler, Erin D; Brooks, Michael

    2009-01-01

    As part of a special issue of The Journal of Head Trauma Rehabilitation, forensic neuropsychology is reviewed as it applies to traumatic brain injury (TBI) and other types of acquired brain injury in which clinical neuropsychologists and rehabilitation psychologists may be asked to render professional opinions about the neurobehavioral effects and outcome of a brain injury. The article introduces and overviews the topic focusing on the process of forensic neuropsychological consultation and practice as it applies to patients with TBI or other types of acquired brain injury. The emphasis is on the application of scientist-practitioner standards as they apply to legal questions about the status of a TBI patient and how best that may be achieved. This article introduces each topic area covered in this special edition.

  16. Prehospital Care of Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    TVSP Murthy

    2008-01-01

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

  17. Brain SPECT in severs traumatic head injury

    International Nuclear Information System (INIS)

    Beaulieu, F.; Eder, V.; Pottier, J.M.; Baulieu, J.L.; Fournier, P.; Legros, B.; Chiaroni, P.; Dalonneau, M.

    2000-01-01

    The aim of this work was to compare the results of the early brain scintigraphy in traumatic brain injury to the long term neuropsychological behavior. Twenty four patients had an ECD-Tc99m SPECT, within one month after the trauma; scintigraphic abnormalities were evaluated according to a semi-quantitative analysis. The neuropsychological clinical investigation was interpreted by a synthetic approach to evaluate abnormalities related to residual motor deficit, frontal behavior, memory and language disorders. Fourteen patients (58%) had sequela symptoms. SPECT revealed 80 abnormalities and CT scan only 31. Statistical analysis of uptake values showed significantly lower uptake in left basal ganglia and brain stem in patients with sequela memory disorders. We conclude that the brain perfusion scintigraphy is able to detect more lesions than CT and that it could really help to predict the neuropsychological behavior after severe head injury. Traumatology could become in the future a widely accepted indication of perfusion SPECT. (authors)

  18. Advanced Neuromonitoring and Imaging in Pediatric Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Stuart H. Friess

    2012-01-01

    Full Text Available While the cornerstone of monitoring following severe pediatric traumatic brain injury is serial neurologic examinations, vital signs, and intracranial pressure monitoring, additional techniques may provide useful insight into early detection of evolving brain injury. This paper provides an overview of recent advances in neuromonitoring, neuroimaging, and biomarker analysis of pediatric patients following traumatic brain injury.

  19. Traumatic Brain Injury: Are We Conducting Enough Resarch

    Science.gov (United States)

    2017-04-17

    FROM: 59 MDW/SGVU SUBJECT: Professional Presentation Approval 7 APR 2017 1. Your paper, entitled Traumatic Brain Injury: Are We Conducting Enough...review and approval.) NA - Pubmed searches w ere the only source of data 6. TITLE OF MATERIAL TO BE PUBLISHED OR PRESENTED: Traumatic Brain Injury...Traumatic Brain Injury: Are We Conducting Enough Research? Capt Mariya Gusman MD, Lt Col Jonathan A Sosnov MD, Jeffrey T Howard PhD Background

  20. The effect of infectious brain edema on NMDA receptor binding in rat's brain

    International Nuclear Information System (INIS)

    Cheng Guansheng; Chen Jianfang; Chen Xiang

    1997-01-01

    PURPOSE: The effect of the infectious brain edema (IBE) induced by Bordetella Pertussis (BP) on the specific binding of 3 H MK-801 in rat's brain in vivo was determined. METHODS: BP was injected via left internal carotid artery in rat model of infectious brain edema. Male SD rats were divided into three groups: 1) Group control (NS, n = 11); 2) Group IBF (BP, n = 12); 3) Group pretreatment of MK-801 + PB (MK-801, n = 4). Normal saline or BP 0.2 ml/kg was injected into left internal carotid artery in NS and BP group respectively. MK-801 0.5 mg/kg per day was injected i.p. two days before injection of BP in group MK-801. Rats were killed by decapitation at 24 hours after injection of BP. The specific binding of N-methyl-D-aspartate (NMDA) receptor were measured with 3 H-MK-801 in the neuronal membrane of cerebral cortex. The Scatchard plots were performed. RESULTS: The B max values were 0.623 +- 0.082 and 0.606 +- 0.087 pmol/mg protein in group NS and BP respectively (t = 0.48, P>0.05). The Kd values were 43.1 +- 4.2 and 30.5 +- 3.0 nmol/L in group NS and BP respectively (t = 7.8, P<0.05). The specific binding of NMDA receptor was decreased by pretreatment of MK-801. CONCLUSIONS: The total number of NMDA receptor had not changed, whereas its affinity increased significantly in the model of brain edema induced by pertussis bacilli in rat. The increase of affinity of NMDA receptor can be blockaded by MK-801 pretreatment in vivo

  1. Brain-derived neurotropic factor polymorphisms, traumatic stress, mild traumatic brain injury, and combat exposure contribute to postdeployment traumatic stress.

    Science.gov (United States)

    Dretsch, Michael N; Williams, Kathy; Emmerich, Tanja; Crynen, Gogce; Ait-Ghezala, Ghania; Chaytow, Helena; Mathura, Venkat; Crawford, Fiona C; Iverson, Grant L

    2016-01-01

    In addition to experiencing traumatic events while deployed in a combat environment, there are other factors that contribute to the development of posttraumatic stress disorder (PTSD) in military service members. This study explored the contribution of genetics, childhood environment, prior trauma, psychological, cognitive, and deployment factors to the development of traumatic stress following deployment. Both pre- and postdeployment data on 231 of 458 soldiers were analyzed. Postdeployment assessments occurred within 30 days from returning stateside and included a battery of psychological health, medical history, and demographic questionnaires; neurocognitive tests; and blood serum for the D2 dopamine receptor (DRD2), apolipoprotein E (APOE), and brain-derived neurotropic factor (BDNF) genes. Soldiers who screened positive for traumatic stress at postdeployment had significantly higher scores in depression (d = 1.91), anxiety (d = 1.61), poor sleep quality (d = 0.92), postconcussion symptoms (d = 2.21), alcohol use (d = 0.63), traumatic life events (d = 0.42), and combat exposure (d = 0.91). BDNF Val66 Met genotype was significantly associated with risk for sustaining a mild traumatic brain injury (mTBI) and screening positive for traumatic stress. Predeployment traumatic stress, greater combat exposure and sustaining an mTBI while deployed, and the BDNF Met/Met genotype accounted for 22% of the variance of postdeployment PTSD scores (R (2)  = 0.22, P PTSD scores. These findings suggest predeployment traumatic stress, genetic, and environmental factors have unique contributions to the development of combat-related traumatic stress in military service members.

  2. [Prognosis in pediatric traumatic brain injury. A dynamic cohort study].

    Science.gov (United States)

    Vázquez-Solís, María G; Villa-Manzano, Alberto I; Sánchez-Mosco, Dalia I; Vargas-Lares, José de Jesús; Plascencia-Fernández, Irma

    2013-01-01

    traumatic brain injury is a main cause of hospital admission and death in children. Our objective was to identify prognostic factors of pediatric traumatic brain injury. this was a dynamic cohort study of traumatic brain injury with 6 months follow-up. The exposition was: mild or moderate/severe traumatic brain injury, searching for prognosis (morbidity-mortality and decreased Glasgow scale). Relative risk and logistic regression was estimated for prognostic factors. we evaluated 440 patients with mild traumatic brain injury and 98 with moderate/severe traumatic brain injury. Morbidity for mild traumatic brain injury was 1 %; for moderate/severe traumatic brain injury, 5 %. There were no deaths. Prognostic factors for moderate/severe traumatic brain injury were associated injuries (RR = 133), fractures (RR = 60), street accidents (RR = 17), night time accidents (RR = 2.3) and weekend accidents (RR = 2). Decreased Glasgow scale was found in 9 %, having as prognostic factors: visible injuries (RR = 3), grown-up supervision (RR = 2.5) and time of progress (RR = 1.6). there should be a prognosis established based on kinetic energy of the injury and not only with Glasgow Scale.

  3. Differential aquaporin 4 expression during edema build-up and resolution phases of brain inflammation

    Directory of Open Access Journals (Sweden)

    Brochet Bruno

    2011-10-01

    Full Text Available Abstract Background Vasogenic edema dynamically accumulates in many brain disorders associated with brain inflammation, with the critical step of edema exacerbation feared in patient care. Water entrance through blood-brain barrier (BBB opening is thought to have a role in edema formation. Nevertheless, the mechanisms of edema resolution remain poorly understood. Because the water channel aquaporin 4 (AQP4 provides an important route for vasogenic edema resolution, we studied the time course of AQP4 expression to better understand its potential effect in countering the exacerbation of vasogenic edema. Methods Focal inflammation was induced in the rat brain by a lysolecithin injection and was evaluated at 1, 3, 7, 14 and 20 days using a combination of in vivo MRI with apparent diffusion coefficient (ADC measurements used as a marker of water content, and molecular and histological approaches for the quantification of AQP4 expression. Markers of active inflammation (macrophages, BBB permeability, and interleukin-1β and markers of scarring (gliosis were also quantified. Results This animal model of brain inflammation demonstrated two phases of edema development: an initial edema build-up phase during active inflammation that peaked after 3 days (ADC increase was followed by an edema resolution phase that lasted from 7 to 20 days post injection (ADC decrease and was accompanied by glial scar formation. A moderate upregulation in AQP4 was observed during the build-up phase, but a much stronger transcriptional and translational level of AQP4 expression was observed during the secondary edema resolution phase. Conclusions We conclude that a time lag in AQP4 expression occurs such that the more significant upregulation was achieved only after a delay period. This change in AQP4 expression appears to act as an important determinant in the exacerbation of edema, considering that AQP4 expression is insufficient to counter the water influx during the build

  4. Overexpression of caveolin-1 attenuates brain edema by inhibiting tight junction degradation.

    Science.gov (United States)

    Choi, Kang-Ho; Kim, Hyung-Seok; Park, Man-Seok; Lee, Eun-Bin; Lee, Jung-Kil; Kim, Joon-Tae; Kim, Ja-Hae; Lee, Min-Cheol; Lee, Hong-Joon; Cho, Ki-Hyun

    2016-10-18

    Cerebral edema from the disruption of the blood-brain barrier (BBB) after cerebral ischemia is a major cause of morbidity and mortality as well as a common event in patients with stroke. Caveolins (Cavs) are thought to regulate BBB functions. Here, we report for the first time that Cav-1 overexpression (OE) decreased brain edema from BBB disruption following ischemic insult. Edema volumes and Cav-1 expression levels were measured following photothrombosis and middle cerebral artery occlusion (MCAO). Endothelial cells that were transduced with a Cav-1 lentiviral expression vector were transplanted into rats. BBB permeability was quantified with Evans blue extravasation. Edema volume was determined from measures of the extravasation area, brain water content, and average fluorescence intensity after Cy5.5 injections. Tight junction (TJ) protein expression was measured with immunoblotting. Cav-1 expression levels and vasogenic brain edema correlated strongly after ischemic insult. Cav-1 expression and BBB disruption peaked 3 d after the MCAO. In addition, intravenous administration of endothelial cells expressing Cav-1 effectively increased the Cav-1 levels 3 d after the MCAO ischemic insult. Importantly, Cav-1 OE ameliorated the vasogenic edema by inhibiting the degradation of TJ protein expression in the acute phase of ischemic stroke. These results suggested that Cav-1 OE protected the integrity of the BBB mainly by preventing the degradation of TJ proteins in rats. These findings need to be confirmed in a clinical setting in human subjects.

  5. Dementia resulting from traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Joana Ramalho

    Full Text Available ABSTRACT Traumatic brain injury (TBI represents a significant public health problem in modern societies. It is primarily a consequence of traffic-related accidents and falls. Other recently recognized causes include sports injuries and indirect forces such as shock waves from battlefield explosions. TBI is an important cause of death and lifelong disability and represents the most well-established environmental risk factor for dementia. With the growing recognition that even mild head injury can lead to neurocognitive deficits, imaging of brain injury has assumed greater importance. However, there is no single imaging modality capable of characterizing TBI. Current advances, particularly in MR imaging, enable visualization and quantification of structural and functional brain changes not hitherto possible. In this review, we summarize data linking TBI with dementia, emphasizing the imaging techniques currently available in clinical practice along with some advances in medical knowledge.

  6. Immunochemical method for quantitative evaluation of vasogenic brain edema following cold injury of rat brain

    International Nuclear Information System (INIS)

    Bodsch, W.; Huerter, T.; Hossmann, K.-A.

    1982-01-01

    An immunochemical method is described for quantitative assessment of serum proteins and hemoglobin content in brain tissue homogenates. Using a combination of affinity chromatography and radioimmunoassay, the sensitivity of the method is 50 ng hemoglobin and 100 ng serum protein per assay, respectively. The method was used to measure cerebral hematocrit, blood volume and serum protein extravasation in rat brain at various times following cold injury. In control rats cerebral blood volume was 6.88 +- 0.15 ml/100 g and cerebral hematocrit 26.4 +- 0.86% (means +- S.E.). Following cold injury blood volume did not significantly change, but there was a gradual increase of extravasated serum proteins, reaching a maximum of 21.54 +- 2.76 mg/g d.w. after 8 hours. Thereafter protein content gradually declined, but even after 64 h it was distinctly increased. Protein extravasation was partly dissociated from the increase of brain water and sodium which reached a maximum already after 2 h and which normalized within 32 and 64 h, respectively. It is concluded that edema fluid associated with cold injury is not simply an ultrafiltrate of blood serum but consists of cytotoxic and vasogenic components which follow a different time course both during formation and resolution of edema. (Auth.)

  7. Traumatic brain injury in modern war

    Science.gov (United States)

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

    2013-05-01

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

  8. Astrocyte roles in traumatic brain injury

    Science.gov (United States)

    Burda, Joshua E.; Bernstein, Alexander M.; Sofroniew, Michael V.

    2015-01-01

    Astrocytes sense changes in neural activity and extracellular space composition. In response, they exert homeostatic mechanisms critical for maintaining neural circuit function, such as buffering neurotransmitters, modulating extracellular osmolarity and calibrating neurovascular coupling. In addition to upholding normal brain activities, astrocytes respond to diverse forms of brain injury with heterogeneous and progressive changes of gene expression, morphology, proliferative capacity and function that are collectively referred to as reactive astrogliosis. Traumatic brain injury (TBI) sets in motion complex events in which noxious mechanical forces cause tissue damage and disrupt central nervous system (CNS) homeostasis, which in turn trigger diverse multi-cellular responses that evolve over time and can lead either to neural repair or secondary cellular injury. In response to TBI, astrocytes in different cellular microenvironments tune their reactivity to varying degrees of axonal injury, vascular disruption, ischemia and inflammation. Here we review different forms of TBI-induced astrocyte reactivity and the functional consequences of these responses for TBI pathobiology. Evidence regarding astrocyte contribution to post-traumatic tissue repair and synaptic remodeling is examined, and the potential for targeting specific aspects of astrogliosis to ameliorate TBI sequelae is considered. PMID:25828533

  9. Human neuronal changes in brain edema and increased intracranial pressure.

    Science.gov (United States)

    Faragó, Nóra; Kocsis, Ágnes Katalin; Braskó, Csilla; Lovas, Sándor; Rózsa, Márton; Baka, Judith; Kovács, Balázs; Mikite, Katalin; Szemenyei, Viktor; Molnár, Gábor; Ozsvár, Attila; Oláh, Gáspár; Piszár, Ildikó; Zvara, Ágnes; Patócs, Attila; Barzó, Pál; Puskás, László G; Tamás, Gábor

    2016-08-04

    Functional and molecular changes associated with pathophysiological conditions are relatively easily detected based on tissue samples collected from patients. Population specific cellular responses to disease might remain undiscovered in samples taken from organs formed by a multitude of cell types. This is particularly apparent in the human cerebral cortex composed of a yet undefined number of neuron types with a potentially different involvement in disease processes. We combined cellular electrophysiology, anatomy and single cell digital PCR in human neurons identified in situ for the first time to assess mRNA expression and corresponding functional changes in response to edema and increased intracranial pressure. In single pyramidal cells, mRNA copy numbers of AQP1, AQP3, HMOX1, KCNN4, SCN3B and SOD2 increased, while CACNA1B, CRH decreased in edema. In addition, single pyramidal cells increased the copy number of AQP1, HTR5A and KCNS1 mRNAs in response to increased intracranial pressure. In contrast to pyramidal cells, AQP1, HMOX1and KCNN4 remained unchanged in single cell digital PCR performed on fast spiking cells in edema. Corroborating single cell digital PCR results, pharmacological and immunohistochemical results also suggested the presence of KCNN4 encoding the α-subunit of KCa3.1 channels in edema on pyramidal cells, but not on interneurons. We measured the frequency of spontaneous EPSPs on pyramidal cells in both pathophysiological conditions and on fast spiking interneurons in edema and found a significant decrease in each case, which was accompanied by an increase in input resistances on both cell types and by a drop in dendritic spine density on pyramidal cells consistent with a loss of excitatory synapses. Our results identify anatomical and/or physiological changes in human pyramidal and fast spiking cells in edema and increased intracranial pressure revealing cell type specific quantitative changes in gene expression. Some of the edema

  10. Traumatic brain injury and olfactory deficits

    DEFF Research Database (Denmark)

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

    2010-01-01

    PRIMARY OBJECTIVE: Olfactory functions are not systematically evaluated following traumatic brain injury (TBI). This study aimed at comparing two smell tests that are used in a clinical setting. RESEARCH DESIGN: The University of Pennsylvania Smell Identification Test (UPSIT) and the Alberta Smell....... RESULTS: The scores of the two smell tests were significantly correlated. Both tests indicated that patients with frontal lesion performed significantly worse than patients with other types of lesion. Mood and injury severity were not associated with olfactory impairment when age was taken into account...

  11. 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...

  12. Integrative Medicine in Traumatic Brain Injury.

    Science.gov (United States)

    Drake, David F; Hudak, Anne M; Robbins, William

    2017-05-01

    Complementary and alternative medicine (CAM) is a group of diverse medical and health care systems, practices, and products that are not presently considered to be a part of conventional medicine. Integrative medicine combines treatment with conventional medical practices and elements of CAM in which there is strong evidence in efficacy and safety. Although there is growing interest in the integrative medical approach in treating the patient population with traumatic brain injury, there is a paucity in high-quality clinical trials supporting its use. This article reviews the background and current clinical data concerning some of the more common CAM interventions. Published by Elsevier Inc.

  13. Diabetes Insipidus after Traumatic Brain Injury

    Science.gov (United States)

    Capatina, Cristina; Paluzzi, Alessandro; Mitchell, Rosalid; Karavitaki, Niki

    2015-01-01

    Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI. PMID:26239685

  14. The Role of Substance P in Secondary Pathophysiology after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Robert Vink

    2017-06-01

    Full Text Available It has recently been shown that substance P (SP plays a major role in the secondary injury process following traumatic brain injury (TBI, particularly with respect to neuroinflammation, increased blood–brain barrier (BBB permeability, and edema formation. Edema formation is associated with the development of increased intracranial pressure (ICP that has been widely associated with increased mortality and morbidity after neurotrauma. However, a pharmacological intervention to specifically reduce ICP is yet to be developed, with current interventions limited to osmotic therapy rather than addressing the cause of increased ICP. Given that previous publications have shown that SP, NK1 receptor antagonists reduce edema after TBI, more recent studies have examined whether these compounds might also reduce ICP and improve brain oxygenation after TBI. We discuss the results of these studies, which demonstrate that NK1 antagonists reduce posttraumatic ICP to near normal levels within 4 h of drug administration, as well as restoring brain oxygenation to near normal levels in the same time frame. The improvements in these parameters occurred in association with an improvement in BBB integrity to serum proteins, suggesting that SP-mediated increases in vascular permeability significantly contribute to the development of increased ICP after acute brain injury. NK1 antagonists may therefore provide a novel, mechanistically targeted approach to the management of increased ICP.

  15. Traumatic Brain Injury and Metabolic Dysfunction Among Head ...

    African Journals Online (AJOL)

    more common in males and young people. Keywords: Traumatic Brain Injury, Plasma Glucose, Cortisol, ... disability and death among young adults through a variety of mechanisms, and is now recognised as a .... such as ischaemic stroke, intracranial haemorrhage or traumatic brain injury and is associated with increased.

  16. Academic consequences of very mild and mild traumatic brain ...

    African Journals Online (AJOL)

    Information on the consequences of mild traumatic brain injuries (MTBI#) on secondary school rugby players has been documented, but studies on the academic consequences of repetitive sub-concussive injuries or so-called very mild traumatic brain injuries (vMTBI) are lacking. The aim of this study was to compare the ...

  17. Centralized rehabilitation after servere traumatic brain injury

    DEFF Research Database (Denmark)

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

    2006-01-01

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

  18. Surgical management of traumatic brain injury

    DEFF Research Database (Denmark)

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

    2014-01-01

    OBJECT: Mass lesions from traumatic brain injury (TBI) often require surgical evacuation as a life-saving measure and to improve outcomes, but optimal timing and surgical technique, including decompressive craniectomy, have not been fully defined. The authors compared neurosurgical approaches...... in the treatment of TBI at 2 academic medical centers to document variations in real-world practice and evaluate the efficacies of different approaches on postsurgical course and long-term outcome. METHODS: Patients 18 years of age or older who required neurosurgical lesion evacuation or decompression for TBI were...... enrolled in the Co-Operative Studies on Brain Injury Depolarizations (COSBID) at King's College Hospital (KCH, n = 27) and Virginia Commonwealth University (VCU, n = 24) from July 2004 to March 2010. Subdural electrode strips were placed at the time of surgery for subsequent electrocorticographic...

  19. 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

  20. Psychiatric disorders and traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Marcelo Schwarzbold

    2008-09-01

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

  1. Arginine-Vasopressin Receptor Blocker Conivaptan Reduces Brain Edema and Blood-Brain Barrier Disruption after Experimental Stroke in Mice.

    Directory of Open Access Journals (Sweden)

    Emil Zeynalov

    Full Text Available Stroke is a major cause of morbidity and mortality. Stroke is complicated by brain edema and blood-brain barrier (BBB disruption, and is often accompanied by increased release of arginine-vasopressin (AVP. AVP acts through V1a and V2 receptors to trigger hyponatremia, vasospasm, and platelet aggregation which can exacerbate brain edema. The AVP receptor blockers conivaptan (V1a and V2 and tolvaptan (V2 are used to correct hyponatremia, but their effect on post-ischemic brain edema and BBB disruption remains to be elucidated. Therefore, we conducted this study to investigate if these drugs can prevent brain edema and BBB disruption in mice after stroke.Experimental mice underwent the filament model of middle cerebral artery occlusion (MCAO with reperfusion. Mice were treated with conivaptan, tolvaptan, or vehicle. Treatments were initiated immediately at reperfusion and administered IV (conivaptan or orally (tolvaptan for 48 hours. Physiological variables, neurological deficit scores (NDS, plasma and urine sodium and osmolality were recorded. Brain water content (BWC and Evans Blue (EB extravasation index were evaluated at the end point.Both conivaptan and tolvaptan produced aquaresis as indicated by changes in plasma and urine sodium levels. However plasma and urine osmolality was changed only by conivaptan. Unlike tolvaptan, conivaptan improved NDS and reduced BWC in the ipsilateral hemisphere: from 81.66 ± 0.43% (vehicle to 78.28 ± 0.48% (conivaptan, 0.2 mg, p < 0.05 vs vehicle. Conivaptan also attenuated the EB extravasation from 1.22 ± 0.08 (vehicle to 1.01 ± 0.02 (conivaptan, 0.2 mg, p < 0.05.Continuous IV infusion with conivaptan for 48 hours after experimental stroke reduces brain edema, and BBB disruption. Conivaptan but not tolvaptan may potentially be used in patients to prevent brain edema after stroke.

  2. Blockage of transient receptor potential vanilloid 4 inhibits brain edema in middle cerebral artery occlusion mice.

    Science.gov (United States)

    Jie, Pinghui; Tian, Yujing; Hong, Zhiwen; Li, Lin; Zhou, Libin; Chen, Lei; Chen, Ling

    2015-01-01

    Brain edema is an important pathological process during stroke. Activation of transient receptor potential vanilloid 4 (TRPV4) causes an up-regulation of matrix metalloproteinases (MMPs) in lung tissue. MMP can digest the endothelial basal lamina to destroy blood brain barrier, leading to vasogenic brain edema. Herein, we tested whether TRPV4-blockage could inhibit brain edema through inhibiting MMPs in middle cerebral artery occlusion (MCAO) mice. We found that the brain water content and Evans blue extravasation at 48 h post-MCAO were reduced by a TRPV4 antagonist HC-067047. The increased MMP-2/9 protein expression in hippocampi of MCAO mice was attenuated by HC-067046, but only the increased MMP-9 activity was blocked by HC-067047. The loss of zonula occludens-1 (ZO-1) and occludin protein in MCAO mice was also attenuated by HC-067047. Moreover, MMP-2/9 protein expression increased in mice treated with a TRPV4 agonist GSK1016790A, but only MMP-9 activity was increased by GSK1016790A. Finally, ZO-1 and occludin protein expression was decreased by GSK1016790A, which was reversed by an MMP-9 inhibitor. We conclude that blockage of TRPV4 may inhibit brain edema in cerebral ischemia through inhibiting MMP-9 activation and the loss of tight junction protein.

  3. The Impact of Traumatic Brain Injury on the Aging Brain.

    Science.gov (United States)

    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.

  4. Report - Cerebral electrical impedance value reflects brain edema caused by cardiopulmonary bypass in infants.

    Science.gov (United States)

    Peng, Mingqing; Guo, Chunbao; Gong, Fang; Li, Min; Li, Yuan; Peng, Qiang; Bo, Lin

    2017-05-01

    The study aimed to investigate if the dynamic changes in cerebral electrical impedance (CEI) values could be used to monitor brain edema during cardiopulmonary bypass (CPB) in infants. Forty infants (mean age: 1.4±0.38y) with acyanotic congenital heart disease who underwent CPB open-heart surgery between September 2009 and March 2010 were prospectively enrolled, and divided into 2 groups based on aortic cross-clamping (ACC) time: CPB-A (ACCbrain edema in infants undergoing CPB, and is an index reflecting brain damage during CPB in infants.

  5. The role in thanatogenesis of generalized brain edema in ischemic cerebral infarction (computer-morphometric research

    Directory of Open Access Journals (Sweden)

    E. A. Dyadyk

    2012-12-01

    Full Text Available This work presents the results of computer-morphometric study of perivascular and pericellular free (oedematous spaces in brain cortex at death from the ischemic cerebral infarction and from reasons unconnected directly with cerebral pathology. It was revealed, that the mean area of perivascular spaces (vasogenic edema index at brain infarction in 13 times exceeds such at extracerebral pathology, and mean area of pericellular spaces (cytotoxic edema index – almost in 12 times, but also it substantially differs on the degree of variation (in 2,5 times higher, than area of perivascular spaces.

  6. Prevention and management of brain edema in patients with acute liver failure

    DEFF Research Database (Denmark)

    Wendon, J.; Larsen, Finn Stolze

    2008-01-01

    1. Intracranial pressure is the pressure exerted by the cranial contents on the dural envelope and consists of the partial pressures of the brain, blood, and cerebrospinal fluid. 2. Severe cases of acute liver failure are frequently complicated by brain edema (due to cytotoxic edema......) and an increase in cerebral blood flow while the cerebrospinal fluid volume remains constant. 3. The development of intracranial hypertension in patients with acute liver failure may be controlled by manipulation of the position, body temperature, plasma tonicity, arterial carbon dioxide tension, and arterial...

  7. Chronic Traumatic Brain Injury in Amateur Boxers

    Directory of Open Access Journals (Sweden)

    M. Rahmati

    2008-04-01

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

  8. Primary blast-induced traumatic brain injury: lessons from lithotripsy

    Science.gov (United States)

    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

  9. Dimethyl fumarate attenuates cerebral edema formation by protecting the blood-brain barrier integrity.

    Science.gov (United States)

    Kunze, Reiner; Urrutia, Andrés; Hoffmann, Angelika; Liu, Hui; Helluy, Xavier; Pham, Mirko; Reischl, Stefan; Korff, Thomas; Marti, Hugo H

    2015-04-01

    Brain edema is a hallmark of various neuropathologies, but the underlying mechanisms are poorly understood. We aim to characterize how tissue hypoxia, together with oxidative stress and inflammation, leads to capillary dysfunction and breakdown of the blood-brain barrier (BBB). In a mouse stroke model we show that systemic treatment with dimethyl fumarate (DMF), an antioxidant drug clinically used for psoriasis and multiple sclerosis, significantly prevented edema formation in vivo. Indeed, DMF stabilized the BBB by preventing disruption of interendothelial tight junctions and gap formation, and decreased matrix metalloproteinase activity in brain tissue. In vitro, DMF directly sustained endothelial tight junctions, inhibited inflammatory cytokine expression, and attenuated leukocyte transmigration. We also demonstrate that these effects are mediated via activation of the redox sensitive transcription factor NF-E2 related factor 2 (Nrf2). DMF activated the Nrf2 pathway as shown by up-regulation of several Nrf2 target genes in the brain in vivo, as well as in cerebral endothelial cells and astrocytes in vitro, where DMF also increased protein abundance of nuclear Nrf2. Finally, Nrf2 knockdown in endothelial cells aggravated subcellular delocalization of tight junction proteins during ischemic conditions, and attenuated the protective effect exerted by DMF. Overall, our data suggest that DMF protects from cerebral edema formation during ischemic stroke by targeting interendothelial junctions in an Nrf2-dependent manner, and provide the basis for a completely new approach to treat brain edema. Copyright © 2015 Elsevier Inc. All rights reserved.

  10. Semi-automated method for brain hematoma and edema quantification using computed tomography.

    Science.gov (United States)

    Bardera, A; Boada, I; Feixas, M; Remollo, S; Blasco, G; Silva, Y; Pedraza, S

    2009-06-01

    In this paper, a semi-automated method for brain hematoma and edema segmentation, and volume measurement using computed tomography imaging is presented. This method combines a region growing approach to segment the hematoma and a level set segmentation technique to segment the edema. The main novelty of this method is the strategy applied to define the propagation function required by the level set approach. To evaluate the method, 18 patients with brain hematoma and edema of different size, shape and location were selected. The obtained results demonstrate that the proposed approach provides objective and reproducible segmentations that are similar to the manually obtained results. Moreover, the processing time of the proposed method is about 4 min compared to the 10 min required for manual segmentation.

  11. Apathy following traumatic brain injury: a review.

    Science.gov (United States)

    Worthington, Andrew; Wood, Rodger Ll

    2018-04-13

    Apathy is a common problem after traumatic brain injury (TBI) and can have a major impact on cognitive function, psychosocial outcome and engagement in rehabilitation. For scientists and clinicians it remains one of the least understood aspects of brain-behaviour relationships encompassing disturbances of cognition, motivation, emotion and action, and is variously an indication of organic brain disease or psychiatric disorder. Apathy can be both sign and symptom and has been proposed as a diagnosis in its own right as well as a secondary feature of other conditions. This review considers previous approaches to apathy in terms of relevant psychological constructs and those neural counterparts most likely to be implicated after TBI. Neurobehavioural disorders of apathy are characterised chiefly by dysfunction of executive control of goal-oriented behaviour or the neural substrates of reward-based and emotional learning. We argue that it is possible to distinguish a primary disorder of apathy as an organic neurobehavioural state from secondary presentations due to an impoverished environment or psychological disturbance which has implications for treatment. Copyright © 2018. Published by Elsevier Ltd.

  12. Nonsurgical interventions after mild traumatic brain injury

    DEFF Research Database (Denmark)

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

    2014-01-01

    OBJECTIVE: To synthesize the best available evidence regarding the impact of nonsurgical interventions on persistent symptoms after mild traumatic brain injury (MTBI). DATA SOURCES: MEDLINE and other databases were searched (2001-2012) with terms including "rehabilitation." Inclusion criteria were...... of 7 studies related to nonsurgical interventions were found to have a low risk of bias. One studied the effect of a scheduled telephone intervention offering counseling and education on outcome and found a significantly better outcome for symptoms (6.6 difference in adjusted mean symptom score; 95...... evidence suggests that early, reassuring educational information is beneficial after MTBI. Well-designed intervention studies are required to develop effective treatments and improve outcomes for adults and children at risk for persistent symptoms after MTBI....

  13. 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.

  14. 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.

  15. Destination memory in traumatic brain injuries.

    Science.gov (United States)

    Wili Wilu, Amina; Coello, Yann; El Haj, Mohamad

    2018-03-17

    Destination memory, which is socially driven, refers to the ability to remember to whom one has sent information. Our study investigated destination memory in patients with traumatic brain injuries (TBIs). Patients and control participants were invited to tell proverbs (e.g., "the pen is mightier than the sword") to pictures of celebrities (e.g., Barack Obama). Then they were asked to indicate to which celebrity they had previously told the proverbs. Besides the assessment of destination memory, participants performed a binding task in which they were required to associate letters with their corresponding location. Analysis demonstrated less destination memory and binding in patients with TBIs than in controls. In both populations, significant correlations were observed between destination memory and performances on the binding task. These findings demonstrate difficulty in the ability to attribute information to its appropriate destination in TBI patients, perhaps owing to difficulties in binding separate information together to form a coherent representation of an event in memory.

  16. Nicotine exacerbates brain edema during in vitro and in vivo focal ischemic conditions.

    Science.gov (United States)

    Paulson, Jennifer R; Yang, Tianzhi; Selvaraj, Pradeep K; Mdzinarishvili, Alexander; Van der Schyf, Cornelis J; Klein, Jochen; Bickel, Ulrich; Abbruscato, Thomas J

    2010-02-01

    We have previously shown that nicotine, the addictive component of tobacco products, alters the blood-brain barrier (BBB) Na(+),K(+),2Cl(-) cotransporter (NKCC) during in vitro hypoxia-aglycemia exposure. Attenuation of abluminal NKCC suggests that accumulation of ions in the brain extracellular fluid would result in an increase of fluid or cytotoxic edema in the brain during hypoxia-aglycemia or stroke conditions. To further investigate whether nicotine products have the potential to worsen stroke outcome by increasing edema formation, two separate models to mimic stroke conditions were utilized to decipher the effects of short-term and long-term administrations of nicotine products on brain edema following stroke. Oxygen glucose deprivation (OGD) was studied in rat hippocampal slices with short-term or long-term exposure to nicotine and cigarette smoke constituents. During short-term exposure, the presence of nicotine at a concentration mimicking heavy smokers increased water content of hippocampal slices during OGD. Furthermore, long-term 1-week administration of nicotine increased water content in hippocampal slices that could be attenuated with nicotine acetylcholine receptor (nAChR) antagonists, suggesting nicotine increase edema during OGD via nAChRs. A second model of focal ischemia, middle cerebral artery occlusion, showed an increase of infarct size during short-term exposure to nicotine and an increase of edema during both short-term and long-term administration of nicotine, compared with saline controls. These findings support the paradigm that nicotine products not only increase the incidence of stroke but also have the potential to worsen stroke outcome by increased edema formation.

  17. Traumatic brain injury among refugees and asylum seekers.

    Science.gov (United States)

    McPherson, Jacob I

    2017-12-28

    Refugees and asylum seekers face many challenges in their pursuit of a safe home. The journey for displaced individuals can be extremely dangerous and many do not survive or go missing. Survivors face significant risks of injury, abuse, and torture. Traumatic brain injury is one of the most common and disabling injuries sustained by these populations. This already complex condition can have profound implications on these groups and their families due to factors related to mental health, cultural perspectives, and their ability to navigate healthcare systems. A literature review was performed to investigate the incidence and prevalence of torture and traumatic brain injury in displaced and fleeing populations. Impacts of traumatic brain injury and residency status on outcomes in these individuals were also examined. The incidence and prevalence of torture and traumatic brain injury among refugees and asylum seekers is significant. These populations may access healthcare systems differently than other groups and as a result may experience a unique health-related outcomes following traumatic brain injury. This information should sensitize healthcare providers to a potential history of traumatic brain injury sustained by patients/clients who are refugees or asylum seekers and may serve to guide some clinical encounters. Implications for rehabilitation Traumatic brain injuries are commonly sustained by refugees and asylum seekers. Cultural factors may complicate how refugees and asylum seekers understand, report, and manage these injuries. The above may be worsened by cognitive, emotional, and behavioral changes following traumatic brain injury. Rehabilitation providers should be aware of potential traumatic brain injury history during encounters with refugee and asylum seeker populations, especially if a history of torture is suspected.

  18. TRAUMATIC BRAIN INJURY IN PEDIATRIC AGE GROUP

    Directory of Open Access Journals (Sweden)

    Hayagriva

    2015-11-01

    Full Text Available Traumatic brain injury is one of the major causes of morbidity and mortality in children. The anatomical features, physiological response to injury, neuronal development, and low myelination in children cause different clinical features compared to the adult traumatic brain injury. Our aim is to study the incidence, predisposing factors, clinical presentations, and outcome in pediatric head injuries. The patients included in this retrospective study are under the age of 14 years admitted in the Neurosurgery Department of King George Hospital, Visakhapatnam, which is a tertiary care centre. The study period is two years’ duration from 1.1.2013 to 31.12.2014. Data collected on the basis of history, physical examination, base line investigations, and the plain CT scan is all cases. The pediatric patients were 226 in total 1643 case of head injury cases. There were 64.6% (n=146 males and 35.4% (n=80 females. The age ranged from 12 days to 14 years. Fall from height was the commonest cause of head injury found in 48.6% (n=110 cases, road traffic accidents (RTA in 34.5% (n=78 and other causes 16.8% (n=38; 49 (21.68% patients had associated injuries. At 55.75% (n=126 cases mild head injury with GCS 13-15 was present and severe head injury with GCS less than 8 in 29 (12.8% patients. The 188 patients are treated conservatively, 38 patients underwent different neurosurgical procedures in which 5 patients died. CONCLUSION: Head injury in pediatric age group carries high risk of morbidity and mortality. Good outcome achieved by early diagnosis and referral from primary care centers to tertiary care centers.

  19. Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study

    Science.gov (United States)

    Song, Juhyun; Park, Joohyun; Kim, Jae Hwan; Choi, Ja Yong; Kim, Jae Young; Lee, Kyoung Min

    2015-01-01

    Ischemic stroke results in the diverse phathophysiologies including blood brain barrier (BBB) disruption, brain edema, neuronal cell death, and synaptic loss in brain. Vitamin C has known as the potent anti-oxidant having multiple functions in various organs, as well as in brain. Dehydroascorbic acid (DHA) as the oxidized form of ascorbic acid (AA) acts as a cellular protector against oxidative stress and easily enters into the brain compared to AA. To determine the role of DHA on edema formation, neuronal cell death, and synaptic dysfunction following cerebral ischemia, we investigated the infarct size of ischemic brain tissue and measured the expression of aquaporin 1 (AQP-1) as the water channel protein. We also examined the expression of claudin 5 for confirming the BBB breakdown, and the expression of bcl 2 associated X protein (Bax), caspase-3, inducible nitric oxide synthase (iNOS) for checking the effect of DHA on the neurotoxicity. Finally, we examined postsynaptic density protein-95 (PSD-95) expression to confirm the effect of DHA on synaptic dysfunction following ischemic stroke. Based on our findings, we propose that DHA might alleviate the pathogenesis of ischemic brain injury by attenuating edema, neuronal loss, and by improving synaptic connection. PMID:25792869

  20. Measurement of brain edema by noninvasive cerebral electrical impedance in patients with massive hemispheric cerebral infarction.

    Science.gov (United States)

    Lou, Jin He; Wang, Jian; Liu, Li Xu; He, Lan Ying; Yang, Hao; Dong, Wei Wei

    2012-01-01

    Malignant cerebral infarction often occurs in patients with massive cerebral infarction. Monitoring brain edema is therefore helpful to make correct clinical decisions. Our previous studies have confirmed that cerebral electrical impedance (CEI) can sensitively reflect the brain edema after stroke. The CEI was measured consecutively by a noninvasive brain edema monitor in 69 patients with massive hemispheric cerebral infarction (MHCI). The results of the CEI were converted into the perturbation index (PI). The characteristics of dynamic changes of the CEI after MHCI were analyzed. Receiver-operating characteristics analysis was used to calculate predictive values for PI and other known parameters including NIHSS score and infarct volume. (1) The overall rate of positive CEI was 88.4% (61/69) in all patients with MHCI. (2) The PI on the infarct side increased significantly within 24 h after stroke onset and reached a peak level 3-5 days after stroke onset (p brain edema in patients with MHCI. Monitoring the CEI may help to predict malignant MHCI and guide treatment decisions. Copyright © 2012 S. Karger AG, Basel.

  1. Racking the brain: detection of cerebral edema on postmortem computed tomography compared with forensic autopsy.

    Science.gov (United States)

    Berger, Nicole; Ampanozi, Garyfalia; Schweitzer, Wolf; Ross, Steffen G; Gascho, Dominic; Ruder, Thomas D; Thali, Michael J; Flach, Patricia M

    2015-04-01

    The purpose of this study was to compare postmortem computed tomography with forensic autopsy regarding their diagnostic reliability of differentiating between pre-existing cerebral edema and physiological postmortem brain swelling. The study collective included a total of 109 cases (n=109/200, 83 male, 26 female, mean age: 53.2 years) and were retrospectively evaluated for the following parameters (as related to the distinct age groups and causes of death): tonsillar herniation, the width of the outer and inner cerebrospinal fluid spaces and the radiodensity measurements (in Hounsfield Units) of the gray and white matter. The results were compared with the findings of subsequent autopsies as the gold standard for diagnosing cerebral edema. p-Values edema (despite normal postmortem swelling) can be reliably assessed using postmortem computed tomography and is indicated by narrowed temporal horns and symmetrical herniation of the cerebellar tonsils (p20 Hounsfield Units), and the gray to white matter ratio was >1.58 when leukoencephalopathy was excluded. Despite normal postmortem changes, generalized brain edema can be differentiated on postmortem computed tomography, and white and gray matter Hounsfield measurements help to determine the cause of death in cases of intoxication or asphyxia. Racking the brain about feasible applications for a precise and reliable brain diagnostic forensic radiology method has just begun. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  2. Vascular endothelial growth factor A protein level and gene expression in intracranial meningiomas with brain edema

    DEFF Research Database (Denmark)

    Nassehi, Damoun; Dyrbye, Henrik; Andresen, Morten

    2011-01-01

    Meningiomas are the second most common primary intracranial tumors in adults. Although meningiomas are mostly benign, more than 50% of patients with meningioma develop peritumoral brain edema (PTBE), which may be fatal because of increased intracranial pressure. Vascular endothelial growth factor...

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

    Directory of Open Access Journals (Sweden)

    Wei Li

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

  4. Brain tissue oxygenation-guided management of diabetic ketoacidosis induced cerebral edema*.

    Science.gov (United States)

    O'Brien, Nicole F; Mella, Cesar

    2012-11-01

    Type 1 diabetes mellitus is the most common chronic disease of childhood. Diabetic ketoacidosis is a well-known complication of diabetes mellitus and can be associated with devastating cerebral edema resulting in severe long-term neurologic disability. Despite the significant morbidity and mortality associated with this condition, relatively few treatments are recommended for these patients. The authors present two patients in which they used both intracranial pressure and brain tissue oxygenation monitoring to manage diabetic ketoacidosis-associated cerebral edema with favorable neurologic outcomes. Pediatric intensive care unit in a tertiary care teaching hospital. Two children presented to the emergency room with vague complaints and were found to have diabetic ketoacidosis. During treatment, both patients became comatose with head computed tomography scans revealing diffuse cerebral edema and herniation syndrome. Intracranial pressure and brain tissue oxygenation monitors were placed to guide therapy. Multiple episodes of brain tissue hypoxia were noted in both patients. Intracranial pressure control with intubation, sedation, and hyperosmolar therapy improved episodes of decreased brain tissue oxygenation associated with intracranial hypertension. Brain tissue oxygenation was also noted to be significantly less than the target value on several occasions even when intracranial pressure was controlled and an age-appropriate cerebral perfusion pressure goal was met. Augmentation of cerebral perfusion pressure above age-appropriate goal with fluid boluses and inotropic agents increased brain tissue oxygenation in these instances. Both children had very low Glasgow Coma Scale scores at admission, but ultimately had favorable neurologic outcomes. Multimodal neuromonitoring of both intracranial pressure and brain tissue oxygenation during episodes of clinically apparent diabetic ketoacidosis-associated cerebral edema allows for the detection and treatment of episodes

  5. Increased brain edema following 5-aminolevulinic acid mediated photodynamic in normal and tumor bearing rats

    Science.gov (United States)

    Hirschberg, Henry; Angell-Petersen, Even; Spetalen, Signe; Mathews, Marlon; Madsen, Steen J.

    2007-02-01

    Introduction: Failure of treatment for high grade gliomas is usually due to local recurrence at the site of surgical resection indicating that a more aggressive form of local therapy, such as PDT, could be of benefit. PDT causes damage to both tumor cells as well as cerebral blood vessels leading to degradation of the blood brain barrier with subsequent increase of brain edema. The increase in brain edema following ALA-PDT was evaluated in terms of animal survival, histopatological changes in normal brain and tumor tissue and MRI scanning. The effect of steroid treatment, to reduce post-treatment PDT induced edema, was also examined. Methods:Tumors were established in the brains of inbred BD-IX and Fisher rats. At various times following tumor induction the animals were injected with ALA ip. and four hours later light treatment at escalating fluences and fluence rates were given. Nontumor bearing control animals were also exposed to ALA-PDT in a similar manner to evaluate damage to normal brain and degree of blood brain barrier (BBB) disruption. Results: Despite a very low level of PpIX production in normal brain, with a 200:1 tumor to normal tissue selectivity ratio measured at a distance of 2 mm from the tumor border, many animals succumbed shortly after treatment. A total radiant energy of 54 J to non-tumor bearing animals resulted in 50% mortality within 5 days of treatment. Treatment of tumor bearing animals with moderate fluence levels produced similar brain edema compared to higher fluence levels. ALA PDT in nontumor bearing animals produced edema that was light dose dependent. PDT appeared to open the BBB for a period of 24-48 hrs after which it was restored. The addition of post operative steroid treatment reduced the incident of post treatment morbidity and mortality. Conclusions: T2 and contrast enhanced T1 MRI scanning proved to be a highly effective and non-evasive modality in following the development of the edema reaction and the degree and time

  6. Central role of maladapted astrocytic plasticity in ischemic brain edema formation

    Directory of Open Access Journals (Sweden)

    Yu-Feng eWang

    2016-05-01

    Full Text Available Brain edema formation and the ensuing brain damages are the major cause of high mortality and long term disability following the occurrence of ischemic stroke. In this process, oxygen and glucose deprivation and the ensuing reperfusion injury play primary roles. In response to the ischemic insult, the neurovascular unit experiences both intracellular and extracellular edemas; the two processes are interactive closely under the driving of maladapted astrocytic plasticity. The astrocytic plasticity includes both morphologic and functional plasticity. The former involves a reactive gliosis and the ensuing glial retraction. It relates to the capacity of astrocytes to buffer changes in extracellular chemical levels, particularly K+ and glutamate, as well as the integrity of the blood-brain barrier. The latter involves the expression and activity of a series of ion and water transport proteins. These molecules are grouped together around glial fibrillary acidic protein and water channel protein aquaporin 4 to form functional networks, regulate hydromineral balance across cell membranes and maintain the integrity of the blood-brain barrier. Intense ischemic challenges can disrupt these capacities of astrocytes and result in their maladaptation. The maladapted astrocytic plasticity in ischemic stroke cannot only disrupt the hydromineral homeostasis across astrocyte membrane and the blood-brain barrier, but also lead to disorders of the whole neurovascular unit. This review focuses on how the maladapted astrocytic plasticity in ischemic stroke plays the central role in the brain edema formation.

  7. Heterogeneity of brain lesions in pediatric traumatic brain injury.

    Science.gov (United States)

    Bigler, Erin D; Abildskov, Tracy J; Petrie, Joann; Farrer, Thomas J; Dennis, Maureen; Simic, Nevena; Taylor, H Gerry; Rubin, Kenneth H; Vannatta, Kathryn; Gerhardt, Cynthia A; Stancin, Terry; Owen Yeates, Keith

    2013-07-01

    Magnetic resonance imaging (MRI) provides a method to identify and quantify abnormalities resulting from traumatic brain injury (TBI). MRI abnormalities in children with TBI have not been fully characterized according to the frequency, location, and quantitative measurement of a range of pathologies critical for studies of neuropsychological outcome. Here, we report MRI findings from a large, multicenter study of childhood TBI, the Social Outcomes of Brain Injury in Kids (SOBIK) study, which compared qualitative and quantitative neuroimaging findings in 72 children with complicated mild-to-severe TBI to 52 children with orthopedic injury (OI). Qualitative analyses of MRI scans coded white matter hyperintensities (WMHs), hemosiderin deposits reflecting prior hemorrhagic lesions, regions of encephalomalacia and/or atrophy, and corpus callosum atrophy and traumatic shear lesions. Two automated quantitative analyses were conducted: (a) FreeSurfer methods computed volumes for total brain, white matter (WM), gray matter (GM), corpus callosum, ventricles, amygdala, hippocampus, basal ganglia, and thalamus along with a ventricle-to-brain ratio (VBR); and (b) voxel-based morphometry (VBM) to identify WM, GM, and cerebrospinal fluid. We also examined performance on the Processing Speed Index (PSI) from the Wechsler Intelligence Scale for Children, Fourth Edition, in relation to the above-mentioned neuroimaging variables. WMHs, hemosiderin deposits, and focal areas of encephalomalacia or atrophy were common in children with TBI, were related to injury severity, and were mostly observed within a frontotemporal distribution. Quantitative analyses showed volumetric changes related to injury severity, especially ventricular enlargement and reduced corpus callosum volume. VBM demonstrated similar findings, but, in addition, GM reductions in the inferior frontal, basal forebrain region, especially in the severe TBI group. The complicated mild TBI group showed few differences from

  8. Risk factors and outcomes associated with post-traumatic headache after mild traumatic brain injury

    NARCIS (Netherlands)

    Yilmaz, Tansel; Roks, Gerwin; de Koning, Myrthe; Scheenen, Myrthe; van der Horn, Harm; Plas, Gerben; Hageman, Gerard; Schoonman, Guus; Spikman, Jacoba; van der Naalt, Joukje

    2017-01-01

    Objectives: To determine the prevalence and potential risk factors of acute and chronic post-traumatic headache (PTH) in patients with mild to moderate traumatic brain injury (TBI) in a prospective longitudinal observational multicentre study. Acute PTH (aPTH) is defined by new or worsening of

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

    Science.gov (United States)

    Sinski, Jennifer Blevins

    2012-01-01

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

  10. Neuropsychological rehabilitation for traumatic brain injury patients

    Directory of Open Access Journals (Sweden)

    Marzena Chantsoulis

    2015-05-01

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

  11. Quantitative Apparent Diffusion Coefficients in the Characterization of Brain Tumors and Associated Peritumoral Edema

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    Server, A.; Schellhorn, T.; Nakstad, P.H. (Dept. of Neuroradiology, Div. of Radiology, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway)); Kulle, B. (Epi-Gen Faculty Div. Akershus Univ. Hospital and Dept. of Biostatistics, Univ. of Oslo, Oslo (Norway)); Maehlen, J.; Kumar, T. (Dept. of Pathology, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway)); Josefsen, R. (Dept. of Neurosurgery, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway)); Langberg, C.W. (Cancer Centre, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway))

    2009-07-15

    Background: Conventional magnetic resonance (MR) imaging has a number of limitations in the diagnosis of the most common intracranial brain tumors, including tumor specification and the detection of tumoral infiltration in regions of peritumoral edema. Purpose: To prospectively assess if diffusion-weighted MR imaging (DWI) could be used to differentiate between different types of brain tumors and to distinguish between peritumoral infiltration in high-grade gliomas, lymphomas, and pure vasogenic edema in metastases and meningiomas. Material and Methods: MR imaging and DWI was performed on 93 patients with newly diagnosed brain tumors: 59 patients had histologically verified high-grade gliomas (37 glioblastomas multiforme, 22 anaplastic astrocytomas), 23 patients had metastatic brain tumors, five patients had primary cerebral lymphomas, and six patients had meningiomas. Apparent diffusion coefficient (ADC) values of tumor (enhancing regions or the solid portion of tumor) and peritumoral edema, and ADC ratios (ADC of tumor or peritumoral edema to ADC of contralateral white matter, ADC of tumor to ADC of peritumoral edema) were compared with the histologic diagnosis. ADC values and ratios of high-grade gliomas, primary cerebral lymphomas, metastases, and meningiomas were compared by using ANOVA and multiple comparisons. Optimal thresholds of ADC values and ADC ratios for distinguishing high-grade gliomas from metastases were determined by receiver operating characteristic (ROC) curve analysis. Results: Statistically significant differences were found for minimum and mean of ADC tumor and ADC tumor ratio values between metastases and high-grade gliomas when including only one factor at a time. Including a combination of in total four parameters (mean ADC tumor, and minimum, maximum and mean ADC tumor ratio) resulted in sensitivity, specificity, positive (PPV), and negative predictive values (NPV) of 72.9, 82.6, 91.5, and 54.3% respectively. In the ROC curve analysis

  12. Quantitative Apparent Diffusion Coefficients in the Characterization of Brain Tumors and Associated Peritumoral Edema

    International Nuclear Information System (INIS)

    Server, A.; Schellhorn, T.; Nakstad, P.H.; Kulle, B.; Maehlen, J.; Kumar, T.; Josefsen, R.; Langberg, C.W.

    2009-01-01

    Background: Conventional magnetic resonance (MR) imaging has a number of limitations in the diagnosis of the most common intracranial brain tumors, including tumor specification and the detection of tumoral infiltration in regions of peritumoral edema. Purpose: To prospectively assess if diffusion-weighted MR imaging (DWI) could be used to differentiate between different types of brain tumors and to distinguish between peritumoral infiltration in high-grade gliomas, lymphomas, and pure vasogenic edema in metastases and meningiomas. Material and Methods: MR imaging and DWI was performed on 93 patients with newly diagnosed brain tumors: 59 patients had histologically verified high-grade gliomas (37 glioblastomas multiforme, 22 anaplastic astrocytomas), 23 patients had metastatic brain tumors, five patients had primary cerebral lymphomas, and six patients had meningiomas. Apparent diffusion coefficient (ADC) values of tumor (enhancing regions or the solid portion of tumor) and peritumoral edema, and ADC ratios (ADC of tumor or peritumoral edema to ADC of contralateral white matter, ADC of tumor to ADC of peritumoral edema) were compared with the histologic diagnosis. ADC values and ratios of high-grade gliomas, primary cerebral lymphomas, metastases, and meningiomas were compared by using ANOVA and multiple comparisons. Optimal thresholds of ADC values and ADC ratios for distinguishing high-grade gliomas from metastases were determined by receiver operating characteristic (ROC) curve analysis. Results: Statistically significant differences were found for minimum and mean of ADC tumor and ADC tumor ratio values between metastases and high-grade gliomas when including only one factor at a time. Including a combination of in total four parameters (mean ADC tumor, and minimum, maximum and mean ADC tumor ratio) resulted in sensitivity, specificity, positive (PPV), and negative predictive values (NPV) of 72.9, 82.6, 91.5, and 54.3% respectively. In the ROC curve analysis

  13. 45 CFR 1308.16 - Eligibility criteria: Traumatic brain injury.

    Science.gov (United States)

    2010-10-01

    ... child is classified as having traumatic brain injury whose brain injuries are caused by an external... adversely affect educational performance. The term includes children with open or closed head injuries, but does not include children with brain injuries that are congenital or degenerative or caused by birth...

  14. Alpha-Tocopherol Reduces Brain Edema and Protects Blood-Brain Barrier Integrity following Focal Cerebral Ischemia in Rats.

    Science.gov (United States)

    Haghnejad Azar, Adel; Oryan, Shahrbanoo; Bohlooli, Shahab; Panahpour, Hamdollah

    2017-01-01

    This study was conducted to examine the neuroprotective effects of α-tocopherol against edema formation and disruption of the blood-brain barrier (BBB) following transient focal cerebral ischemia in rats. Ninety-six male Sprague-Dawley rats were divided into 3 major groups (n = 32 in each), namely the sham, and control and α-tocopherol-treated (30 mg/kg) ischemic groups. Transient focal cerebral ischemia (90 min) was induced by occlusion of the left middle cerebral artery. At the end of the 24-hour reperfusion period, the animals were randomly selected and used for 4 investigations (n = 8) in each of the 3 main groups: (a) assessment of neurological score and measurement of infarct size, (b) detection of brain edema formation by the wet/dry method, (c) evaluation of BBB permeability using the Evans blue (EB) extravasation technique, and (d) assessment of the malondialdehyde (MDA) and reduced glutathione (GSH) concentrations using high-performance liquid chromatography methods. Induction of cerebral ischemia in the control group produced extensive brain edema (brain water content 83.8 ± 0.11%) and EB leakage into brain parenchyma (14.58 ± 1.29 µg/g) in conjunction with reduced GSH and elevated MDA levels (5.86 ± 0.31 mmol/mg and 63.57 ± 5.42 nmol/mg, respectively). Treatment with α-tocopherol significantly lowered brain edema formation and reduced EB leakage compared with the control group (p edema formation and produced protective effects on BBB function following ischemic stroke occurrence. This effect could be through increasing antioxidant activity. © 2016 S. Karger AG, Basel.

  15. Spreading depolarisations and outcome after traumatic brain injury

    DEFF Research Database (Denmark)

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

    2011-01-01

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

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

    Data.gov (United States)

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

  17. Preliminary questions before studying mild traumatic brain injury outcome.

    Science.gov (United States)

    Fayol, P; Carrière, H; Habonimana, D; Dumond, J-J

    2009-07-01

    To point out from the literature the issues in mild traumatic brain injury outcome. METHODOLOGY-RESULTS: The literature review allows to point out several different factors involved in the difficulty to study mild traumatic brain injury: mild traumatic brain injury definition, postconcussional syndrome definition, diagnosis threshold, severity and functional symptoms outcome, neuropsychological tests, unspecific syndrome feature, individual factors, confounding factors and treatment interventions. The mild traumatic brain injury outcome study is complicated by the definitions issues and especially their practical use and by the multiplicity and the intricate interrelationships among involved factors. The individual outcome and social cost weight is widely emphasized for an event still considered as medically trivial. The well-ordered preventive interventions necessity and the targeted treatment programs need for the persisting postconcussive symptoms complete our critical review.

  18. Antioxidant therapies in traumatic brain injury: a review

    Directory of Open Access Journals (Sweden)

    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.

  19. Acute, transient hemorrhagic hypotension does not aggravate structural damage or neurologic motor deficits but delays the long-term cognitive recovery following mild to moderate traumatic brain injury

    Science.gov (United States)

    Schütz, Christian; Stover, John F.; Thompson, Hilaire J.; Hoover, Rachel C.; Morales, Diego M.; Schouten, Joost W.; McMillan, Asenia; Soltesz, Kristie; Motta, Melissa; Spangler, Zachery; Neugebauer, Edmund; McIntosh, Tracy K.

    2008-01-01

    Objectives Posttraumatic hypotension is believed to increase morbidity and mortality in traumatically brain-injured patients. Using a clinically relevant model of combined traumatic brain injury with superimposed hemorrhagic hypotension in rats, the present study evaluated whether a reduction in mean arterial blood pressure aggravates regional brain edema formation, regional cell death, and neurologic motor/cognitive deficits associated with traumatic brain injury. Design Experimental prospective, randomized study in rodents. Setting Experimental laboratory at a university hospital. Subjects One hundred nineteen male Sprague-Dawley rats weighing 350-385 g. Interventions Experimental traumatic brain injury of mild to moderate severity was induced using the lateral fluid percussion brain injury model in anesthetized rats (n = 89). Following traumatic brain injury, in surviving animals one group of animals was subjected to pressure-controlled hemorrhagic hypotension, maintaining the mean arterial blood pressure at 50-60 mm Hg for 30 mins (n = 47). The animals were subsequently either resuscitated with lactated Ringer’s solution (three times shed blood volume, n = 18) or left uncompensated (n = 29). Other groups of animals included those with isolated traumatic brain injury (n = 34), those with isolated hemorrhagic hypotension (n = 8), and sham-injured control animals receiving anesthesia and surgery alone (n = 22). Measurements and Main Results The withdrawal of 6-7 mL of arterial blood significantly reduced mean arterial blood pressure by 50% without decreasing arterial oxygen saturation or Pao2. Brain injury induced significant cerebral edema (p hypotension. Brain injury-induced neurologic deficits persisted up to 20 wks after injury and were also not aggravated by the hemorrhagic hypotension. Cognitive dysfunction persisted for up to 16 wks postinjury. The superimposition of hemorrhagic hypotension significantly delayed the time course of cognitive recovery

  20. 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.

  1. [Application of noninvasive cerebral electrical impedance measurement on brain edema in patient with cerebral infarction].

    Science.gov (United States)

    He, Lan-Ying; Wang, Jian; Zhang, Bei; Dong, Wei-Wei; Luo, Yong

    2010-11-23

    to investigate the change of brain edema in patients with cerebral infarction (CI) by the measurement of noninvasive cerebral electrical impedance (CEI). an invariable secure current at a frequency 50 kHz and an intensity of 0.1 mA was applied into a person's brain. The CEI of values for both hemispheres of 200 healthy volunteers and 107 CI patients was measured. The results were compared with the volume of edema on CT. (1) in healthy volunteers, the CEI values in the left and right hemisphere were 8.0 ± 1.0 and 8.0 ± 0.7 respectively. And there was no significant difference between either side (P > 0.05). Age, sex and different measuring time points did not obviously affect the CEI values (P > 0.05). (2) In CI patients, the CEI was more sensitive in the volumes of lesion which was more than 20 ml (80.0%), the CEI was75.9% and 83.3% in the volumes of lesion which was 20 - 50 ml and more than 50 ml respectively. The CEI was low when the volume fell under 20 ml; (3) The CEI of the ipsilateral side was higher than contralateral side in the patients at Day 3 after onset. It increased obviously at Days 3 - 5 after onset. The difference of two sides was the most significant. CEI of two sides was 9.2 ± 2.1 and 8.8 ± 1.8 (n = 91, P 0.05); (4) There was a positive correlation between the ispilateral CEI and the volume of infarction detected within 24 hours (n = 31, r = 0.682, P brain edema in CI patients. The higher the CEI, the more severe edema resulted. The sensitivity of CEI is higher when the volume of infarction exceeds 20 ml. CEI is a new technique for judging the patient condition of brain edema noninvasively.

  2. Transcranial measurement of diffuse light reflectance from brain edema in rats: effect of change in the blood flow

    Science.gov (United States)

    Ueda, Yoshinori; Sato, Shunichi; Ooigawa, Hidetoshi; Nawashiro, Hiroshi; Saitoh, Daizoh; Shima, Katsuji; Okada, Yoshiaki; Ashida, Hiroshi; Obara, Minoru

    2005-04-01

    We assumed that edema causes a decrease in the scattering coefficient of brain tissue and hence a decrease in the intensity of diffuse reflectance from the brain. On the basis of this assumption, we attempted to transcranially detect a formation of brain edema by measuring diffuse light reflectance. In rats, edema was induced by making a cold injury in the brain. The skull was irradiated with 633-nm and 532-nm laser light delivered through an optical fiber, and the diffuse light reflectance from the brain was collected with another optical fiber. We observed that reflectance intensities were significantly decreased around the cold injury both at 633 nm and 532 nm, suggesting that scattering coefficient of brain tissue was reduced due to a formation of edema in this area. In the injury, reflectance intensity was increased at 532 nm, indicating that cerebral blood volume was decreased in this region.

  3. Pharmacological Treatment of Glutamate Excitotoxicity Following Traumatic Brain Injury

    Science.gov (United States)

    2009-01-14

    In 1969, Olney found that subcutaneous injection of monosodium glutamate resulted in necrotic brain lesions in the hypothalamus of newborn mice...Thesis: "Pharmacological Treatment of Glutamate Excitotoxicity Following Traumatic Brain Injury" Name of Candidate: Michael Doh Molecular & Cell...TYPE 3. DATES COVERED 00-00-2009 to 00-00-2009 4. TITLE AND SUBTITLE Pharmacological Treatment Of Glutamate Excitotoxicity Following Traumatic

  4. Cerebral edema following iodine-131 therapy for thyroid carcinoma metastatic to the brain

    International Nuclear Information System (INIS)

    Datz, F.L.

    1986-01-01

    Brain metastases are rare in well-differentiated thyroid carcinoma but when present they can lead to the patient's death. Iodine-131 therapy for intracerebral thyroid carcinoma metastases causes radiation-induced acute cerebral edema that can lead to CNS complications and even death. We present a case in which a patient with intracerebral 131 I uptake developed seizures, slurred speech, and muscle weakness 12 hr following 131 I therapy. The patient's CT scan, post-therapy, confirmed an intracranial metastasis with a significant amount of surrounding edema. Radiotherapists, when using external beam radiation to treat intracerebral metastases, commonly place these patients on steroids, glycerol, or mannitol prior to instituting therapy, to prevent complications from radiation-induced cerebral edema. This technique could be applied to 131 I therapy of intracranial thyroid carcinoma metastases as well

  5. Rehabilitation of persons with traumatic brain injury.

    Science.gov (United States)

    The objective of this NIH Consensus Statement is to inform the biomedical research and clinical practice communities of the results of the NIH Consensus Development Conference on Rehabilitation of Persons with Traumatic Brain Injury. The statement provides state-of-the-art information regarding effective rehabilitation measures for persons who have suffered a traumatic brain injury (TBI) and presents the conclusions and recommendations of the consensus panel regarding these issues. In addition, the statement identifies those areas that deserve further investigation. Upon completion of this educational activity, the reader should possess a clear working clinical knowledge of the state of the art regarding this topic. The target audience for this statement includes, but is not limited to, pediatricians, family practitioners, internists, neurologists, physiatrists, psychologists, and behavioral medicine specialists. Participants were a non-Federal, nonadvocate, 16-member panel representing the fields of neuropsychology, neurology, psychiatry, behavioral medicine, family medicine, pediatrics, physical medicine and rehabilitation, speech and hearing, occupational therapy, nursing, epidemiology, biostatistics and the public. In addition, 23 experts from these same fields presented data to the panel and a conference audience of 883. The literature was searched through Medline and an extensive bibliography of references was provided to the panel and the conference audience. Experts prepared abstracts with relevant citations from the literature. A compendium of evidence was prepared by the panel which included a contribution from a patient with TBI, a report from an Evidence Based Practice Center of the Agency for Health Care Policy and Research, and a report from the National Center for Injury Prevention and Control at the Centers for Disease Control and Prevention. Scientific evidence was given precedence over clinical anecdotal experience. The panel, answering predefined

  6. Dexamethasone exacerbates cerebral edema and brain injury following lithium-pilocarpine induced status epilepticus.

    Science.gov (United States)

    Duffy, B A; Chun, K P; Ma, D; Lythgoe, M F; Scott, R C

    2014-03-01

    Anti-inflammatory therapies are the current most plausible drug candidates for anti-epileptogenesis and neuroprotection following prolonged seizures. Given that vasogenic edema is widely considered to be detrimental for outcome following status epilepticus, the anti-inflammatory agent dexamethasone is sometimes used in clinic for alleviating cerebral edema. In this study we perform longitudinal magnetic resonance imaging in order to assess the contribution of dexamethasone on cerebral edema and subsequent neuroprotection following status epilepticus. Lithium-pilocarpine was used to induce status epilepticus in rats. Following status epilepticus, rats were either post-treated with saline or with dexamethasone sodium phosphate (10mg/kg or 2mg/kg). Brain edema was assessed by means of magnetic resonance imaging (T2 relaxometry) and hippocampal volumetry was used as a marker of neuronal injury. T2 relaxometry was performed prior to, 48 h and 96 h following status epilepticus. Volume measurements were performed between 18 and 21 days after status epilepticus. Unexpectedly, cerebral edema was worse in rats that were treated with dexamethasone compared to controls. Furthermore, dexamethasone treated rats had lower hippocampal volumes compared to controls 3 weeks after the initial insult. The T2 measurements at 2 days and 4 days in the hippocampus correlated with hippocampal volumes at 3 weeks. Finally, the mortality rate in the first week following status epilepticus increased from 14% in untreated rats to 33% and 46% in rats treated with 2mg/kg and 10mg/kg dexamethasone respectively. These findings suggest that dexamethasone can exacerbate the acute cerebral edema and brain injury associated with status epilepticus. Copyright © 2013. Published by Elsevier Inc.

  7. Magnetic resonance studies on the brain edema by the administration of the osmotic agents

    International Nuclear Information System (INIS)

    Niino, Masaki; Asakura, Tetsuhiko; Nakamura, Katsumi; Yatsushiro, Kazutaka; Kadota, Koki; Sasahira, Masahiro; Fujimoto, Toshiro; Shimooki, Susumu.

    1990-01-01

    Changes of proton relaxation times (T 1 and T 2 ) and MR imaging of the brain edema by the administration of the osmotic agents (mannitol or glycerol) were studied. Subjects were 11 patients who were composed of 4 gliomas, 2 metastatic brain tumors, 2 meningiomas, 2 hypertensive intracerebral hematomas, and a C-P angle tumor. 20% mannitol or 10% glycerol 550 ml was rapidly injected intravenously. Scanning was done before injection, just after injection, and post injection until 2 hours with passing times. We regarded the peritumoral or perihemorrahgical low density area on the CT scan as the edema, and then, relaxation times of the edema was obtained from the ROI of the calculated images corresponding to the surrounding low density area on the CT scan. The results were as follows. 1) In general, relaxation times of the edema showed a tendency to decrease after injection of the osmotic agents. Normal white matter, in the same way, showed the decreasing tendency, but the degree of the decreasing was more clearly in the edematous areas than in the white matter. 2) The changes of relaxation times did not show a uniform pattern. In most cases, relaxation times decreased just after injection. But in a few cases, relaxation times increased just after injection, transiently. In some cases, decreased relaxation times continued more than 2 hours, in the other cases, relaxation times increased at 2 hours. 3) The changes of relaxation times thought to be varied by some factors, that is --kinds of the lesions causing edema, degree of malignancy of the lesions, or phase of edema (acute or chronic) etc. 4) Osmotic agents were supposed to dehydrate the edematous lesions. In the current MR systems, there are considerably large standard deviations and inequality in the magnetic field, therefore, further investigations should be done moreover. (author)

  8. Peritumoral brain edema in intracranial meningiomas evaluated by dynamic perfusion-weighted MR imaging: a preliminary study

    Energy Technology Data Exchange (ETDEWEB)

    Uematsu, Hidemasa; Itoh, Harumi [Department of Radiology, Fukui Medical University, Fukui (Japan); Maeda, Masayuki [Department of Radiology, Mie University School of Medicine, Mie (Japan)

    2003-04-01

    Our objective was to semi-quantitatively evaluate the cerebral perfusion in the peritumoral brain edema of meningiomas using dynamic perfusion-weighted MR imaging. Six patients with intracranial meningiomas accompanied by peritumoral brain edema were prospectively examined by perfusion-weighted MR imaging. One patient was examined twice, once before and once 5 months after the surgical resection. The relative regional cerebral blood volume (rrCBV), the relative regional cerebral blood flow (rrCBF), and the relative regional mean transit time (rrMTT) were calculated for peritumoral brain edema and the contralateral white matter. These parameters were compared between peritumoral brain edema and the contralateral white matter. The time-concentration curve of the peritumoral brain edema was less prominent than that of the contralateral white matter, resulting in a significantly lower rrCBV (mean 46%) and rrCBF (mean 45%) in peritumoral brain edema than those of contralateral white matter. The serial perfusion-weighted MR imaging also demonstrated the recovery of these parameters after the removal of meningioma by means of surgical resection. Perfusion-weighted MR imaging can demonstrate significantly decreased rrCBV and rrCBF in peritumoral brain edema compared with those in normal white matter. (orig.)

  9. Peritumoral brain edema in intracranial meningiomas evaluated by dynamic perfusion-weighted MR imaging: a preliminary study

    International Nuclear Information System (INIS)

    Uematsu, Hidemasa; Itoh, Harumi; Maeda, Masayuki

    2003-01-01

    Our objective was to semi-quantitatively evaluate the cerebral perfusion in the peritumoral brain edema of meningiomas using dynamic perfusion-weighted MR imaging. Six patients with intracranial meningiomas accompanied by peritumoral brain edema were prospectively examined by perfusion-weighted MR imaging. One patient was examined twice, once before and once 5 months after the surgical resection. The relative regional cerebral blood volume (rrCBV), the relative regional cerebral blood flow (rrCBF), and the relative regional mean transit time (rrMTT) were calculated for peritumoral brain edema and the contralateral white matter. These parameters were compared between peritumoral brain edema and the contralateral white matter. The time-concentration curve of the peritumoral brain edema was less prominent than that of the contralateral white matter, resulting in a significantly lower rrCBV (mean 46%) and rrCBF (mean 45%) in peritumoral brain edema than those of contralateral white matter. The serial perfusion-weighted MR imaging also demonstrated the recovery of these parameters after the removal of meningioma by means of surgical resection. Perfusion-weighted MR imaging can demonstrate significantly decreased rrCBV and rrCBF in peritumoral brain edema compared with those in normal white matter. (orig.)

  10. Acute and Subacute Presentations of Cerebral Edema following Deep Brain Stimulation Lead Implantation.

    Science.gov (United States)

    Fenoy, Albert J; Villarreal, Sebastian J; Schiess, Mya C

    2017-01-01

    Postoperative cerebral edema around a deep brain stimulation (DBS) electrode is an uncommon reported complication. The goal of this study was to identify instances of postoperative edema based on clinical presentation, and to remark on their management. A retrospective chart review was performed on all patients who underwent DBS electrode implantation over a 3-year period. Routine CT imaging on postoperative day (POD) 1 was negative. Patients were identified based on clinical neurological changes, leading to imaging and subsequent diagnosis. Five of 145 patients (3.4%) presented with new neurological symptoms from POD 1 to 14, which were confirmed by CT imaging to show perilead and/or subcortical edema around 6 of 281 electrodes (2.1%). Four of 5 patients had unilateral edema despite bilateral implantation. Clinical presentations varied widely. Two patients presenting on POD 1 with deteriorating conditions required longer inpatient stays with supportive measures than those presenting later (p = 0.0002). All patients were treated with corticosteroids and returned to baseline by 3 months after surgery. Acute instances of DBS lead edema may occur as early as POD 1 and can rapidly progress into profound deficits. Treatment with supportive care and corticosteroids is otherwise identical to those cases presenting later. © 2017 S. Karger AG, Basel.

  11. Racking the brain: Detection of cerebral edema on postmortem computed tomography compared with forensic autopsy

    Energy Technology Data Exchange (ETDEWEB)

    Berger, Nicole [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Institute of Diagnostic and Interventional Radiology, University Hospital of Zurich, Raemistrasse 100, 8091 Zurich (Switzerland); Ampanozi, Garyfalia; Schweitzer, Wolf; Ross, Steffen G.; Gascho, Dominic [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Ruder, Thomas D. [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Institute of Diagnostic, Interventional and Pediatric Radiology, University Hospital of Bern, Freiburgstrasse, 3010 Bern (Switzerland); Thali, Michael J. [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Flach, Patricia M., E-mail: patricia.flach@irm.uzh.ch [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Institute of Diagnostic and Interventional Radiology, University Hospital of Zurich, Raemistrasse 100, 8091 Zurich (Switzerland)

    2015-04-15

    Graphical abstract: -- Highlights: •Postmortem swelling of the brain is a typical finding on PMCT and occurs concomitant with potential antemortem or agonal brain edema. •Cerebral edema despite normal postmortem swelling is indicated by narrowed temporal horns and symmetrical herniation of the cerebral tonsils on PMCT. •Cases with intoxication or asphyxia demonstrated higher deviations of the attenuation between white and gray matter (>20 Hounsfield Units) and a ratio >1.58 between the gray and white matter. •The Hounsfield measurements of the white and gray matter help to determine the cause of death in cases of intoxication or asphyxia. -- Abstract: Purpose: The purpose of this study was to compare postmortem computed tomography with forensic autopsy regarding their diagnostic reliability of differentiating between pre-existing cerebral edema and physiological postmortem brain swelling. Materials and methods: The study collective included a total of 109 cases (n = 109/200, 83 male, 26 female, mean age: 53.2 years) and were retrospectively evaluated for the following parameters (as related to the distinct age groups and causes of death): tonsillar herniation, the width of the outer and inner cerebrospinal fluid spaces and the radiodensity measurements (in Hounsfield Units) of the gray and white matter. The results were compared with the findings of subsequent autopsies as the gold standard for diagnosing cerebral edema. p-Values <0.05 were considered statistically significant. Results: Cerebellar edema (despite normal postmortem swelling) can be reliably assessed using postmortem computed tomography and is indicated by narrowed temporal horns and symmetrical herniation of the cerebellar tonsils (p < 0.001). There was a significant difference (p < 0.001) between intoxication (or asphyxia) and all other causes of death; the former causes demonstrated higher deviations of the attenuation between white and gray matter (>20 Hounsfield Units), and the gray to

  12. Racking the brain: Detection of cerebral edema on postmortem computed tomography compared with forensic autopsy

    International Nuclear Information System (INIS)

    Berger, Nicole; Ampanozi, Garyfalia; Schweitzer, Wolf; Ross, Steffen G.; Gascho, Dominic; Ruder, Thomas D.; Thali, Michael J.; Flach, Patricia M.

    2015-01-01

    Graphical abstract: -- Highlights: •Postmortem swelling of the brain is a typical finding on PMCT and occurs concomitant with potential antemortem or agonal brain edema. •Cerebral edema despite normal postmortem swelling is indicated by narrowed temporal horns and symmetrical herniation of the cerebral tonsils on PMCT. •Cases with intoxication or asphyxia demonstrated higher deviations of the attenuation between white and gray matter (>20 Hounsfield Units) and a ratio >1.58 between the gray and white matter. •The Hounsfield measurements of the white and gray matter help to determine the cause of death in cases of intoxication or asphyxia. -- Abstract: Purpose: The purpose of this study was to compare postmortem computed tomography with forensic autopsy regarding their diagnostic reliability of differentiating between pre-existing cerebral edema and physiological postmortem brain swelling. Materials and methods: The study collective included a total of 109 cases (n = 109/200, 83 male, 26 female, mean age: 53.2 years) and were retrospectively evaluated for the following parameters (as related to the distinct age groups and causes of death): tonsillar herniation, the width of the outer and inner cerebrospinal fluid spaces and the radiodensity measurements (in Hounsfield Units) of the gray and white matter. The results were compared with the findings of subsequent autopsies as the gold standard for diagnosing cerebral edema. p-Values <0.05 were considered statistically significant. Results: Cerebellar edema (despite normal postmortem swelling) can be reliably assessed using postmortem computed tomography and is indicated by narrowed temporal horns and symmetrical herniation of the cerebellar tonsils (p < 0.001). There was a significant difference (p < 0.001) between intoxication (or asphyxia) and all other causes of death; the former causes demonstrated higher deviations of the attenuation between white and gray matter (>20 Hounsfield Units), and the gray to

  13. Persuasive discourse impairments in traumatic brain injury.

    Science.gov (United States)

    Ghayoumi, Zahra; Yadegari, Fariba; Mahmoodi-Bakhtiari, Behrooz; Fakharian, Esmaeil; Rahgozar, Mehdi; Rasouli, Maryam

    2015-03-01

    Considering the cognitive and linguistic complexity of discourse production, it is expected that individuals with traumatic brain injury (TBI) should face difficulties in this task. Therefore, clinical examination of discourse has become a useful tool for studying and assessment of communication skills of people suffering from TBI. Among different genres of discourse, persuasive discourse is considered as a more cognitively demanding task. However, little is known about persuasive discourse in individuals suffering from TBI. The purpose of this study was to evaluate the performance of adults with TBI on a task of spoken persuasive discourse to determine the impaired linguistic measures. Thirteen TBI nonaphasic Persian speaking individuals, ranged between 19 to 40 years (Mean = 25.64 years; SD = 6.10) and 59 healthy adults matched by age, were asked to perform the persuasive discourse task. The task included asking the participants to express their opinion on a topic, and after the analysis of the produced discourse, the two groups were compared on the basis of their language productivity, sentential complexity, maze ratio and cohesion ratio. The TBI group produced discourses with less productivity, sentential complexity, cohesion ratio and more maze ratio compared the control group. As it is important to consider acquired communication disorders particularly discourse impairment of brain injured patients along with their other clinical impairments and regarding the fact that persuasive discourse is crucial in academic and social situations, the persuasive discourse task presented in this study could be a useful tool for speech therapists, intending to evaluate communication disorders in patients with TBI.

  14. Social functioning after traumatic brain injury.

    Science.gov (United States)

    Temkin, Nancy R; Corrigan, John D; Dikmen, Sureyya S; Machamer, Joan

    2009-01-01

    To determine the relationship between adult-onset traumatic brain injury (TBI) and social functioning including employment, social relationships, independent living, recreation, functional status, and quality of life 6 months or longer after injury. Not applicable. Systematic review of the published, peer-reviewed literature. Not applicable. Fourteen primary and 25 secondary studies were identified that allowed comparison to controls for adults who were at least 6 months post-TBI. TBI decreases the probability of employment after injury in those who were workers before their injury, lengthens the timing of their return if they do return to work, and decreases the likelihood that they will return to the same position. Those with moderate and severe TBI are clearly affected, but there was insufficient evidence of a relationship between unemployment and mild TBI. Penetrating head injury sustained in wartime is clearly associated with increased unemployment. TBI also adversely affects leisure and recreation, social relationships, functional status, quality of life, and independent living. Although there is a dose-response relationship between severity of injury and social outcomes, there is insufficient evidence to determine at what level of severity the adverse effects are demonstrated. TBI clearly has adverse effects on social functioning for adults. While some consequences might arise from injuries to other parts of the body, those with moderate to severe TBI have more impaired functioning than do those with other injuries alone.

  15. Iatrogenic traumatic brain injury during tooth extraction.

    Science.gov (United States)

    Troxel, Mark

    2015-01-01

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

  16. Dysautonomia after severe traumatic brain injury.

    Science.gov (United States)

    Hendricks, H T; Heeren, A H; Vos, P E

    2010-09-01

    Dysautonomia after traumatic brain injury (TBI) is characterized by episodes of increased heart rate, respiratory rate, temperature, blood pressure, muscle tone, decorticate or decerebrate posturing, and profuse sweating. This study addresses the incidence of dysautonomia after severe TBI, the clinical variables that are associated with dysautonomia, and the functional outcome of patients with dysautonomia. A historic cohort study in patients with severe TBI [Glasgow Coma Scale (GCS) dysautonomia was 11.8%. Episodes of dysautonomia were prevalent during a mean period of 20.1 days (range 3-68) and were often initiated by discomfort. Patients with dysautonomia showed significant longer periods of coma (24.78 vs. 7.99 days) and mechanical ventilation (22.67 vs. 7.21 days). Dysautonomia was associated with diffuse axonal injury (DAI) [relative risk (RR) 20.83, CI 4.92-83.33] and the development of spasticity (RR 16.94, CI 3.96-71.42). Patients with dysautonomia experienced more secondary complications. They tended to have poorer outcome. Dysautonomia occurs in approximately 10% of patients surviving severe TBI and is associated with DAI and the development of spasticity at follow-up. The initiation of dysautonomia by discomfort supports the Excitatory: Inhibitory Ratio model as pathophysiological mechanism.

  17. Visual problems associated with traumatic brain injury.

    Science.gov (United States)

    Armstrong, Richard A

    2018-02-28

    Traumatic brain injury (TBI) and its associated concussion are major causes of disability and death. All ages can be affected but children, young adults and the elderly are particularly susceptible. A decline in mortality has resulted in many more individuals living with a disability caused by TBI including those affecting vision. This review describes: (1) the major clinical and pathological features of TBI; (2) the visual signs and symptoms associated with the disorder; and (3) discusses the assessment of quality of life and visual rehabilitation of the patient. Defects in primary vision such as visual acuity and visual fields, eye movement including vergence, saccadic and smooth pursuit movements, and in more complex aspects of vision involving visual perception, motion vision ('akinopsia'), and visuo-spatial function have all been reported in TBI. Eye movement dysfunction may be an early sign of TBI. Hence, TBI can result in a variety of visual problems, many patients exhibiting multiple visual defects in combination with a decline in overall health. Patients with chronic dysfunction following TBI may require occupational, vestibular, cognitive and other forms of physical therapy. Such patients may also benefit from visual rehabilitation, including reading-related oculomotor training and the prescribing of spectacles with a variety of tints and prism combinations. © 2018 Optometry Australia.

  18. Traumatic Brain Injury as a Disorder of Brain Connectivity

    Science.gov (United States)

    Hayes, Jasmeet P.; Bigler, Erin D.; Verfaellie, Mieke

    2017-01-01

    Objectives Recent advances in neuroimaging methodologies sensitive to axonal injury have made it possible to assess in vivo the extent of traumatic brain injury (TBI) -related disruption in neural structures and their connections. The objective of this paper is to review studies examining connectivity in TBI with an emphasis on structural and functional MRI methods that have proven to be valuable in uncovering neural abnormalities associated with this condition. Methods We review studies that have examined white matter integrity in TBI of varying etiology and levels of severity, and consider how findings at different times post-injury may inform underlying mechanisms of post-injury progression and recovery. Moreover, in light of recent advances in neuroimaging methods to study the functional connectivity among brain regions that form integrated networks, we review TBI studies that use resting-state functional connectivity MRI methodology to examine neural networks disrupted by putative axonal injury. Results The findings suggest that TBI is associated with altered structural and functional connectivity, characterized by decreased integrity of white matter pathways and imbalance and inefficiency of functional networks. These structural and functional alterations are often associated with neurocognitive dysfunction and poor functional outcomes. Conclusions TBI has a negative impact on distributed brain networks that lead to behavioral disturbance. PMID:26888612

  19. 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.

  20. Maxillofacial injuries and traumatic brain injury--a pilot study.

    Science.gov (United States)

    Rajandram, Rama Krsna; Syed Omar, Syed Nabil; Rashdi, Muhd Fazly Nizam; Abdul Jabar, Mohd Nazimi

    2014-04-01

    Maxillofacial injuries comprising hard tissue as well as soft tissue injuries can be associated with traumatic brain injuries due to the impact of forces transmitted through the head and neck. To date, the role of maxillofacial injury on brain injury has not been properly documented with some saying it has a protective function on the brain while others opposing this idea. This cross-sectional retrospective study evaluated all patients with maxillofacial injuries. The aim of the study was to analyze the occurrence and relationship of maxillofacial injuries with traumatic brain injuries. We retrospectively studied the hospital charts of all trauma patients seen at the accident and emergency department of UKM Medical Centre from November 2010 until November 2011. A detail analysis was then carried out on all patients who satisfied the inclusion and exclusion criteria. A total of 11294 patients were classified as trauma patients in which 176 patients had facial fractures and 292 did not have facial fractures. Middle face fractures was the most common pattern of facial fracture seen. Traumatic brain injury was present in 36.7% of maxillofacial cases. A significant association was found between facial fractures and traumatic brain injury (P maxillofacial injuries with or without facial fractures are at risk of acute or delayed traumatic brain injury. All patients should always have proper radiological investigations together with a proper observation and follow-up schedule. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  1. Ischemic Postconditioning Alleviates Brain Edema After Focal Cerebral Ischemia Reperfusion in Rats Through Down-Regulation of Aquaporin-4.

    Science.gov (United States)

    Han, Dong; Sun, Miao; He, Ping-Ping; Wen, Lu-Lu; Zhang, Hong; Feng, Juan

    2015-07-01

    Cerebral edema is a serious complication associated with cerebral ischemia/reperfusion (I/R). Aquaporin-4 (AQP4) plays a role in generating postischemic edema after reperfusion. Recently, ischemic postconditioning (Postcond) has been shown to produce neuroprotective effects and reduce brain edema in rats after cerebral I/R. It is unclear if ischemic Postcond alleviates brain edema injury through regulation of AQP4. In this study, middle cerebral artery occlusion (MCAO) was induced in rats by filament insertion for 2 h following 24-h reperfusion: ischemic Postcond treatment was performed before reperfusion in the experimental group. We used the wet-dry weight ratio and transmission electron microscopy to evaluate brain edema after 24 h of reperfusion. We used immunohistochemistry and Western blot analyses to evaluate the distribution and expression of AQP4. Ischemic Postcond significantly reduced the water content of the brain tissue and swelling of the astrocytic foot processes. AQP4 expression increased in the I/R and Postcond groups compared to the sham group, but it decreased in the Postcond group compared to the I/R group. The results of our study suggest that ischemic Postcond effectively reduces brain edema after reperfusion by inhibiting AQP4 expression. The data in this study support the use of ischemic Postcond for alleviating brain edema after cerebral I/R.

  2. 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.

  3. Feasibility of using diffuse reflectance spectroscopy for the quantification of brain edema

    Science.gov (United States)

    Rodriguez, Juan G.; Sisson, Cynthia; Hendricks, Chad; Pattillo, Chris; McWaters, Megan; Hardjasudarma, Mardjohan; Quarles, Chad; Yaroslavsky, Anna N.; Yaroslavsky, Ilya V.; Battarbee, Harold

    2001-05-01

    Many diseased states of the brain can result in the displacement of brain tissues and restrict cerebral blood flow, disrupting function in a life-threatening manner. Clinical examples where displacements are observed include venous thromboses, hematomas, strokes, tumors, abscesses, and, particularly, brain edema. For the latter, the brain tissue swells, displacing the cerebral spinal fluid (CSF) layer that surrounds it, eventually pressing itself against the skull. Under such conditions, catheters are often inserted into the brain's ventricles or the subarachnoid space to monitor increased pressure. These are invasive procedures that incur increased risk of infection and consequently are used reluctantly by clinicians. Recent studies in the field of biomedical optics have suggested that the presence or absence of the CSF layer can lead to dramatic changes in NIR signals obtained from diffuse reflectance measurements around the head. In this study, we consider how this sensitivity of NIR signals to CSF might be exploited to non-invasively monitor the onset and resolution of brain edema.

  4. Neuropsychological Consequences of Traumatic Brain Injury in Children and Adolescents.

    Science.gov (United States)

    Lord-Maes, Janiece; Obrzut, John E.

    1996-01-01

    This article discusses recent findings concerning cognitive outcomes in traumatic brain injury (TBI) in children and adolescents, with a particular focus on age differences with TBI. It suggests a relationship between specific learning disorders and brain dysfunction, addresses differential hemispheric functioning with TBI, and outlines recent…

  5. 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,

  6. 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....

  7. Functional and Morphological Evaluation of Traumatized Eyes With Berlin's Edema Affecting the Macula Using mfERG, Microperimetry, and SD-OCT.

    Science.gov (United States)

    Boss, Joseph Daniel; Tosi, Joaquin; Glybina, Inna; Tewari, Asheesh; Abrams, Gary W

    2017-02-01

    To describe the structural and functional changes that occur in traumatic Berlin's edema involving the macula through assessment with multifocal electroretinogram (mfERG), microperimetry, fundus photography, and spectral-domain optical coherence tomography (SD-OCT). Retrospective case series of five eyes from four patients with macular traumatic Berlin's edema. Patients underwent baseline mfERG (three eyes), MP1 microperimetry (three eyes), fundus photography (five eyes), and SD-OCT (five eyes). All eyes with Berlin's edema showed abnormal findings on baseline SD-OCT, including disruption and fragmentation of the inner segment/ outer segment layer. In two patients with unilateral blunt ocular trauma who underwent mfERG, there was complete loss of the foveal peak in affected eyes. All three eyes that underwent microperimetry showed depressed retinal sensitivity in the area of Berlin's edema. SD-OCT, microperimetry, and mfERG can be used to help diagnose, stratify traumatic severity, and follow structural and functional progression over time in patients with Berlin's edema. [Ophthalmic Surg Lasers Imaging Retina. 2017;48:114-121.]. Copyright 2017, SLACK Incorporated.

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

    Directory of Open Access Journals (Sweden)

    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.

  9. Pediatric traumatic brain injury affects multisensory integration.

    Science.gov (United States)

    Königs, Marsh; Weeda, Wouter D; van Heurn, L W Ernest; Vermeulen, R Jeroen; Goslings, J Carel; Luitse, Jan S K; Poll-The, Bwee Tien; Beelen, Anita; van der Wees, Marleen; Kemps, Rachèl J J K; Catsman-Berrevoets, Coriene E; Oosterlaan, Jaap

    2017-02-01

    To investigate the impact of pediatric traumatic brain injury (TBI) on multisensory integration in relation to general neurocognitive functioning. Children with a hospital admission for TBI aged between 6 and 13 years (n = 94) were compared with children with trauma control (TC) injuries (n = 39), while differentiating between mild TBI without risk factors for complicated TBI (mild RF- ; n = 19), mild TBI with ≥1 risk factor (mild RF+ ; n = 45), and moderate/severe TBI (n = 30). We measured set-shifting performance based on visual information (visual shift condition) and set-shifting performance based on audiovisual information, requiring multisensory integration (audiovisual shift condition). Effects of TBI on set-shifting performance were traced back to task strategy (i.e., boundary separation), processing efficiency (i.e., drift rate), or extradecisional processes (i.e., nondecision time) using diffusion model analysis. General neurocognitive functioning was measured using estimated full-scale IQ (FSIQ). The TBI group showed selectively reduced performance in the audiovisual shift condition (p = .009, Cohen's d = -0.51). Follow-up analyses in the audiovisual shift condition revealed reduced performance in the mildRF+ TBI group and moderate/severe TBI group (ps ≤ .025, ds ≤ -0.61). These effects were traced back to lower drift rate (ps ≤ .048, ds ≤ -0.44), reflecting reduced multisensory integration efficiency. Notably, accuracy and drift rate in the audiovisual shift condition partially mediated the relation between TBI and FSIQ. Children with mildRF+ or moderate/severe TBI are at risk for reduced multisensory integration efficiency, possibly contributing to decreased general neurocognitive functioning. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

  10. Traumatic Brain Injury in the Workplace.

    Science.gov (United States)

    Paci, Michael; Infante-Rivard, Claire; Marcoux, Judith

    2017-09-01

    Work-related traumatic brain injuries (TBIs) are not well documented in the literature. Published studies mostly rely on worker databases that fail to provide clinically relevant information. Our objective is to describe the characteristics of hospitalized patients and their work-related TBI. We used the Québec provincial trauma and TBI program databases to identify all patients with a diagnosis of work-related TBI admitted to the Montreal General Hospital, a level 1 trauma center, between 2000 and 2014. Data from their medical records were extracted using a predetermined information sheet. Simple descriptive statistics (means and percentages) were used to summarize the data. A total of 285 cases were analyzed. Workplace TBI patients were middle-aged (mean, 43.62 years), overwhelmingly male (male:female 18:1), mostly healthy, and had completed a high school level education. Most workers were from the construction industry; falling was the most common mechanism of injury. The majority of patients (76.8%) presented with a mild TBI; only a minority (14%) required neurosurgery. The most common finding on computed tomography was skull fracture. The median length of hospitalization was 7 days, after which most patients were discharged directly home. A total of 8.1% died of their injuries. Our study found that most hospitalized victims of work-related TBI had mild injury; however, some required neurosurgical intervention and a non-negligible proportion died of their injury. Improving fall prevention, accurately document helmet use and increasing the safety practice in the construction industry may help decrease work-related TBI burden.

  11. Relationship between apathy and tumor location, size, and brain edema in patients with intracranial meningioma

    Directory of Open Access Journals (Sweden)

    Peng Y

    2015-07-01

    Full Text Available Yihua Peng,1,* Chunhong Shao,1,* Ye Gong,2 Xuehai Wu,2 Weijun Tang,3 Shenxun Shi1 1Psychiatry Department, 2Neurosurgery Department, 3Radiology Department, Huashan Hospital, Fudan University, People’s Republic of China *These authors contributed equally to this work Background: The purpose of this study is to assess the relationship between apathy and tumor location, size, and brain edema in patients with intracranial meningioma. Methods: We enrolled 65 consecutive patients with meningioma and 31 normal controls matched for age, gender, and education. The patients were divided into frontal or non-frontal (NF meningioma groups based on magnetic resonance imaging; the frontal group was then subdivided to dorsolateral frontal (DLF, medial frontal (MF, and ventral frontal (VF groups. Tumor size and brain edema were also recorded. Apathy was assessed by the Apathy Evaluation Scale (AES. Assessments were carried out 1 week before and 3 months after surgery, respectively. Logistic regression analysis was performed to identify the predictive effect of tumor size, location, and brain edema on apathy. Analysis of variance and chi-square analysis were applied to compare apathy scores and apathy rates among the frontal, NF, and normal control groups, and all subgroups within the frontal group. Results: Compared with the NF and control groups, the mean AES score was much higher in the frontal group (34.0±8.3 versus 28.63±6.0, P=0.008, and 26.8±4.2, P<0.001. Subgroup analysis showed that AES scores in the MF group (42.1±6.6 and VF group (34.7±8.0 were higher than in the DLF group (28.5±4.36, NF group, and control group (P<0.05. The apathy rate was 63.6% in the MF group and 25% in the VF group, and significantly higher than in the DLF (5.6%, NF (5.3%, and control (0% groups (P<0.001. A moderate correlation was found between AES score and mean diameter of the meningioma in all patient groups. Further analysis demonstrated that the correlation existed in

  12. Edema is not a reliable diagnostic sign to exclude small brain metastases.

    Directory of Open Access Journals (Sweden)

    Tanja Schneider

    Full Text Available No prior systematic study on the extent of vasogenic edema (VE in patients with brain metastases (BM exists. Here, we aim to determine 1 the general volumetric relationship between BM and VE, 2 a threshold diameter above which a BM shows VE, and 3 the influence of the primary tumor and location of the BM in order to improve diagnostic processes and understanding of edema formation. This single center, retrospective study includes 173 untreated patients with histologically proven BM. Semi-manual segmentation of 1416 BM on contrast-enhanced T1-weighted images and of 865 VE on fluid-attenuated inversion recovery/T2-weighted images was conducted. Statistical analyses were performed using a paired-samples t-test, linear regression/generalized mixed-effects model, and receiver-operating characteristic (ROC curve controlling for the possible effect of non-uniformly distributed metastases among patients. For BM with non-confluent edema (n = 545, there was a statistically significant positive correlation between the volumes of the BM and the VE (P < 0.001. The optimal threshold for edema formation was a diameter of 9.4 mm for all BM. The primary tumors as interaction term in multivariate analysis had a significant influence on VE formation whereas location had not. Hence VE development is dependent on the volume of the underlying BM and the site of the primary neoplasm, but not from the location of the BM.

  13. Hexachlorophene-induced brain edema in rat observed by proton magnetic resonance.

    Science.gov (United States)

    Kinoshita, Y; Matsumura, H; Igisu, H; Yokota, A

    2000-08-04

    Rat brain was examined with 4.7 T proton magnetic resonance (MR). On administering hexachlorophene (HCP) 30 mg/kg/day for 5 days, myelin-rich structures stood out in T2-weighted images. Apparent diffusion coefficient (ADC) was markedly suppressed in all regions examined except for cerebral cortex. Seven days after terminating the exposure to HCP, without enhancement in T2-weighted images, ADC was still decreased in corpus callosum, optic nerve and trigeminal nerve. Rat administered with HCP and followed with high magnetic field proton MR seems to provide a good model for cytotoxic brain edema, and it may also be useful to visualize heavily myelinated structures.

  14. 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

  15. MRI findings of acute cerebral swelling and brain edema in the acute stage

    International Nuclear Information System (INIS)

    Oki, Hideo; Ueda, Shin; Matsumoto, Keizo; Kashihara, Michiharu; Furuichi, Masashi.

    1988-01-01

    We report two cases, one of acute cerebral swelling and the other with a major stroke, whose MRI has shown very interesting findings. Case 1, a 32-year-old male, was admitted to our service because of a lowering of his consciousness immediately after a head injury. On admission, the patient was semicomatous (E 1 M 2 V 1 , with anisocoria (R > L). His plain skull X-ray was normal. A CT scan, however, demonstrated right isodensity hemispheric swelling associated with a subarachnoid hemorrhage in the right Sylvian fissure. A right carotid angiogram showed no vascular disorders. MR imaging of the spin density demonstrated a hyperintensitive thickening of the gray matter in the whole right hemisphere. Case 2, a 58-year-old female, was admitted because of a sudden onset of loss of consciousness, with right hemiparesis and dysarthria. On admission, her consciousness was semicomatous (E 1 M 3 V 1 ), and it deteriorated to a deep coma 1 hour later. A CT scan demonstrated a diffuse left hemispheric low density, with a finding of hemorrhagic infarction in the basal ganglia. MR imaging of the spin density showed a hyperintensitive thickening of the gray matter resembling that of Case 1. The findings of the spin-echo images of our two cases showed a hyperintensitive thickening of the gray matter in both. The hyperintensity and thickening of the gray matter apparently indicated a sort of hyperemia and brain edema. These findings led us to suspect that the hyperemia associated with acute cerebral swelling and ischemic brain edema of our two cases originated in the gray matter, although it has been considered that the pathogenesis of acute cerebral swelling is not known and that brain edema, especially vasogenic edema, will mostly develop in the white matter rather than in the gray matter. (author)

  16. 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.)

  17. Neuropsychological and neuroimaging findings in traumatic brain injury and post-traumatic stress disorder

    OpenAIRE

    Brenner, Lisa A.

    2011-01-01

    Advances in imaging technology, coupled with military personnel returning home from Iraq and Afghanistan with traumatic brain injury (TBI) and/or post-traumatic stress disorder (PTSD), have increased interest in the neuropsychology and neurobiology of these two conditions. There has been a particular focus on differential diagnosis. This paper provides an overviev of findings regarding the neuropsychological and neurobiological underpinnings of TBI andfor PTSD. A specific focus is on assessme...

  18. Genesis of the use of corticosteroids in the treatment and prevention of brain edema.

    Science.gov (United States)

    McClelland, Shearwood; Long, Donlin M

    2008-04-01

    Since the groundbreaking article from the University of Minnesota in 1961 by Drs. Galicich, French, and Melby describing the use of dexamethasone for peritumoral cerebral edema, the use of corticosteroids in patients with brain tumors has become routine. Unfortunately, little has been reported regarding the environment that fostered arguably the greatest translational research contribution in the history of neurosurgery. During a pilot study to assess corticosteroid uptake in brain tumors, Dr. Galicich observed that patients given a large dose of corticosteroids just before craniotomy had a relatively benign postoperative course. This led, in October 1959, to the administration of high-dose corticosteroids to a patient with a large recurrent glioblastoma who was semicomatose and severely hemiparetic. The results were dramatic, with almost complete resolution of neurological deficit during a period of several days and marked reduction of midline shift on repeat angiograms. This finding prompted the studies that confirmed the efficacy of high-dose corticosteroids in reducing peritumoral brain edema in humans reported in the 1961 article. After publication, a revolution in brain tumor management occurred because corticosteroid therapy markedly reduced the morbidity and mortality associated with brain tumors both in the United States and worldwide. The combination of astute clinical observation and follow up by rigorous clinical research at the University of Minnesota resulted in one of the greatest contributions in the history of neurosurgery, rivaled only by the operative microscope in its effect on morbidity, and unsurpassed in reduction of mortality.

  19. Clinical and neuroradiological studies of eclampsia. Cerebral vasospasm and relation to the brain edema

    Energy Technology Data Exchange (ETDEWEB)

    Ito, Yasuhiro; Niwa, Hisayoshi; Ando, Tetsuo; Yasuda, Takeshi; Yanagi, Tsutomu [Nagoya Daini Red Cross Hospital, Aichi (Japan)

    1995-04-01

    Clinical and neuroradiological studies involving cerebral angiography were conducted in four patients with eclampsia. In three cases (case 1, 2 and 4), neurological focal signs, abnormal low density areas on cranial CT and T{sub 2} high intensity areas on cranial MRI disappeared within a month. But in one case (case 3), cerebral infarction occurred and right hemiparesis and aphasia persisted. Cerebral angiography in the acute phase demonstrated vasospasm in all cases and arterial occlusion in the middle cerebral artery due to vasospasm in case 3. Angiography demonstrated several types of spasms, including diffuse, peripheral and multi local. Furthermore, in some cases, diffuse vasospasms were recognized at the siphon and extracranial portions of the internal carotid artery. In one case (Case 4), segmental vasospasms were detected in the bilateral vertebral arteries. Three to four weeks later, follow-up cerebral angiography was performed in three cases. Cerebral vasospasms had partially or completely recovered. Subarachnoid hemorrhage (SAH) was excluded by lumbar puncture and neuroradiological findings in all cases. We concluded that eclampsia itself causes cerebral vasospasm and that the mechanism of vasospasm is different from that of SAH, since cerebral vasospasm occurred in the extracranial cerebral arteries. We suspected that cerebral vasospasm in eclampsia causes cerebral ischemia, which leads to cytotoxic edema and dysfunction of the blood-brain barrier (BBB) and cerebral autoregulation. With this background, brain edema, especially vasogenic edema, may easily occur and clinical symptoms of eclampsia may appear when the blood pressure rapidly increases. (author).

  20. Regulation of Caveolin-1 Expression Determines Early Brain Edema After Experimental Focal Cerebral Ischemia.

    Science.gov (United States)

    Choi, Kang-Ho; Kim, Hyung-Seok; Park, Man-Seok; Kim, Joon-Tae; Kim, Ja-Hae; Cho, Kyung-Ah; Lee, Min-Cheol; Lee, Hong-Joon; Cho, Ki-Hyun

    2016-05-01

    Most patients with cerebral infarction die of brain edema because of the breakdown of the blood-brain barrier (BBB) in ischemic tissue. Caveolins (a group of proteins) are key modulators of vascular permeability; however, a direct role of caveolin-1 (Cav-1) in the regulation of BBB permeability during ischemic injury has yet to be identified. Cav-1 expression was measured by immunoblotting after photothrombotic ischemia. A direct functional role of Cav-1 in cerebral edema and BBB permeability during cerebral ischemia was investigated by genetic manipulation (gene disruption and re-expression) of Cav-1 protein expression in mice. There was a significant correlation between the extent of BBB disruption and the Cav-1 expression. In Cav-1-deficient (Cav-1(-/-)) mice, the extent of BBB disruption after cerebral ischemia was increased compared with wild-type (Cav-1(+/+)) mice, whereas the increase in cerebral edema volume was ameliorated by lentiviral-mediated re-expression of Cav-1. Furthermore, Cav-1(-/-) mice had significantly higher degradation of tight junction proteins and proteolytic activity of matrix metalloproteinase than Cav-1(+/+) mice. Conversely, re-expression of Cav-1 in Cav-1(-/-) mice restored tight junction protein expression and reduced matrix metalloproteinase proteolytic activity. These results indicate that Cav-1 is a critical determinant of BBB permeability. Strategies for regulating Cav-1 represent a novel therapeutic approach to controlling BBB disruption and subsequent neurological deterioration during cerebral ischemia. © 2016 American Heart Association, Inc.

  1. Clinical and neuroradiological studies of eclampsia. Cerebral vasospasm and relation to the brain edema

    International Nuclear Information System (INIS)

    Ito, Yasuhiro; Niwa, Hisayoshi; Ando, Tetsuo; Yasuda, Takeshi; Yanagi, Tsutomu

    1995-01-01

    Clinical and neuroradiological studies involving cerebral angiography were conducted in four patients with eclampsia. In three cases (case 1, 2 and 4), neurological focal signs, abnormal low density areas on cranial CT and T 2 high intensity areas on cranial MRI disappeared within a month. But in one case (case 3), cerebral infarction occurred and right hemiparesis and aphasia persisted. Cerebral angiography in the acute phase demonstrated vasospasm in all cases and arterial occlusion in the middle cerebral artery due to vasospasm in case 3. Angiography demonstrated several types of spasms, including diffuse, peripheral and multi local. Furthermore, in some cases, diffuse vasospasms were recognized at the siphon and extracranial portions of the internal carotid artery. In one case (Case 4), segmental vasospasms were detected in the bilateral vertebral arteries. Three to four weeks later, follow-up cerebral angiography was performed in three cases. Cerebral vasospasms had partially or completely recovered. Subarachnoid hemorrhage (SAH) was excluded by lumbar puncture and neuroradiological findings in all cases. We concluded that eclampsia itself causes cerebral vasospasm and that the mechanism of vasospasm is different from that of SAH, since cerebral vasospasm occurred in the extracranial cerebral arteries. We suspected that cerebral vasospasm in eclampsia causes cerebral ischemia, which leads to cytotoxic edema and dysfunction of the blood-brain barrier (BBB) and cerebral autoregulation. With this background, brain edema, especially vasogenic edema, may easily occur and clinical symptoms of eclampsia may appear when the blood pressure rapidly increases. (author)

  2. Vascular endothelial growth factor A protein level and gene expression in intracranial meningiomas with brain edema

    DEFF Research Database (Denmark)

    Nassehi, Damoun; Dyrbye, Henrik; Andresen, Morten

    2011-01-01

    Meningiomas are the second most common primary intracranial tumors in adults. Although meningiomas are mostly benign, more than 50% of patients with meningioma develop peritumoral brain edema (PTBE), which may be fatal because of increased intracranial pressure. Vascular endothelial growth factor...... (VEGF) is an endothelial cell-specific mitogen and angiogen. VEGF-A protein, which is identical to vascular permeability factor, is a regulator of angiogenesis. In this study, 101 patients with meningiomas, and possible co-factors to PTBE, such as meningioma subtypes and tumor location, were examined....... Forty-three patients had primary, solitary, supratentorial meningiomas with PTBE. In these, correlations in PTBE, edema index, VEGF-A protein, VEGF gene expression, capillary length, and tumor water content were investigated. DNA-branched hybridization was used for measuring VEGF gene expression...

  3. Pathophysiological studies of experimental brain edema and cerebral ischemia using MRI/S

    International Nuclear Information System (INIS)

    Naruse, Shoji; Higuchi, Toshihiro; Horikawa, Yoshiharu; Tanaka, Chuzo; Hirakawa, Kimiyoshi

    1987-01-01

    Pathophysiological changes in experimental brain edema and cerebral ischemia were examined by the in vivo 1 H- and 31 P-NMR method. Two types of experimental brain edema were induced in rats by cold injury and by triethyltin (TET) intoxication. Experimental cerebral ischemia was induced in rats by the four-vessel occlusion method. During the course of these pathological conditions, the 1 H-MRIs and 31 P-NMR spectra were measured sequentially with a single NMR spectrometer (4.8 tesla, 9 cm bore magnet). In the cold-injury edema, high-intensity lesions were detected in the gray and white matters of the injured hemisphere by means of SE images with a long Te 3 hours after the injury. The intensity reached its maximum 16 to 24 hours after the injury, and then returned to normal 7 days later. These high-intensity lesions indicated an increase in the T2 value in the edematous tissue. There were no changes in the 31 P-NMR spectra during the course of edema formation and absorption. In the TET-induced edema, high-intensity lesions were also detected in the bilateral white matter by means of SE images with a long Te from the 3rd day up to the 7th day during the injection of TET. These high-intensity lesions subsided 42 days after the discontinuance of injecting TET. There were no changes in the 31 P-NMR spectra during the whole course of TET-induced edema. In the cerebral ischemia, no remarkable changes in the MRI were detected in either SE or IR images during the ischemic and recirculated periods. However, dynamic changes in the 31 P-NMR spectra were detected during the course of cerebral ischemia. In the pre-ischemic period, the peaks of the ATP, PCr, phosphodiesters (PDE), Pi, and phosphomonoesters (PME) were detected. After the induction of ischemia, the ATP and PCr peaks decreased, while one Pi peak increased rapidly. (J.P.N.)

  4. Predictors of malignant brain edema in middle cerebral artery infarction observed on CT angiography.

    Science.gov (United States)

    Kim, Hoon; Jin, Seon Tak; Kim, Young Woo; Kim, Seong Rim; Park, Ik Seong; Jo, Kwang Wook

    2015-03-01

    Patients with middle cerebral artery (MCA) infarction accompanied by MCA occlusion with or without internal carotid artery (ICA) occlusion have a poor prognosis, as a result of brain cell damage caused by both the infarction and by space-occupying and life-threatening edema formation. Multiple treatments can reduce the likelihood of edema formation, but tend to show limited efficacy. Decompressive hemicraniectomy with duroplasty has been promising for improving functional outcomes and reducing mortality, particularly improved functional outcomes can be achieved with early decompressive surgery. Therefore, identifying patients at risk for developing fatal edema is important and should be performed as early as possible. Sixty-four patients diagnosed with major MCA infarction with MCA occlusion within 8 hours of symptom onset were retrospectively reviewed. Early clinical, laboratory, and computed tomography angiography (CTA) parameters were analyzed for malignant brain edema (MBE). Twenty of the 64 patients (31%) had MBE, and the clinical outcome was poor (3month modified Rankin Scale >2) in 95% of them. The National Institutes of Health Stroke Scale (NIHSS) score, Alberta Stroke Program Early Computed Tomography Score, Clot Burden Score, and Collateral Score (CS) showed statically significant differences in both groups. Multivariable analyses adjusted for age and sex identified the independent predictors of MBE: NIHSS score >18 (odds ratio [OR]: 4.4, 95% confidence interval [CI]: 1.2-16.0, p=0.023) and CS on CTA <2 (OR: 7.28, 95% CI: 1.7-30.3,p=0.006). Our results provide useful information for selecting patients in need of aggressive treatment such as decompressive surgery. Crown Copyright © 2014. Published by Elsevier Ltd. All rights reserved.

  5. Volumetric Electromagnetic Phase-Shift Spectroscopy of Brain Edema and Hematoma

    Science.gov (United States)

    Gonzalez, Cesar A.; Valencia, Jose A.; Mora, Alfredo; Gonzalez, Fernando; Velasco, Beatriz; Porras, Martin A.; Salgado, Javier; Polo, Salvador M.; Hevia-Montiel, Nidiyare; Cordero, Sergio; Rubinsky, Boris

    2013-01-01

    Motivated by the need of poor and rural Mexico, where the population has limited access to advanced medical technology and services, we have developed a new paradigm for medical diagnostic based on the technology of “Volumetric Electromagnetic Phase Shift Spectroscopy” (VEPS), as an inexpensive partial substitute to medical imaging. VEPS, can detect changes in tissue properties inside the body through non-contact, multi-frequency electromagnetic measurements from the exterior of the body, and thereby provide rapid and inexpensive diagnostics in a way that is amenable for use in economically disadvantaged parts of the world. We describe the technology and report results from a limited pilot study with 46 healthy volunteers and eight patients with CT radiology confirmed brain edema and brain hematoma. Data analysis with a non-parametric statistical Mann-Whitney U test, shows that in the frequency range of from 26 MHz to 39 MHz, VEPS can distinguish non-invasively and without contact, with a statistical significance of p<0.05, between healthy subjects and those with a medical conditions in the brain. In the frequency range of between 153 MHz to 166 MHz it can distinguish with a statistical significance of p<0.05 between subjects with brain edema and those with a hematoma in the brain. A classifier build from measurements in these two frequency ranges can provide instantaneous diagnostic of the medical condition of the brain of a patient, from a single set of measurements. While this is a small-scale pilot study, it illustrates the potential of VEPS to change the paradigm of medical diagnostic of brain injury through a VEPS classifier-based technology. Obviously substantially larger-scale studies are needed to verify and expand on the findings in this small pilot study. PMID:23691001

  6. Misconceptions on neuropsychological rehabilitation and traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Alberto García- Molina

    2013-12-01

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

  7. Crotalus helleri venom preconditioning reduces postoperative cerebral edema and improves neurological outcomes after surgical brain injury.

    Science.gov (United States)

    Kim, Cherine H; McBride, Devin W; Sherchan, Prativa; Person, Carl E; Gren, Eric C K; Kelln, Wayne; Lekic, Tim; Hayes, William K; Tang, Jiping; Zhang, John H

    2017-11-01

    Postoperative cerebral edema is a devastating complication in neurosurgical patients. Loss of blood-brain barrier integrity has been shown to lead to the development of brain edema following neurosurgical procedures. The aim of this study was to evaluate preconditioning with Crotalus helleri venom (Cv-PC) as a potential preventive therapy for reducing postoperative brain edema in the rodent SBI model. C. helleri venom is known to contain phospholipase A2 (PLA2), an enzyme upstream to cyclooxygenase-2 (COX-2) in the inflammatory cascade, acts to increase the production of inflammatory mediators, such as prostaglandins. We hypothesize that Cv-PC will downregulate the response of the COX-2 pathway to injury, thereby reducing the inflammatory response and the development of brain edema after SBI. 75 male Sprague Dawley rats (280-330g) were divided to the following groups-naïve+vehicle, naïve+Cv-PC, sham, vehicle, Cv-PC, Cv-PC+NS398 (COX-2 inhibitor). Vehicle preconditioned and Cv-PC animals received either three daily subcutaneous doses of saline or C. helleri venom at 72h, 48h, and 24h prior to surgery. In Cv-PC+NS398 animals, NS398 was administered intraperitoneally 1h prior to each Cv-PC injection. Sham-operated animals received craniotomy only, whereas SBI animals received a partial right frontal lobectomy. Neurological testing and brain water content were assessed at 24h and 72h after SBI; COX-2 and PGE 2 expression was assessed at 24h postoperatively by Western blot and immunohistochemistry, respectively. At 24h after SBI, the vehicle-treated animals were observed to have increased brain water content (83.1±0.2%) compared to that of sham animals (80.2±0.1%). The brain water content of vehicle-treated animals at 72h post-SBI was elevated at 83.3±0.2%. Cv-PC-treated animals with doses of 10% LD 50 had significantly reduced brain water content of 81.92±0.7% and 81.82±0.3% at 24h and 72h, respectively, after SBI compared to that of vehicle-treated animals

  8. Perforin Expression by CD8 T Cells Is Sufficient To Cause Fatal Brain Edema during Experimental Cerebral Malaria.

    Science.gov (United States)

    Huggins, Matthew A; Johnson, Holly L; Jin, Fang; N Songo, Aurelie; Hanson, Lisa M; LaFrance, Stephanie J; Butler, Noah S; Harty, John T; Johnson, Aaron J

    2017-05-01

    Human cerebral malaria (HCM) is a serious complication of Plasmodium falciparum infection. The most severe outcomes for patients include coma, permanent neurological deficits, and death. Recently, a large-scale magnetic resonance imaging (MRI) study in humans identified brain swelling as the most prominent predictor of fatal HCM. Therefore, in this study, we sought to define the mechanism controlling brain edema through the use of the murine experimental cerebral malaria (ECM) model. Specifically, we investigated the ability of CD8 T cells to initiate brain edema during ECM. We determined that areas of blood-brain barrier (BBB) permeability colocalized with a reduction of the cerebral endothelial cell tight-junction proteins claudin-5 and occludin. Furthermore, through small-animal MRI, we analyzed edema and vascular leakage. Using gadolinium-enhanced T1-weighted MRI, we determined that vascular permeability is not homogeneous but rather confined to specific regions of the brain. Our findings show that BBB permeability was localized within the brainstem, olfactory bulb, and lateral ventricle. Concurrently with the initiation of vascular permeability, T2-weighted MRI revealed edema and brain swelling. Importantly, ablation of the cytolytic effector molecule perforin fully protected against vascular permeability and edema. Furthermore, perforin production specifically by CD8 T cells was required to cause fatal edema during ECM. We propose that CD8 T cells initiate BBB breakdown through perforin-mediated disruption of tight junctions. In turn, leakage from the vasculature into the parenchyma causes brain swelling and edema. This results in a breakdown of homeostatic maintenance that likely contributes to ECM pathology. Copyright © 2017 American Society for Microbiology.

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

    Science.gov (United States)

    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.

  10. Minocycline-induced hypersensitivity syndrome presenting with meningitis and brain edema: a case report

    Directory of Open Access Journals (Sweden)

    Lefebvre Nicolas

    2007-05-01

    Full Text Available Background Hypersentivity Syndrome (HS may be a life-threatening condition. It frequently presents with fever, rash, eosinophilia and systemic manifestations. Mortality can be as high as 10% and is primarily due to hepatic failure. We describe what we believe to be the first case of minocycline-induced HS with accompanying lymphocytic meningitis and cerebral edema reported in the literature. Case presentation A 31-year-old HIV-positive female of African origin presented with acute fever, lymphocytic meningitis, brain edema, rash, eosinophilia, and cytolytic hepatitis. She had been started on minocycline for inflammatory acne 21 days prior to the onset of symptoms. HS was diagnosed clinically and after exclusion of infectious causes. Minocycline was withdrawn and steroids were administered from the second day after presentation because of the severity of the symptoms. All signs resolved by the seventh day and steroids were tailed off over a period of 8 months. Conclusion Clinicians should maintain a high index of suspicion for serious adverse reactions to minocycline including lymphocytic meningitis and cerebral edema among HIV-positive patients, especially if they are of African origin. Safer alternatives should be considered for treatment of acne vulgaris. Early recognition of the symptoms and prompt withdrawal of the drug are important to improve the outcome.

  11. Hemosiderin deposition in the brain as footprint of high-altitude cerebral edema.

    Science.gov (United States)

    Schommer, Kai; Kallenberg, Kai; Lutz, Kira; Bärtsch, Peter; Knauth, Michael

    2013-11-12

    Based on recent findings of microhemorrhages (MHs) in the corpus callosum (CC) in 3 individuals after nonfatal high-altitude cerebral edema (HACE), we hypothesized that hemosiderin depositions in the brain after high-altitude exposure are specific for HACE and remain detectable over many years. This was a cross-sectional study involving 37 mountaineers in 4 groups: 10 had experienced HACE, 8 high-altitude pulmonary edema, 11 severe acute mountain sickness, and 8 had climbed to altitudes ≥6,962 m without developing any high-altitude illness. HACE was defined as ataxia necessitating assistance with walking and/or decreased consciousness. Within hemosiderin depositions, which were quantified by a score. Unequivocal MHs located in the splenium of the CC were found in 8 subjects and questionable MHs were found in 2 subjects 1 to 35 months after HACE. They were located outside the CC in 5 more severe cases. MHs remained unchanged in those reexamined after 12 to 50 months. A few unequivocal MHs in the splenium of the CC were found in one subject after severe acute mountain sickness, while one subject with high-altitude pulmonary edema and 2 of the extreme altitude climbers had questionable lesions. In all other subjects, MHs were unequivocally absent. MHs detectable by susceptibility-weighted MRI predominantly in the splenium of the CC are long-lasting footprints of HACE.

  12. The Brain Tourniquet: Physiological Isolation of Brain Regions Damaged by Traumatic Head Injury

    Science.gov (United States)

    2008-06-19

    brain slices were treated after injury with either a nootropic agent (aniracetam, cyclothiazide, IDRA 21, or 1-BCP) or the antiepileptic drug...pharmacological approach. 15. SUBJECT TERMS traumatic brain injury, cell necrosis, neuroprotection, nootropics , epilepsy, long-term potentiation...render their use problematic in an effective brain tourniquet system. We chose to focus our investigations on the nootropic (cognition enhancing) drugs

  13. Centralized rehabilitation after servere traumatic brain injury

    DEFF Research Database (Denmark)

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

    2006-01-01

    in the prospective study, six died, and 92 (1.27 per 100,000 population per year) survived after a post-traumatic amnesia (PTA) period of at least 28 days. All 19 patients with PTA 7-27 days and 48% of survivors with PTA at least 4 weeks were discharged directly home. The incidence of patients vegetative at 1 month...

  14. Role of water content and water state in characterizing vasogenic brain edema

    International Nuclear Information System (INIS)

    Fatouros, P.P.; Kraft, K.A.; Inao, S.; Marmarou, A.; Clarke, G.D.; Kishore, P.R.S.

    1987-01-01

    Characterization of edematous brain tissue with MR imaging requires a knowledge of the water content and of the amount and type of protein present. The authors determined the frequency dependence of the hydration layer's T1 for gelatin solutions of different water concentrations by simultaneously measuring the relaxation rates (at 5, 41, 63, and 100 MHz) and the bound water fractions by differential scanning calorimetry. Similar measurements of different protein concentrations in serum were carried out at 100 MHz. The results indicate the critical role of both water content and protein concentration in the characterization of vasogenic edema and its ultimate resolution

  15. Lost Polarization of Aquaporin4 and Dystroglycan in the Core Lesion after Traumatic Brain Injury Suggests Functional Divergence in Evolution

    Directory of Open Access Journals (Sweden)

    Hui Liu

    2015-01-01

    Full Text Available Objective. To understand how aquaporin4 (AQP4 and dystroglycan (DG polarized distribution change and their roles in brain edema formation after traumatic brain injury (TBI. Methods. Brain water content, Evans blue detection, real-time PCR, western blot, and immunofluorescence were used. Results. At an early stage of TBI, AQP4 and DG maintained vessel-like pattern in perivascular endfeet; M1, M23, and M1/M23 were increased in the core lesion. At a later stage of TBI, DG expression was lost in perivascular area, accompanied with similar but delayed change of AQP4 expression; expression of M1, M23, and DG and the ratio of M1/M2 were increased. Conclusion. At an early stage, AQP4 and DG maintained the polarized distribution. Upregulated M1 and M23 could retard the cytotoxic edema formation. At a later stage AQP4 and DG polarized expression were lost from perivascular endfeet and induced the worst cytotoxic brain edema. The alteration of DG expression could regulate that of AQP4 expression after TBI.

  16. The protective effect of HET0016 on brain edema and blood-brain barrier dysfunction after cerebral ischemia/reperfusion.

    Science.gov (United States)

    Liu, Yu; Wang, Di; Wang, Huan; Qu, Youyang; Xiao, Xingjun; Zhu, Yulan

    2014-01-28

    N-hydroxy-N-(4-butyl-2-methylphenyl) formamidine (HET0016) is a specific 20-hydroxyeicosatetraenoic acid (20-HETE) inhibitor which was first synthesized in 2001. It has been demonstrated that HET0016 reduces cerebral infarction volume in rat middle cerebral artery occlusion (MCAO) models. However, little is known about the role of HET0016 in the blood-brain barrier (BBB) dysfunction after cerebral ischemia/reperfusion (I/R) injury. The present study was designed to examine the effect of HET0016 in a MCAO and reperfusion rat model to determine whether it protects against brain edema and BBB disruption. Rats were subjected to 90 min MCAO, followed by 4, 24, 48, and 72 h reperfusion. Brain edema was measured according to the wet and dry weight method. BBB permeability based on the extravasation of Evans blue and sodium fluorescein was detected. BBB ultrastructure alterations were presented through transmission electron microscope. Superoxide production in ischemic tissue was also measured by dihydroethidium fluorescent probe. Western blot was used to analyze the expression of Claudin-5, ZO-1, MMP-9, and JNK pathway. At 24h after reperfusion, HET0016 reduced brain edema and BBB leakage. Ultrastructural damage of BBB and the increase of superoxide production were attenuated by HET0016 treatment. Western blot showed that HET0016 suppressed the activation of MMP-9 and JNK pathway but restored the expression of Claudin-5 and ZO-1. In conclusion, these results suggest that HET0016 protects BBB dysfunction after I/R by regulating the expression of MMP-9 and tight junction proteins. Furthermore, inhibition of oxidative stress and JNK pathway may be involved in this protecting effect. © 2013 Published by Elsevier B.V.

  17. The Cost of Treating Post Traumatic Stress Disorder and Mild Traumatic Brain Injuries

    Science.gov (United States)

    2010-03-01

    It is important that these individuals receive social support in order to help with the healing process. Comorbid Symptoms Comorbid symptoms...and may increase the risk for Alzheimer ‟s disease and Parkinson‟s disease as the person ages (Traumatic Brain Injury: Hope Through Research, 2002

  18. Oligodendrogenesis after Cerebral Ischaemia and Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Zheng Gang Zhang

    2013-08-01

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

  19. Dedifferentiation Does Not Account for Hyperconnectivity after Traumatic Brain Injury

    OpenAIRE

    Bernier, Rachel Anne; Roy, Arnab; Venkatesan, Umesh Meyyappan; Grossner, Emily C.; Brenner, Einat K.; Hillary, Frank Gerard

    2017-01-01

    Objective Changes in functional network connectivity following traumatic brain injury (TBI) have received increasing attention in recent neuroimaging literature. This study sought to understand how disrupted systems adapt to injury during resting and goal-directed brain states. Hyperconnectivity has been a common finding, and dedifferentiation (or loss of segregation of networks) is one possible explanation for this finding. We hypothesized that individuals with TBI would show dedifferenti...

  20. Effect of Coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats

    Directory of Open Access Journals (Sweden)

    Hanci Volkan

    2011-07-01

    Full Text Available Abstract Background Head trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q10 (CoQ10, a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ10 in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ10 administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out. Results In the biochemical tests, tissue malondialdehyde (MDA levels were significantly higher in the traumatic brain-injury group compared to the sham group (p 10 after trauma was shown to be protective because it significantly lowered the increased MDA levels (p 10 group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ10 and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p Conclusion Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ10 use in rats with traumatic brain injury.

  1. Cognitive Task Demands and Discourse Performance after Traumatic Brain Injury

    Science.gov (United States)

    Byom, Lindsey; Turkstra, Lyn S.

    2017-01-01

    Background: Social communication problems are common in adults with traumatic brain injury (TBI), particularly problems in spoken discourse. Social communication problems are thought to reflect underlying cognitive impairments. Aims: To measure the contribution of two cognitive processes, executive functioning (EF) and theory of mind (ToM), to the…

  2. Headache in traumatic brain injuries from blunt head trauma

    OpenAIRE

    Chelse, Ana B.; Epstein, Leon G.

    2015-01-01

    Investigators from New York Presbyterian Morgan Stanley Children’s Hospital examined whether having an isolated headache following minor blunt head trauma was suggestive of traumatic brain injury (TBI) among a large cohort of children 2-18 years of age.

  3. Integration of Neuropsychology in Educational Planning Following Traumatic Brain Injury

    Science.gov (United States)

    Stavinoha, Peter L.

    2005-01-01

    Traumatic brain injuries (TBIs) have the potential to significantly disrupt a student's cognitive, academic, social, emotional, behavioral, and physical functioning. It is important for educators to appreciate the array of difficulties students with TBI may experience in order to appropriately assess needs and create an educational plan that…

  4. Traumatic Brain Injury and Special Education: An Information Resource Guide.

    Science.gov (United States)

    Stevens, Alice M.

    This resource guide of annotated references on traumatic brain injury (TBI) was created to help educators locate information from such disciplines as neurology, neuropsychology, rehabilitation, and pediatric medicine. Twenty-four resources published from 1990 to 1994 are listed, with annotations. The resources include research reports/reviews,…

  5. Traumatic Brain Injury and Metabolic Dysfunction Among Head ...

    African Journals Online (AJOL)

    Traumatic Brain Injury (TBI) is a common health problem which is one of the main causes of chronic disability and it is associated with hormonal and metabolic disorders. This work was carried out to investigate the relationship between some stress hormones (i.e. prolactin and cortisol) and plasma glucose level in TBI ...

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

    Science.gov (United States)

    Grove, Michael J.

    2013-01-01

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

  7. Facial Expression Recognition for Traumatic Brain Injured Patients

    DEFF Research Database (Denmark)

    Ilyas, Chaudhary Muhammad Aqdus; Nasrollahi, Kamal; Moeslund, Thomas B.

    2018-01-01

    In this paper, we investigate the issues associated with facial expression recognition of Traumatic Brain Insured (TBI) patients in a realistic scenario. These patients have restricted or limited muscle movements with reduced facial expressions along with non-cooperative behavior, impaired reason...

  8. Quantifying the funding gap for management of traumatic brain ...

    African Journals Online (AJOL)

    We used data from a prospective digital trauma registry to cost Traumatic Brain Injury (TBI) at our institution over a two-year period and to estimate the funding gap that exists in the care of TBI. Methods: All patients who were admitted to the Pietermaritzburg Metropolitan Trauma Service (PMTS) with TBI were identified from ...

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

    Science.gov (United States)

    2015-09-01

    compulsive buying and the burden perceived by caregivers after moderate-to-severe traumatic brain injury. Psychopathology. 2011;44:158-164. Rochat L...well as the progression from abuse to compulsive drug taking and addiction (Coluzzi and Pappagallo, 2005; Koob and Volkow, 2010). Physical dependence

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

    Science.gov (United States)

    2014-07-01

    impulsivity relates to compulsive buying and the burden perceived by caregivers after moderate-to-severe traumatic brain injury. Psychopathology...mechanism for the continued misuse/abuse of opioid drugs as well as the progression from abuse to compulsive drug taking and addiction (Coluzzi and

  11. Working with Parents of Students with Traumatic Brain Injuries.

    Science.gov (United States)

    Rhein, Barbara; And Others

    Intended for educators working with children who have suffered traumatic brain injuries (TBI), this brief paper addresses parent issues, administrative issues, and programmatic issues. Noted are the five stages of adjustment typically experienced by parents: shock, elation, reality, crisis, and mourning. Professionals are encouraged to be informed…

  12. Traumatic Brain Injury in the Accident and Emergency Department of ...

    African Journals Online (AJOL)

    Background: Traumatic brain injury is a major public health problem in Nigeria, as it could be associated with long term and life long deficits. Unlike other parts of the world, in our country, motorcycles are possibly the main cause of this injury. Unfortunately, we do not have a national epidemiological data base yet. This study ...

  13. Adolescents\\' experience of a parental traumatic brain injury | Harris ...

    African Journals Online (AJOL)

    The phenomenon of parental traumatic brain injury was characterised by denial, anger, grief, guilt, anxiety, over-protectiveness, social isolation, and change in many areas of the participants' lives. The adolescents coped using both approaches and avoidance styles of coping. Religion was a theme in the lives of all four ...

  14. Traumatic brain injury in children | Coughlan | South African Family ...

    African Journals Online (AJOL)

    South African Family Practice. Journal Home · ABOUT THIS JOURNAL · Advanced Search · Current Issue · Archives · Journal Home > Vol 45, No 5 (2003) >. Log in or Register to get access to full text downloads. Username, Password, Remember me, or Register. Traumatic brain injury in children. M Coughlan, G Fieggen ...

  15. Demographic profile of severe traumatic brain injury admissions to ...

    African Journals Online (AJOL)

    This retrospective, descriptive, quantitative study included children admitted to the RCWMCH with severe traumatic brain injury (TBI) between June 2006 and April 2011, who required intracranial monitoring. We used the Division of Paediatric Neurosurgery's TBI database to identify cases for inclusion in the study and to ...

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

    NARCIS (Netherlands)

    J.T.M. van Baalen (Bianca)

    2008-01-01

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

  17. 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 ...

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

    African Journals Online (AJOL)

    Objectives. This retrospective review of a prospectively entered and maintained hybrid electronic trauma registry was intended to develop a comprehensive overview of traumatic brain injury (TBI) in children and adolescents and to compare it with previous audits from our local environment and from other developing world ...

  19. 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 ...

  20. Minor traumatic brain injuries – what is new? | Hollander ...

    African Journals Online (AJOL)

    Minor traumatic brain injuries – what is new? D Hollander, J Coventry, M Du Trevou. Abstract. No Abstract. Full Text: EMAIL FREE FULL TEXT EMAIL FREE FULL TEXT · DOWNLOAD FULL TEXT DOWNLOAD FULL TEXT · AJOL African Journals Online. HOW TO USE AJOL... for Researchers · for Librarians · for Authors ...

  1. Oxidative stress following traumatic brain injury: enhancement of ...

    African Journals Online (AJOL)

    Background: Management of brain injury can pose enormous challenges to the health team. There are many studies aimed at discovering or developing pharmacotherapeutic agents targeted at improving outcome of head-injured patients. This paper reviews the role of oxidative stress in neuronal loss following traumatic ...

  2. Minor traumatic brain injuries – what is new?

    African Journals Online (AJOL)

    Research has concentrated on indications for neuroimaging, management guidelines for sports-related concussion and sequelae of minor traumatic brain injuries (mTBIs). Despite the emergence of several guidelines there is little agreement on several important issues, including the definition of mTBIs and concussion.

  3. Clostridium butyricum exerts a neuroprotective effect in a mouse model of traumatic brain injury via the gut-brain axis.

    Science.gov (United States)

    Li, H; Sun, J; Du, J; Wang, F; Fang, R; Yu, C; Xiong, J; Chen, W; Lu, Z; Liu, J

    2017-11-27

    Traumatic brain injury (TBI) is a common occurrence following gastrointestinal dysfunction. Recently, more and more attentions are being focused on gut microbiota in brain and behavior. Glucagon-like peptide-1 (GLP-1) is considered as a mediator that links the gut-brain axis. The aim of this study was to explore the neuroprotective effects of Clostridium butyricum (Cb) on brain damage in a mouse model of TBI. Male C57BL/6 mice were subjected to a model of TBI-induced by weight-drop impact head injury and were treated intragastrically with Cb. The cognitive deficits, brain water content, neuronal death, and blood-brain barrier (BBB) permeability were evaluated. The expression of tight junction (TJ) proteins, Bcl-2, Bax, GLP-1 receptor (GLP-1R), and phosphorylation of Akt (p-Akt) in the brain were also measured. Moreover, the intestinal barrier permeability, the expression of TJ protein and GLP-1, and IL-6 level in the intestine were detected. Cb treatment significantly improved neurological dysfunction, brain edema, neurodegeneration, and BBB impairment. Meanwhile, Cb treatment also significantly increased the expression of TJ proteins (occludin and zonula occluden-1), p-Akt and Bcl-2, but decreased expression of Bax. Moreover, Cb treatment exhibited more prominent effects on decreasing the levels of plasma d-lactate and colonic IL-6, upregulating expression of Occludin, and protecting intestinal barrier integrity. Furthermore, Cb-treated mice showed increased the secretion of intestinal GLP-1 and upregulated expression of cerebral GLP-1R. Our findings demonstrated the neuroprotective effect of Cb in TBI mice and the involved mechanisms were partially attributed to the elevating GLP-1 secretion through the gut-brain axis. © 2017 John Wiley & Sons Ltd.

  4. Amelioration of cold injury-induced cortical brain edema formation by selective endothelin ETB receptor antagonists in mice.

    Science.gov (United States)

    Michinaga, Shotaro; Nagase, Marina; Matsuyama, Emi; Yamanaka, Daisuke; Seno, Naoki; Fuka, Mayu; Yamamoto, Yui; Koyama, Yutaka

    2014-01-01

    Brain edema is a potentially fatal pathological condition that often occurs in stroke and head trauma. Following brain insults, endothelins (ETs) are increased and promote several pathophysiological responses. This study examined the effects of ETB antagonists on brain edema formation and disruption of the blood-brain barrier in a mouse cold injury model (Five- to six-week-old male ddY mice). Cold injury increased the water content of the injured cerebrum, and promoted extravasation of both Evans blue and endogenous albumin. In the injury area, expression of prepro-ET-1 mRNA and ET-1 peptide increased. Intracerebroventricular (ICV) administration of BQ788 (ETB antagonist), IRL-2500 (ETB antagonist), or FR139317 (ETA antagonist) prior to cold injury significantly attenuated the increase in brain water content. Bolus administration of BQ788, IRL-2500, or FR139317 also inhibited the cold injury-induced extravasation of Evans blue and albumin. Repeated administration of BQ788 and IRL-2500 beginning at 24 h after cold injury attenuated both the increase in brain water content and extravasation of markers. In contrast, FR139317 had no effect on edema formation when administrated after cold injury. Cold injury stimulated induction of glial fibrillary acidic protein-positive reactive astrocytes in the injured cerebrum. Induction of reactive astrocytes after cold injury was attenuated by ICV administration of BQ788 or IRL-2500. These results suggest that ETB receptor antagonists may be an effective approach to ameliorate brain edema formation following brain insults.

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

    Directory of Open Access Journals (Sweden)

    Michael A. Kiraly

    2007-01-01

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

  6. Pentoxifylline attenuates TNF-α protein levels and brain edema following temporary focal cerebral ischemia in rats.

    Science.gov (United States)

    Vakili, Abedin; Mojarrad, Somye; Akhavan, Maziar Mohammad; Rashidy-Pour, Ali

    2011-03-04

    Cerebral edema is the most common cause of neurological deterioration and mortality during acute ischemic stroke. Despite the clinical importance of cerebral ischemia, the underlying mechanisms remain poorly understood. Recent studies suggest a role for TNF-α in the brain edema formation. To further investigate whether TNF-α would play a role in brain edema formation, we examined the effects of pentoxifylline (PTX, an inhibitor of TNF-α synthesis) on the brain edema and TNF-α levels in a model of transient focal cerebral ischemia. The right middle cerebral artery (MCA) of rats was occluded for 60 min using the intraluminal filament method. The animals received PTX (60 mg/kg) immediately, 1, 3, or 6h post-ischemic induction. Twenty-four hours after induction of ischemic injury, permeability of the blood-brain barrier (BBB) and brain edema were determined by in situ brain perfusion of Evans Blue (EB) and wet-to-dry weight ratio, respectively. TNF-α protein levels in ischemic cortex were also measured at 1, 4, and 24h after the beginning of an ischemic stroke by using an enzyme-linked immunosorbent assay method. The administration of PTX up to 6h after occlusion of the MCA significantly reduced the brain edema. Moreover, PTX significantly reduced the concentration of TNF-α in ischemic brain cortex up to 4h post-transient focal stroke (Pedema in a model of transient focal cerebral ischemia. The beneficial effects of PTX may be mediated, at least in part, through a decline in TNF-α production and BBB breakdown. Copyright © 2011 Elsevier B.V. All rights reserved.

  7. Acute non-traumatic marrow edema syndrome in the knee: MRI findings at presentation, correlation with spinal DEXA and outcome

    International Nuclear Information System (INIS)

    Karantanas, Apostolos H.; Drakonaki, Elena; Karachalios, Theophilos; Korompilias, Anastasios V.; Malizos, Konstantinos

    2008-01-01

    Purpose: The aim of the study was to present the MRI findings of non-traumatic edema-like lesions presented acutely in the adult knee and to correlate them with the 3-year outcome and the bone mineral density (BMD) in the spine. Materials and methods: Ninety-eight patients (40 men, 58 women, mean age 60.1 ± 11 years, age range 27-82 years), were followed up clinically as well as with MR imaging, when indicated, for at least 3 years. Patients were classified according to presentation in 3 groups (A: bone marrow edema (BME), B: BME and subchondral fracture, C: BME and articular collapse) and according to outcome in 2 groups (A: reversible BME, B: articular collapse). BMD measurements of the spine were carried out in males over 70 and females over 60 years old using DEXA. Results: The isolated BME pattern was observed in 64.3% (Group A), subchondral fractures without articular collapse in 11.2% (Group B) and articular collapse in 24.5% (Group C). Significant differences were found among the 3 groups at presentation, regarding the age, sex, BMD, affected area and duration of symptoms prior to imaging (p < 0.05). Localization of the lesions in the weight-bearing areas of the knee was shown in 100% of C, in 90.9% of B and in 50.8% of A. The duration of symptoms prior to imaging was longer in C (7.6 ± 2.8 m) than in A (2.5 ± 1.7 m) and B (4.0 ± 3.2 m) (p < 0.05). Group B progressed to articular collapse in 45.5%, the rest demonstrating a favourable outcome. Group C showed clinical improvement in 75% and persistent symptoms that required knee arthroplasty in 25% of cases. Articular collapse was the final outcome in 29.6% and transient BME in 70.4% of patients. These two groups showed significant differences regarding the age (p ∼ 0), sex (p = 0.002), low BMD (p = 0.004), affected area (p ∼ 0), presence of subchondral sparing (p ∼ 0), duration of symptoms prior to imaging (p ∼ 0), time from onset of symptoms to the final outcome (p ∼ 0) and need for

  8. Acute non-traumatic marrow edema syndrome in the knee: MRI findings at presentation, correlation with spinal DEXA and outcome

    Energy Technology Data Exchange (ETDEWEB)

    Karantanas, Apostolos H. [Department of Radiology, University of Crete, Heraklion 711 10 Greece (Greece)], E-mail: apolsen@yahoo.com; Drakonaki, Elena [Department of Radiology, University of Crete, Heraklion 711 10 Greece (Greece); Karachalios, Theophilos [Department of Orthopaedic Surgery, University of Thessaly, Larissa 411 10 Greece (Greece); Korompilias, Anastasios V. [Department of Orthopaedic Surgery, University of Ioannina, Ioannina 451 10 (Greece); Malizos, Konstantinos [Department of Orthopaedic Surgery, University of Thessaly, Larissa 411 10 Greece (Greece)

    2008-07-15

    Purpose: The aim of the study was to present the MRI findings of non-traumatic edema-like lesions presented acutely in the adult knee and to correlate them with the 3-year outcome and the bone mineral density (BMD) in the spine. Materials and methods: Ninety-eight patients (40 men, 58 women, mean age 60.1 {+-} 11 years, age range 27-82 years), were followed up clinically as well as with MR imaging, when indicated, for at least 3 years. Patients were classified according to presentation in 3 groups (A: bone marrow edema (BME), B: BME and subchondral fracture, C: BME and articular collapse) and according to outcome in 2 groups (A: reversible BME, B: articular collapse). BMD measurements of the spine were carried out in males over 70 and females over 60 years old using DEXA. Results: The isolated BME pattern was observed in 64.3% (Group A), subchondral fractures without articular collapse in 11.2% (Group B) and articular collapse in 24.5% (Group C). Significant differences were found among the 3 groups at presentation, regarding the age, sex, BMD, affected area and duration of symptoms prior to imaging (p < 0.05). Localization of the lesions in the weight-bearing areas of the knee was shown in 100% of C, in 90.9% of B and in 50.8% of A. The duration of symptoms prior to imaging was longer in C (7.6 {+-} 2.8 m) than in A (2.5 {+-} 1.7 m) and B (4.0 {+-} 3.2 m) (p < 0.05). Group B progressed to articular collapse in 45.5%, the rest demonstrating a favourable outcome. Group C showed clinical improvement in 75% and persistent symptoms that required knee arthroplasty in 25% of cases. Articular collapse was the final outcome in 29.6% and transient BME in 70.4% of patients. These two groups showed significant differences regarding the age (p {approx} 0), sex (p = 0.002), low BMD (p = 0.004), affected area (p {approx} 0), presence of subchondral sparing (p {approx} 0), duration of symptoms prior to imaging (p {approx} 0), time from onset of symptoms to the final outcome (p

  9. Fresh Frozen Plasma Modulates Brain Gene Expression in a Swine Model of Traumatic Brain Injury and Shock

    DEFF Research Database (Denmark)

    Sillesen, Martin; Bambakidis, Ted; Dekker, Simone E

    2017-01-01

    BACKGROUND: Resuscitation with fresh frozen plasma (FFP) decreases brain lesion size and swelling in a swine model of traumatic brain injury and hemorrhagic shock. We hypothesized that brain gene expression profiles after traumatic brain injury and hemorrhagic shock would be modulated by FFP resu...

  10. Mild traumatic brain injury does not produce post-traumatic stress disorder.

    Science.gov (United States)

    Sbordone, R J; Liter, J C

    1995-01-01

    It has been widely assumed that patients who sustain mild traumatic brain injury (MTBI) or post-concussive syndrome develop post-traumatic stress disorder (PTSD) in response to their cognitive difficulties, diminished coping skills, or other losses. This study examined 70 patients who had previously been diagnosed as having either PTSD or MTBI. Each patient was asked to provide a highly detailed chronological history of the events which preceded, followed, and occurred during the traumatic event, to indicate whether they were rendered unconscious or had amnesia for the event, and to describe the various symptoms they developed. All (100.0%) of the PTSD patients were able to provide a highly detailed and emotionally charged recollection of the events which occurred within 15 minutes of the traumatic event in comparison to none (0.0%) of the MTBI patients. None of the MTBI patients reported symptoms such as intrusive recollections of the traumatic event, nightmares, hypervigilance, phobic or startle reactions, or became upset when they were asked to describe the traumatic event or were exposed to stimuli associated with it. These data suggest that PTSD and MTBI are two mutually exclusive disorders, and that it is highly unlikely that MTBI patients develop PTSD symptoms. Furthermore, these findings suggest that clinicians should exercise considerable caution in ruling out PTSD prior to making the diagnosis of MTBI.

  11. [Utility of diffusion-weighted magnetic resonance imaging in severe focal traumatic brain injuries].

    Science.gov (United States)

    Prieto-Valderrey, F; Muñiz-Montes, J R; López-García, J A; Villegas-Del Ojo, J; Málaga-Gil, J; Galván-García, R

    2013-01-01

    To describe the apparent diffusion coefficient (ADC) in a series of severe traumatic brain injuries, their clinical and outcome features, and possible implications. A descriptive, observational case-series study was carried out. Patients with severe traumatic brain injuries (TBIs) admitted to the ICU were subjected to MRI study using a 1.5 T scanner. Diffusion-weighted images (DWMR) were obtained using the following echo-planar pulse sequence: TR 10000 ms, TE 126.9 ms, with b values 1000 s/mm2 in the three spatial dimensions. Combining the three sets of images, an isotropic image conforming a map of the mean ADCs was obtained. DWMR was performed in 23 patients with severe TBI admitted to the ICU between 2001 and 2004. In the MR images we selected 26 regions of interest (ROIs) where ADC was recorded. We observed a clear increase in diffusion in non-treated space-occupying lesions versus other types of injuries and the normal values. A poorer outcome was recorded in patients with lower ADC values. Mean ADC in the lesions was greater than the normal values and greater in contusions than in other types of injuries, as an expression of extracellular edema. ADCs were decreased in patients with a poor outcome, suggesting an association between ischemia and the patient prognosis. Copyright © 2011 Elsevier España, S.L. and SEMICYUC. All rights reserved.

  12. The significance of morphological changes in the brain-tumor interface for the pathogenesis of brain edema in meningioma: Magnetic resonance tomography and intraoperative findings

    International Nuclear Information System (INIS)

    Bitzer, M.; Klose, U.; Naegele, T.; Mundinger, P.; Voigt, K.; Freudenstein, D.; Heiss, E.

    1999-01-01

    Purpose: The aim of the study was to verify a possible correlation between macroscopic changes of the brain-tumor interface (BTI) and the development of a peritumoral brain edema in meningiomas. Methods: 27 meningiomas were investigated in this prospective study using an optimized inversion-recovery (IR) sequence. After i.v. administration of 0.2 mmol Gd-DTPA/kg axial and coronary images were acquired (slice thickness=2 mm). The distances of signal altered cortex and obliterations of the subarachnoid space (SAS) were measured at the BTI and related to the pial tumor circumference (cortical-index and SAS-index). Intraoperatively the BTI was divided into the following categories: 0: SAS not obliterated, 1: SAS partially obliterated, 2: Direct contact between tumor and white matter, 3: Tumor infiltration into brain. Results: Edema-associated meningiomas showed a significantly (p=0.0001) increased SAS-index (0.47 vs. 0.07) and cortical index (0.45 vs. 0.0) compared to cases without edema. Intraoperatively 95% of meningiomas with brain edema showed SAS-obliterations, compared to 50% of cases without an edema. Conclusions: Arachnoid adhesions at the BTI with obliteration of the SAS seem to play an essential role in the induction of brain edema in meningiomas. (orig.) [de

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

    Directory of Open Access Journals (Sweden)

    Zhao Song

    2012-06-01

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

  14. Neuropathology and brain weight in traumatic-crush asphyxia.

    Science.gov (United States)

    Al-Sarraj, Safa; Laxton, Ross; Swift, Ben; Kolar, Alexander J; Chapman, Rob C; Fegan-Earl, Ashley W; Cary, Nat R B

    2017-11-01

    Traumatic (crush) asphyxia is a rare condition caused by severe compression of the chest and trunk leading to often extreme so-called asphyxial signs, including cyanosis in head and neck regions, multiple petechiae, and subconjunctival haemorrhage as well as neurological manifestations. To investigate the neuropathology and brain weight in traumatic asphyxia caused by different accidents such as industrial accidents and road traffic collision. Post mortem records of 20 cases of traumatic asphyxia (TA) resulting from different causes of which four brains are available for comprehensive neuropathological examination. The expected brain weights for given body height and associated 95% confidence range were calculated according to the following formula: baseline brain weight (BBW) + body height x rate (g/cm). The 95% confidence range was calculated by adding and subtracting the standard error (SE) x 1.96 (7-8). There was a trend for higher brain weight in the TA cohort but it was not significant (1494 g vs 1404 g, p = 0.1). The upper limits of the brain weight of 95% confidence was 1680 g vs 1660 g, p = 0.9. The neuropathological examination of four available brains from the TA cohort showed severe congestion of blood vessels, perivascular haemorrhages and occasional βAPP deposits consistent with early axonal disruption. Brain examination is informative as part of investigation of TA. Developing ischaemic changes and an increase in brain weight are the most likely indicators of a prolonged period of patient's survival. Copyright © 2017 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.

  15. Epidemiology of mild traumatic brain injury and neurodegenerative disease.

    Science.gov (United States)

    Gardner, Raquel C; Yaffe, Kristine

    2015-05-01

    Every year an estimated 42 million people worldwide suffer a mild traumatic brain injury (MTBI) or concussion. More severe traumatic brain injury (TBI) is a well-established risk factor for a variety of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). Recently, large epidemiological studies have additionally identified MTBI as a risk factor for dementia. The role of MTBI in risk of PD or ALS is less well established. Repetitive MTBI and repetitive sub-concussive head trauma have been linked to increased risk for a variety of neurodegenerative diseases including chronic traumatic encephalopathy (CTE). CTE is a unique neurodegenerative tauopathy first described in boxers but more recently described in a variety of contact sport athletes, military veterans, and civilians exposed to repetitive MTBI. Studies of repetitive MTBI and CTE have been limited by referral bias, lack of consensus clinical criteria for CTE, challenges of quantifying MTBI exposure, and potential for confounding. The prevalence of CTE is unknown and the amount of MTBI or sub-concussive trauma exposure necessary to produce CTE is unclear. This review will summarize the current literature regarding the epidemiology of MTBI, post-TBI dementia and Parkinson's disease, and CTE while highlighting methodological challenges and critical future directions of research in this field. This article is part of a Special Issue entitled SI:Traumatic Brain Injury. Published by Elsevier Inc.

  16. Traumatic brain injury and disturbed sleep and wakefulness.

    Science.gov (United States)

    Baumann, Christian R

    2012-09-01

    Traumatic brain injury is a frequent condition worldwide, and sleep-wake disturbances often complicate the course after the injuring event. Current evidence suggests that the most common sleep-wake disturbances following traumatic brain injury include excessive daytime sleepiness and posttraumatic hypersomnia, that is, increased sleep need per 24 h. The neuromolecular basis of posttraumatic sleep pressure enhancement is not entirely clear. First neuropathological and clinical studies suggest that impaired hypocretin (orexin) signalling might contribute to sleepiness, but direct or indirect traumatic injury also to other sleep-wake modulating systems in the brainstem and the mesencephalon is likely. Posttraumatic insomnia may be less common than posttraumatic sleepiness, but studies on its frequency revealed conflicting results. Furthermore, insomnia is often associated with psychiatric comorbidities, and some patients with posttraumatic disruption of their circadian rhythm may be misdiagnosed as insomnia patients. The pathophysiology of posttraumatic circadian sleep disorders remains elusive; however, there is some evidence that reduced evening melatonin production due to traumatic brain damage may cause disruption of circadian regulation of sleep and wakefulness.

  17. Suicide after traumatic brain injury: a population study

    DEFF Research Database (Denmark)

    Teasdale, T W; Engberg, A W

    2001-01-01

    OBJECTIVES: To determine the rates of suicide among patients who have had a traumatic brain injury. METHODS: From a Danish population register of admissions to hospital covering the years 1979-93 patients were selected who had had either a concussion (n=126 114), a cranial fracture (n=7560...... in hospital. Cox regression analyses for proportional hazards confirmed that there was a significantly greater risk of suicide among patients with cerebral contusions or traumatic intracranial haemorrhages than among patients with concussion or cranial fractures (hazard ratios=1.42 and 1.50 respectively...

  18. Cerebral Infarction after Traumatic Brain Injury: Incidence and Risk Factors

    OpenAIRE

    Bae, Dong-Hyeon; Choi, Kyu-Sun; Yi, Hyeong-Joong; Chun, Hyoung-Joon; Ko, Yong; Bak, Koang Hum

    2014-01-01

    Objective Post-traumatic cerebral infarction (PTCI) is one of the most severe secondary insults after traumatic brain injury (TBI), and is known to be associated with poor outcome and high mortality rate. We assessed the practical incidence and risk factors for the development of PTCI. Methods We conducted retrospective study on 986 consecutive patients with TBI from the period May 2005 to November 2012 at our institution. The definition of PTCI was made on non-enhanced CT scan based on a wel...

  19. Computational modelling of traumatic brain injury predicts the location of chronic traumatic encephalopathy pathology.

    Science.gov (United States)

    Ghajari, Mazdak; Hellyer, Peter J; Sharp, David J

    2017-02-01

    Traumatic brain injury can lead to the neurodegenerative disease chronic traumatic encephalopathy. This condition has a clear neuropathological definition but the relationship between the initial head impact and the pattern of progressive brain pathology is poorly understood. We test the hypothesis that mechanical strain and strain rate are greatest in sulci, where neuropathology is prominently seen in chronic traumatic encephalopathy, and whether human neuroimaging observations converge with computational predictions. Three distinct types of injury were simulated. Chronic traumatic encephalopathy can occur after sporting injuries, so we studied a helmet-to-helmet impact in an American football game. In addition, we investigated an occipital head impact due to a fall from ground level and a helmeted head impact in a road traffic accident involving a motorcycle and a car. A high fidelity 3D computational model of brain injury biomechanics was developed and the contours of strain and strain rate at the grey matter-white matter boundary were mapped. Diffusion tensor imaging abnormalities in a cohort of 97 traumatic brain injury patients were also mapped at the grey matter-white matter boundary. Fifty-one healthy subjects served as controls. The computational models predicted large strain most prominent at the depths of sulci. The volume fraction of sulcal regions exceeding brain injury thresholds were significantly larger than that of gyral regions. Strain and strain rates were highest for the road traffic accident and sporting injury. Strain was greater in the sulci for all injury types, but strain rate was greater only in the road traffic and sporting injuries. Diffusion tensor imaging showed converging imaging abnormalities within sulcal regions with a significant decrease in fractional anisotropy in the patient group compared to controls within the sulci. Our results show that brain tissue deformation induced by head impact loading is greatest in sulcal locations

  20. Quantitative autoradiography of 14C-D-glucose metabolism of normal and traumatized rat brain using micro-absorption photometry

    International Nuclear Information System (INIS)

    Bonorden, S.

    1980-01-01

    It could be shown using 14 C-glucose as energy-providing substrate for brain tissue metabolism that for bolus type application a retarded and even channelling of the substrate into the metabolic process takes place. The presence of tracer in the tissue was established using autoradiography. A linear correlation between the amount of tissue-incorporated 14 C section thickness and exposure time could be established by means of densitometric measurement of brain sections of various thicknesses, by applying various 14 C-activities and by different exposure times. From these correlations direct conclusions may be made regarding the specific activity of the tissue provided that exposure time and section thickness of the sample are known. Comparative studies between cortex and narrow and between traumatized and non-traumatized brain tissue show that the rate of metabolism in brain cortex is markedly higher than in the marrow and that 14 C-incorporation is higher in traumatized tissue than in non-traumatized tissue. Whilst the difference in rate of metabolism between brain cortex and marrow can be clearly related to the differing cell count/unit surface area for cortex and marrow, the different energy conversion rates for functionally damaged and normal brain tissue is a specific characteristic of injury. Apart from the fact that an increased 14 C-deposition is in no way indicative of an increased metabolic activity, the possibility of quantifying 14 C-tissue content provides a basis for estimating therapeutic effects e.g. in the treatment of trauma-caused brain edema. (orig.) [de

  1. Assessment of cerebral perfusion in post-traumatic brain injury patients with the use of ICG-bolus tracking method.

    Science.gov (United States)

    Weigl, W; Milej, D; Gerega, A; Toczylowska, B; Kacprzak, M; Sawosz, P; Botwicz, M; Maniewski, R; Mayzner-Zawadzka, E; Liebert, A

    2014-01-15

    The aim of this study was to verify the usefulness of the time-resolved optical method utilizing diffusely reflected photons and fluorescence signals combined with intravenous injection of indocyanine green (ICG) in the assessment of brain perfusion in post-traumatic brain injury patients. The distributions of times of flight (DTOFs) of diffusely reflected photons were acquired together with the distributions of times of arrival (DTAs) of fluorescence photons. The data analysis methodology was based on the observation of delays between the signals of statistical moments (number of photons, mean time of flight and variance) of DTOFs and DTAs related to the inflow of ICG to the extra- and intracerebral tissue compartments. Eleven patients with brain hematoma, 15 patients with brain edema and a group of 9 healthy subjects were included in this study. Statistically significant differences between parameters obtained in healthy subjects and patients with brain hematoma and brain edema were observed. The best optical parameter to differentiate patients and control group was variance of the DTOFs or DTAs. Results of the study suggest that time-resolved optical monitoring of inflow of the ICG seems to be a promising tool for detecting cerebral perfusion insufficiencies in critically ill patients. © 2013 Elsevier Inc. All rights reserved.

  2. Expression and roles of aquaporin 1 in hippocampus of mice model with traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Bo QIU

    2014-03-01

    Full Text Available Background The "secondary brain insult" including ischemia, hypoxia and edema after primary traumatic brain injury (TBI may deteriorate the brain damages and greatly influence the prognosis. As a selective vulnerable region, the hippocampus is especially sensitive to ischemia, hypoxia or edema and yields irreversible sequelae. Aquaporin 1 (AQP1 has been reported to be related to cerebral edema, but the expression and role of AQP1 in hippocampal edema after TBI have seldomly been investigated. In this study, we established BALB/c mouse closed craniocerebral injury models and investigated the changes of AQP1 expression in hippocampus of mouse models after TBI, thereby discussing its effects on relevant pathophysiological processes.  Methods Seventy-five BALB/c mice were used to establish experimental closed TBI models with a free-falling weight drop device, and the equal numbers of mice were subject to sham operation and categorized as sham group. The neurological function of each mouse in either TBI group or sham group was scored at different time points (1, 6, 24 and 72 h after TBI or sham operation, and brain edema formation of the mice in both groups was also evaluated accordingly at 6, 24 and 72 h. The apoptotic hippocampal cells were stained in situ and detected using TdT-mediated dUTP-biotin nick end labeling (TUNEL method at different time points (6, 24 and 72 h, then AQP1 expression in hippocampus was also correspondingly detected using immunohistochemistry and Western blotting. All the data were finally compared with those in sham operation group and analyzed.  Results Experimental TBI models were successfully established and confirmed by the neurological function score and hippocampal edema evaluation. Six hours after craniocerebral injury, the apoptotic cells increased significantly in the hippocampus of mice in TBI group compared with those in sham group [(44.26 ± 15.18% vs (8.61 ± 8.25% , t = - 9.676, P = 0.002]. The apoptotic

  3. Spatial patterns of progressive brain volume loss after moderate-severe traumatic brain injury

    Science.gov (United States)

    Jolly, Amy; de Simoni, Sara; Bourke, Niall; Patel, Maneesh C; Scott, Gregory; Sharp, David J

    2018-01-01

    Abstract Traumatic brain injury leads to significant loss of brain volume, which continues into the chronic stage. This can be sensitively measured using volumetric analysis of MRI. Here we: (i) investigated longitudinal patterns of brain atrophy; (ii) tested whether atrophy is greatest in sulcal cortical regions; and (iii) showed how atrophy could be used to power intervention trials aimed at slowing neurodegeneration. In 61 patients with moderate-severe traumatic brain injury (mean age = 41.55 years ± 12.77) and 32 healthy controls (mean age = 34.22 years ± 10.29), cross-sectional and longitudinal (1-year follow-up) brain structure was assessed using voxel-based morphometry on T1-weighted scans. Longitudinal brain volume changes were characterized using a novel neuroimaging analysis pipeline that generates a Jacobian determinant metric, reflecting spatial warping between baseline and follow-up scans. Jacobian determinant values were summarized regionally and compared with clinical and neuropsychological measures. Patients with traumatic brain injury showed lower grey and white matter volume in multiple brain regions compared to controls at baseline. Atrophy over 1 year was pronounced following traumatic brain injury. Patients with traumatic brain injury lost a mean (± standard deviation) of 1.55% ± 2.19 of grey matter volume per year, 1.49% ± 2.20 of white matter volume or 1.51% ± 1.60 of whole brain volume. Healthy controls lost 0.55% ± 1.13 of grey matter volume and gained 0.26% ± 1.11 of white matter volume; equating to a 0.22% ± 0.83 reduction in whole brain volume. Atrophy was greatest in white matter, where the majority (84%) of regions were affected. This effect was independent of and substantially greater than that of ageing. Increased atrophy was also seen in cortical sulci compared to gyri. There was no relationship between atrophy and time since injury or age at baseline. Atrophy rates were related to memory performance at the end of the

  4. Purinergic receptor stimulation reduces cytotoxic edema and brain infarcts in mouse induced by photothrombosis by energizing glial mitochondria.

    Directory of Open Access Journals (Sweden)

    Wei Zheng

    2010-12-01

    Full Text Available Treatments to improve the neurological outcome of edema and cerebral ischemic stroke are severely limited. Here, we present the first in vivo single cell images of cortical mouse astrocytes documenting the impact of single vessel photothrombosis on cytotoxic edema and cerebral infarcts. The volume of astrocytes expressing green fluorescent protein (GFP increased by over 600% within 3 hours of ischemia. The subsequent growth of cerebral infarcts was easily followed as the loss of GFP fluorescence as astrocytes lysed. Cytotoxic edema and the magnitude of ischemic lesions were significantly reduced by treatment with the purinergic ligand 2-methylthioladenosine 5' diphosphate (2-MeSADP, an agonist with high specificity for the purinergic receptor type 1 isoform (P2Y(1R. At 24 hours, cytotoxic edema in astrocytes was still apparent at the penumbra and preceded the cell lysis that defined the infarct. Delayed 2MeSADP treatment, 24 hours after the initial thrombosis, also significantly reduced cytotoxic edema and the continued growth of the brain infarction. Pharmacological and genetic evidence are presented indicating that 2MeSADP protection is mediated by enhanced astrocyte mitochondrial metabolism via increased inositol trisphosphate (IP(3-dependent Ca(2+ release. We suggest that mitochondria play a critical role in astrocyte energy metabolism in the penumbra of ischemic lesions, where low ATP levels are widely accepted to be responsible for cytotoxic edema. Enhancement of this energy source could have similar protective benefits for a wide range of brain injuries.

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

    Directory of Open Access Journals (Sweden)

    Robert L. Ruff

    2016-08-01

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

  6. 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.

  7. A prospective pilot investigation of brain volume, white matter hyperintensities and haemorrhagic lesions after mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Michael eJarrett

    2016-02-01

    Full Text Available Traumatic brain injury (TBI is among the most common neurological disorders. Haemorrhagic lesions and white matter hyperintensities (WMH are radiological features associated with moderate and severe traumatic brain injury TBI. Brain volume reductions have also been observed during the months following injury. In concussion, no signs of injury are observed on conventional MRI, which may be a true feature of concussion or merely due to the limited sensitivity of imaging techniques used so far. Moreover, it is not known whether volume reductions are due to the resolution of trauma related edema or a true volume loss. Forty five collegiate level ice hockey players (20 female and 15 controls (9 female 40 players underwent 3T MRI for haemorrhages (multi echo susceptibility weighted imaging (SWI, WMH (three dimensional FLAIR and brain volume at the beginning and the end of the hockey season. Concussed athletes underwent additional imaging and neuropsychological testing atthree days, two weeks, and two months after injury. At the end of the hockey season, brain volume was reduced compared to controls by 0.32% (p<0.034 in the whole cohort and by 0.26% (p<0.09 in the concussed athletes. Two weeks and two months after concussion, brain volume was reduced by -0.08% (p=0.027 and -0.23% (p=0.035, respectively. In athletes, the WMH were significantly closer to the interface between grey matter and white matter compared to controls. No significant changes in thenumber of WMH over the duration of the study were found in athletes. No microhaemorrhages were detected as a result of concussion or playing a season of ice hockey. We conclude that mild TBI does not lead to transient increases in brain volume and no new microbleeds or WMH are detectable after concussion. Brain volume reductions appear by two weeks after concussion and persist until at least two months after concussion. Brain volume is reduced between the beginning and the end of the icehockey season.

  8. 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...

  9. [Traumatic brain injuries--forensic and expertise aspects].

    Science.gov (United States)

    Vuleković, Petar; Simić, Milan; Misić-Pavkov, Gordana; Cigić, Tomislav; Kojadinović, Zeljko; Dilvesi, Dula

    2008-01-01

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

  10. Acute Inflammatory Response in Rodent Brain and Blood Following a Blast Induced Traumatic Brain Injury

    Science.gov (United States)

    2014-11-01

    dehydrated with 30% sucrose before storing at -80 °C. Thirty micron coronal sections were stained with a primary antibody against microglia ...strongly Iba-1 stained cells as compared to controls. These results indicate blast exposure induces activation of microglia in the hippocampus... Neuroinflammation after traumatic brain injury: Opportunities for therapeutic intervention. Brain, behaviour and Immunity 26: 1191-1201. Loane, D. J

  11. Circulating brain-derived neurotrophic factor has diagnostic and prognostic value in traumatic brain injury

    NARCIS (Netherlands)

    F.K. Korley (Frederick K.); R. Diaz-Arrastia (Ramon); A.H.B. Wu (Alan H. B.); J.K. Yue (John); G. Manley (Geoffrey); H.I. Sair (Haris I.); J.E. van Eyk (Jennifer); A.D. Everett (Allen D.); D. Okonkwo (David); A.B. Valadka (Alex); W.A. Gordon (Wayne A.); A.I.R. Maas (Andrew I.R.); P. Mukherjee (Pratik); E.L. Yuh (Esther); H.F. Lingsma (Hester); A.M. Puccio (Ava); D.M. Schnyer (David)

    2016-01-01

    textabstractBrain-derived neurotrophic factor (BDNF) is important for neuronal survival and regeneration. We investigated the diagnostic and prognostic values of serum BDNF in traumatic brain injury (TBI). We examined serum BDNF in two independent cohorts of TBI cases presenting to the emergency

  12. Comparison of brain perfusion SPECT abnormalities with anatomical imaging in mild traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Majid Asadi

    2007-02-01

    Full Text Available Background: Trauma is the most common cause of morbidity and mortality in industrialized countries and also in Iran. Anatomical imaging (AI CT and MRI is helpful in the diagnosis of acute traumatic complications however it is not efficient in the diagnosis of disabling injury syndrome. In contrast, brain perfusion SPECT (Single Photon Emission Computed Tomography can be more useful for evaluation of microvascular structure. This study was designed to compare these two diagnostic methods. Methods: A total of 50 patients who had been suffering from traumatic brain injury for more than 1 year, and were followed as mild traumatic brain injury group according to “the Brain Injury Interdisciplinary Special Interest Group of the Ameri can Congress of Rehabilitation Medicine” criteria, were examined by brain perfusion SPECT and AI. The common anatomical classification of the lobes of brain was used. Results: The male to female ratio was 3:2. The mean age was 32.32±11.8 years and mean post-traumatic time was 1.48±0.65 years. The most common symptoms were headache (60%, agusia (36% and anosmia (32%. Among 400 examined brain lobes in this study, brain perfusion SPECT revealed remarkable abnormality in 76 lobes (19%, but AI determined abnormalities in 38 lobes (9.5% therefore, SPECT was twice sensitive than AI in mild traumatic brain injury (P<0.001. The correlation between SPECT and AI findings was 84%. SPECT was more sensitive than AI in demonstrating brain abnormalities in frontal lobe it was more obvious in the male group however, there was no significant difference between more and less than 30 years old groups. Conclusion: According to the findings of this study, we recommend using brain perfusion SPECT for all patients with chronic complications of head trauma, particularly those who have signs and symptoms of hypofrontalism, even though with some abnormalities in AI.

  13. Neurodegeneration after mild and repetitive traumatic brain injury: Chronic traumatic encepalopathy

    Directory of Open Access Journals (Sweden)

    Stanescu Ioana

    2015-09-01

    Full Text Available Repetitive brain trauma is associated with a progressive neurological deterioration, now termed as chronic traumatic encephalopathy (CTE. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently under research. CTE can be diagnosed only by post mortem neuropathological examination of the brain. Great efforts are being made to better understand the clinical signs and symptoms of CTE, obtained in most cases retrospectively from families of affected persons.Patients with CTE are described as having behavioral, mood, cognitive and motor impairments, occurring after a long latency from the traumatic events. Recent pathogenetic studies have provided new insights to CTE mechanisms, offering important clues in understanding neurodegenerative process and relations between physical factors and pathologic protein deposition. Further research is needed to better identify the genetic and environmental risk factors for CTE, as well as rehabilitation and treatment strategies.

  14. Acute symptomatic peri-lead edema 33 hours after deep brain stimulation surgery: a case report.

    Science.gov (United States)

    Schoen, Nathan B; Jermakowicz, Walter J; Luca, Corneliu C; Jagid, Jonathan R

    2017-04-14

    Symptomatic peri-lead edema is a rare complication of deep brain stimulation that has been reported to develop 4 to 120 days postoperatively. Here we report the case of a 63-year-old Hispanic man with an 8-year history of Parkinson's disease who underwent bilateral placement of subthalamic nucleus deep brain stimulation leads and presented with acute, symptomatic, unilateral, peri-lead edema just 33 hours after surgery. We document a thorough radiographic time course showing the evolution of these peri-lead changes and their regression with steroid therapy, and discuss the therapeutic implications of these findings. We propose that the unilateral peri-lead edema after bilateral deep brain stimulation is the result of severe microtrauma with blood-brain barrier disruption. Knowledge of such early manifestation of peri-lead edema after deep brain stimulation is critical for ruling out stroke and infection and preventing unnecessary diagnostic testing or hardware removal in this rare patient population.

  15. 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....

  16. Resuscitation with Pooled and Pathogen-Reduced Plasma Attenuates the Increase in Brain Water Content following Traumatic Brain Injury and Hemorrhagic Shock in Rats

    DEFF Research Database (Denmark)

    Genét, Gustav Folmer; Bentzer, Peter; Ostrowski, Sisse Rye

    2017-01-01

    Traumatic brain injury and hemorrhagic shock is associated with blood-brain barrier (BBB) breakdown and edema formation. Recent animal studies have shown that fresh frozen plasma (FFP) resuscitation reduces brain swelling and improves endothelial function compared to isotonic NaCl (NS). The aim o......)-treated plasma attenuates the post-traumatic increase in brain water content, and that this effect may, in part, be explained by a high crystalloid and colloid osmotic pressure in SD-treated plasma....... brain injury, hemorrhage (20 mL/kg), and 90-min shock, 48 male Sprague-Dawley rats were randomized to resuscitation with OCTA, FFP, or NS (n = 16/group). Brain water content (wet/dry weight) and BBB permeability (transfer constant for51Cr-EDTA) were measured at 24 h. Plasma osmolality, oncotic pressure...... permeability. Plasma osmolality and oncotic pressures were highest in FFP and OCTA resuscitated, and osmolality was further highest in OCTA versus FFP (p = 0.027). In addition, syndecan-1 was highest in FFP and OCTA resuscitated (p = 0.010). These results suggest that pooled solvent-detergent (SD...

  17. The neuropathology and neurobiology of traumatic brain injury.

    Science.gov (United States)

    Blennow, Kaj; Hardy, John; Zetterberg, Henrik

    2012-12-06

    The acute and long-term consequences of traumatic brain injury (TBI) have received increased attention in recent years. In this Review, we discuss the neuropathology and neural mechanisms associated with TBI, drawing on findings from sports-induced TBI in athletes, in whom acute TBI damages axons and elicits both regenerative and degenerative tissue responses in the brain and in whom repeated concussions may initiate a long-term neurodegenerative process called dementia pugilistica or chronic traumatic encephalopathy (CTE). We also consider how the neuropathology and neurobiology of CTE in many ways resembles other neurodegenerative illnesses such as Alzheimer's disease, particularly with respect to mismetabolism and aggregation of tau, β-amyloid, and TDP-43. Finally, we explore how translational research in animal models of acceleration/deceleration types of injury relevant for concussion together with clinical studies employing imaging and biochemical markers may further elucidate the neurobiology of TBI and CTE. Copyright © 2012 Elsevier Inc. All rights reserved.

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

    OpenAIRE

    Bigler, Erin D.

    2016-01-01

    The patient who sustains a traumatic brain injury (TBI) typically undergoes neuroimaging studies, usually in the form of computed tomography (CT) and magnetic resonance imaging (MRI). In most cases the neuroimaging findings are clinically assessed with descriptive statements that provide qualitative information about the presence/absence of visually identifiable abnormalities; though little if any of the potential information in a scan is analyzed in any quantitative manner, except in researc...

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

    OpenAIRE

    Flanagan, Steve

    2008-01-01

    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 probl...

  20. Neuropsychology of Neuroendocrine Dysregulation after Traumatic Brain Injury

    OpenAIRE

    Zihl, J.; Almeida, O.

    2015-01-01

    Endocrine dysfunction is a common effect of traumatic brain injury (TBI). In addition to affecting the regulation of important body functions, the disruption of endocrine physiology can significantly impair mental functions, such as attention, memory, executive function, and mood. This mini-review focuses on alterations in mental functioning that are associated with neuroendocrine disturbances in adults who suffered TBI. It summarizes the contribution of hormones to the regulation of mental f...

  1. Mild Traumatic Brain Injury and Dynamic Simulated Shooting Performance

    Science.gov (United States)

    2016-02-01

    USAARL Report No. 2016-16 Mild Traumatic Brain Injury and Dynamic Simulated Shooting Performance By Ben Lawson1, Bethany Ranes1, Amanda... Form 298 (Rev. 8/98) REPORT DOCUMENTATION PAGE Prescribed by ANSI Std. Z39.18 Form Approved OMB No. 0704-0188 The public reporting burden for this...collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. 1. REPORT

  2. Longitudinal Locomotor and Postural Control Following Mild Traumatic Brain Injury

    OpenAIRE

    Fino, Peter C.

    2016-01-01

    Millions of people sustain a mild traumatic brain injury (concussion) each year. While most clinical signs and symptoms resolve within 7-10 days for the majority of typical concussions, some gait and balance tasks have shown abnormalities lasting beyond the resolution of clinical symptoms. These abnormalities can persist after athletes have been medically cleared for competition, yet the implications of such changes are unclear. Most prior research has examined straight gait and standard meas...

  3. Treatment for Depression after Traumatic Brain Injury: A Systematic Review

    OpenAIRE

    Fann, Jesse R.; Hart, Tessa; Schomer, Katherine G.

    2009-01-01

    The aim of this systematic review was to critically evaluate the evidence on interventions for depression following traumatic brain injury (TBI) and provide recommendations for clinical practice and future research. We reviewed pharmacological, other biological, psychotherapeutic, and rehabilitation interventions for depression following TBI from the following data sources: PubMed, CINAHL, PsycINFO, ProQuest, Web of Science, and Google Scholar. We included studies written in English published...

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

    Science.gov (United States)

    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.

  5. Severe traumatic brain injury managed with decompressive ...

    African Journals Online (AJOL)

    2012-05-29

    May 29, 2012 ... adequate decompression for patients with severe TBI. Studies of potential gains in cranial volume against size of craniectomy have shown that small craniectomies risk brain herniation with venous infarction at the bone margins.[2]. In our patient, a large fronto-temporo-parietal free bone flap was raised.

  6. Executive dysfunction in psychosis following traumatic brain injury (PFTBI).

    Science.gov (United States)

    Batty, Rachel; Francis, Andrew; Thomas, Neil; Hopwood, Malcolm; Ponsford, Jennie; Johnston, Lisa; Rossell, Susan

    2015-01-01

    Executive dysfunction is well established in patients with traumatic brain injury and in schizophrenia (SCZ). However, assessments of executive function in psychosis following traumatic brain injury (PFTBI) are limited and inconsistent, and often do not reflect the deficits demonstrated in patients with traumatic brain injury (TBI) or SCZ. We sought to determine the extent of executive dysfunction in PFTBI relative to three comparison cohorts. Measures of executive function were administered to dually diagnosed patients with PFTBI (n = 10) including tests of mental inhibition and switching, processing speed, and attention: the Stroop Task, Trail Making Test (TMT), and the Attention subtest of the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Demographically comparable patients with TBI (n = 10), SCZ (n = 23), and healthy controls (n = 23) underwent an identical battery. Significant executive dysfunction was evident in patients with PFTBI on all measures. Relative to all three comparison cohorts patients with PFTBI performed most poorly. These data present novel evidence of substantially impaired executive function across four task types in PFTBI and suggest that TBI and psychosis have an additive influence on executive function deficits. Treatment programs requiring substantial executive engagement are not suitable for patients dually diagnosed with PFTBI.

  7. Emerging pharmacological agents to improve survival from traumatic brain injury.

    Science.gov (United States)

    Radosevich, John J; Patanwala, Asad E; Erstad, Brian L

    2013-01-01

    To review emerging pharmacological agents for the treatment of traumatic brain injury with regard to survival outcomes and provide recommendations regarding their use. An Ovid MEDLINE (up to May 2013) and the Cochrane Central Register of Controlled Trials (up to May 2013) search was conducted to identify emerging pharmacological therapies for the treatment of traumatic brain injury. The search was limited to English language and humans. Pharmacological agents that were evaluated with respect to survival as an outcome were included. Based on the search, the investigators identified the following new therapies: beta-receptor antagonists, erythropoiesis stimulating agents, hydroxymethylglutaryl-CoA reductase inhibitors (statins) and progesterone. With the exception of progesterone, which was studied in several small, randomized, controlled trials, the remaining agents were primarily studied in observational retrospective cohorts. For each of the agents identified, a potential increase in survival was noted. Emerging pharmacological agents represent promising treatment options for traumatic brain injury to improve survival. Most of these agents are commercially available for other indications. However, limitations in study design, sample size, duration of treatment, timing of treatment and inclusion of heterogeneous patient populations make it difficult to draw definitive conclusions from the literature.

  8. Specificity of Cognitive and Behavioral Complaints in Post-Traumatic Stress Disorder and Mild Traumatic Brain Injury

    OpenAIRE

    Pineau, H?l?ne; Marchand, Andr?; Guay, St?phane

    2015-01-01

    Characterization of cognitive and behavioral complaints is explored in Post-traumatic stress disorder (PTSD) and mild traumatic brain injury (MTBI) samples according to the severity of PTSD, depression and general anxiety conditions. Self-reported questionnaires on cognitive and behavioral changes are administered to PTSD, MTBI, MTBI/PTSD and control groups. Confounding variables are controlled. All groups report more complaints since the traumatic event. PTSD and MTBI/PTSD groups report more...

  9. The emergence of artistic ability following traumatic brain injury

    OpenAIRE

    Midorikawa, Akira; Kawamura, Mitsuru

    2014-01-01

    In this study, the case of a patient who developed artistic ability following a traumatic brain injury is reported. The subject was a 49-year-old male who suffered brain injury at the age of 44 due to an accidental fall. At age 48, he began drawing with great enthusiasm and quickly developed a personal style with his own biomorphic iconography. At first, his drawing was restricted to realistic reproductions of photographs of buildings, but his style of drawing changed and became more personal...

  10. Acute respiratory distress syndrome assessment after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Shahrooz Kazemi

    2016-01-01

    Full Text Available Background: Acute respiratory distress syndrome (ARDS is one of the most important complications associated with traumatic brain injury (TBI. ARDS is caused by inflammation of the lungs and hypoxic damage with lung physiology abnormalities associated with acute respiratory distress syndrome. Aim of this study is to determine the epidemiology of ARDS and the prevalence of risk factors. Methods: This prospective study performed on patients with acute traumatic head injury hospitalization in the intensive care unit of the Shohaday-e Haftom-e-Tir Hospital (September 2012 to September 2013 done. About 12 months, the data were evaluated. Information including age, sex, education, employment, drug and alcohol addiction, were collected and analyzed. The inclusion criteria were head traumatic patients and exclusion was the patients with chest trauma. Questionnaire was designed with doctors supervision of neurosurgery. Then the collected data were analysis. Results: In this study, the incidence of ARDS was 23.8% and prevalence of metabolic acidosis was 31.4%. Most injury with metabolic acidosis was Subarachnoid hemorrhage (SAH 48 (60% and Subdural hemorrhage (SDH was Next Level with 39 (48% Correlation between Glasgow Coma Scale (GCS and Respiratory Distress Syndrome (ARDS were significantly decreased (P< 0.0001. The level of consciousness in patients with skull fractures significantly lower than those without fractures (P= 0.009 [(2.3±4.6 vs (4.02±7.07]. Prevalence of metabolic acidosis during hospitalization was 80 patients (31.4%. Conclusion: Acute respiratory distress syndrome is a common complication of traumatic brain injury. Management and treatment is essential to reduce the mortality. In this study it was found the age of patients with ARDS was higher than patients without complications. ARDS risk factor for high blood pressure was higher in men. Most victims were pedestrians. The most common injury associated with ARDS was SDH. Our analysis

  11. Application of non-invasive cerebral electrical impedance measurement on brain edema in patients with cerebral infarction.

    Science.gov (United States)

    He, Lan Ying; Wang, Jian; Luo, Yong; Dong, Wei Wei; Liu, Li Xu

    2010-09-01

    To investigate the change of brain edema in patients with cerebral infarction by non-invasive cerebral electrical impedance (CEI) measurements. An invariable secure current at a frequency of 50 kHz and an intensity of 0.1 mA was given into a person's brain. CEI values of the bilateral hemisphere of 200 healthy volunteers and 107 patients with cerebral infarction were measured by non-invasive brain edema monitor. The results of perturbative index (PI) converted from CEI were compared with the volumes of brain edema, which were calculated by an image analysing system according to magnetic resonance imaging or computed tomography. (1) In the healthy volunteers, PI values in the left and right hemisphere were 7.98 +/- 0.95 and 8.02 +/- 0.71 respectively, and there was no significant difference between the two sides (p>0.05). Age, gender and different measuring times did not obviously affect PI values (p>0.05). (2) In the cerebral infarction group, CEI measurements were more sensitive to the volumes of lesion, which were more than 20 ml. The positive ratio of PI was higher when the volumes of infarction were >20 ml (80.0%): the ratio of PI was 75.9% when the volumes of infarction were 20-50 ml and it was 83.3% when the volumes of lesion were more than 50 ml. PI was lower when the volumes were less than 20 ml. (3) PI of the infarction side increased obviously 3-5 days after onset; the difference of two sides was the most significant. There was a positive correlation between PI of the infarction side and volume of infarction. PI may be a sensitive parameter for non-invasive monitoring of the change of brain edema in patients with cerebral infarction. CEI is a valuable method for the early detection of brain edema.

  12. Cerebral Taurine Levels are Associated with Brain Edema and Delayed Cerebral Infarction in Patients with Aneurysmal Subarachnoid Hemorrhage.

    Science.gov (United States)

    Kofler, Mario; Schiefecker, Alois; Ferger, Boris; Beer, Ronny; Sohm, Florian; Broessner, Gregor; Hackl, Werner; Rhomberg, Paul; Lackner, Peter; Pfausler, Bettina; Thomé, Claudius; Schmutzhard, Erich; Helbok, Raimund

    2015-12-01

    Cerebral edema and delayed cerebral infarction (DCI) are common complications after aneurysmal subarachnoid hemorrhage (aSAH) and associated with poor functional outcome. Experimental data suggest that the amino acid taurine is released into the brain extracellular space secondary to cytotoxic edema and brain tissue hypoxia, and therefore may serve as a biomarker for secondary brain injury after aSAH. On the other hand, neuroprotective mechanisms of taurine treatment have been described in the experimental setting. We analyzed cerebral taurine levels using high-performance liquid chromatography in the brain extracellular fluid of 25 consecutive aSAH patients with multimodal neuromonitoring including cerebral microdialysis (CMD). Patient characteristics and clinical course were prospectively recorded. Associations with CMD-taurine levels were analyzed using generalized estimating equations with an autoregressive process to handle repeated observations within subjects. CMD-taurine levels were highest in the first days after aSAH (11.2 ± 3.2 µM/l) and significantly decreased over time (p taurine levels compared to those without (Wald = 7.3, df = 1, p taurine supplementation and brain extracellular taurine (p = 0.6). Moreover, a significant correlation with brain extracellular glutamate (r = 0.82, p taurine levels were found in patients with brain edema or DCI after aneurysmal subarachnoid hemorrhage. Its value as a potential biomarker deserves further investigation.

  13. Current pre-hospital traumatic brain injury management in China

    Science.gov (United States)

    Kou, Kou; Hou, Xiang-yu; Sun, Jian-dong; Chu, Kevin

    2014-01-01

    BACKGROUND: Traumatic brain injury (TBI) is associated with most trauma-related deaths. Secondary brain injury is the leading cause of in-hospital deaths after traumatic brain injury. By early prevention and slowing of the initial pathophysiological mechanism of secondary brain injury, pre-hospital service can significantly reduce case-fatality rates of TBI. In China, the incidence of TBI is increasing and the proportion of severe TBI is much higher than that in other countries. The objective of this paper is to review the pre-hospital management of TBI in China. DATA SOURCES: A literature search was conducted in January 2014 using the China National Knowledge Infrastructure (CNKI). Articles on the assessment and treatment of TBI in pre-hospital settings practiced by Chinese doctors were identified. The information on the assessment and treatment of hypoxemia, hypotension, and brain herniation was extracted from the identified articles. RESULTS: Of the 471 articles identified, 65 met the selection criteria. The existing literature indicated that current practices of pre-hospital TBI management in China were sub-optimal and varied considerably across different regions. CONCLUSION: Since pre-hospital care is the weakest part of Chinese emergency care, appropriate training programs on pre-hospital TBI management are urgently needed in China. PMID:25548596

  14. Electrical bioimpedance enabling prompt intervention in traumatic brain injury

    Science.gov (United States)

    Seoane, Fernando; Atefi, S. Reza

    2017-05-01

    Electrical Bioimpedance (EBI) is a well spread technology used in clinical practice across the world. Advancements in Textile material technology with conductive textile fabrics and textile-electronics integration have allowed exploring potential applications for Wearable Measurement Sensors and Systems exploiting. The sensing principle of electrical bioimpedance is based on the intrinsic passive dielectric properties of biological tissue. Using a pair of electrodes, tissue is electrically stimulated and the electrical response can be sensed with another pair of surface electrodes. EBI spectroscopy application for cerebral monitoring of neurological conditions such as stroke and perinatal asphyxia in newborns have been justified using animal studies and computational simulations. Such studies have shown proof of principle that neurological pathologies indeed modify the dielectric composition of the brain that is detectable via EBI. Similar to stroke, Traumatic Brain Injury (TBI) also affects the dielectric properties of brain tissue that can be detected via EBI measurements. Considering the portable and noninvasive characteristics of EBI it is potentially useful for prehospital triage of TBI patients where. In the battlefield blast induced Traumatic Brain Injuries are very common. Brain damage must be assessed promptly to have a chance to prevent severe damage or eventually death. The relatively low-complexity of the sensing hardware required for EBI sensing and the already proven compatibility with textile electrodes suggest the EBI technology is indeed a candidate for developing a handheld device equipped with a sensorized textile cap to produce an examination in minutes for enabling medically-guided prompt intervention.

  15. FGF2 Attenuates Neural Cell Death via Suppressing Autophagy after Rat Mild Traumatic Brain Injury.

    Science.gov (United States)

    Tang, Chonghui; Shan, Yudong; Hu, Yilan; Fang, Zhanjian; Tong, Yun; Chen, Mengdan; Wei, Xiaojie; Fu, Xiaojun; Xu, Xinlong

    2017-01-01

    Traumatic brain injury (TBI) can lead to physical and cognitive deficits, which are caused by the secondary injury process. Effective pharmacotherapies for TBI patients are still lacking. Fibroblast growth factor-2 (FGF2) is an important neurotrophic factor that can stimulate neurogenesis and angiogenesis and has been shown to have neuroprotective effects after brain insults. Previous studies indicated that FGF2's neuroprotective effects might be related to its function of regulating autophagy. The present study investigated FGF2's beneficial effects in the early stage of rat mild TBI and the underlying mechanisms. One hundred and forty-four rats were used for creating controlled cortical impact (CCI) models to simulate the pathological damage after TBI. Our results indicated that pretreatment of FGF2 played a neuroprotective role in the early stage of rat mild TBI through alleviating brain edema, reducing neurological deficits, preventing tissue loss, and increasing the number of surviving neurons in injured cortex and the ipsilateral hippocampus. FGF2 could also protect cells from various forms of death such as apoptosis or necrosis through inhibition of autophagy. Finally, autophagy activator rapamycin could abolish the protective effects of FGF2. This study extended our understanding of FGF2's neuroprotective effects and shed lights on the pharmacological therapy after TBI.

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

    Science.gov (United States)

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

    2016-09-01

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

  17. Prediction of Clinically Important Traumatic Brain Injury in Pediatric Minor Head Trauma; proposing Pediatric Traumatic Brain Injury (PTBI Prognostic Rule

    Directory of Open Access Journals (Sweden)

    Babak Nakhjavan-Shahraki

    2017-01-01

    Full Text Available Background: The present study assesses independent predictors of clinically important traumatic brain injury (ciTBI in order to design a prognostic rule for identification of high risk children with mild head injury. Materials and Methods: In a retrospective cross-sectional study, 3,199 children with mild traumatic brain injury (TBI brought to emergency ward of three hospitals in Tehran, Iran were gathered, from April 2014 to April 2016. The associations between probable predictors of ciTBI in children with mild TBI were assessed and a prediction rule for identification of high risk children in need of computed tomography (CT scan was designed based on a stepwise multivariate logistic regression. Results: 592 (18.5% children had ciTBI. History of loss of conciseness (odds ratio [OR]=3.0; p

  18. Reducing Secondary Insults in Traumatic Brain Injury

    Science.gov (United States)

    2015-03-01

    currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. 1. REPORT DATE (DD-MM-YYYY) 24 Jun 2015 2. REPORT TYPE Journal...transport, intracranial pressure, monitoring, hypoxia, hypotension 16. SECURITY CLASSIFICATION OF: 17. LIMITATION OF ABSTRACT SAR 18. NUMBER OF...of productivity8 Previous studies suggest that secondary insults such as hypoxia and hypotension may worsen a brain injury.9-’ 9 Recent recognition

  19. Protection of Vascular Endothelial Growth Factor to Brain Edema Following Intracerebral Hemorrhage and Its Involved Mechanisms: Effect of Aquaporin-4.

    Directory of Open Access Journals (Sweden)

    Heling Chu

    Full Text Available Vascular endothelial growth factor (VEGF has protective effects on many neurological diseases. However, whether VEGF acts on brain edema following intracerebral hemorrhage (ICH is largely unknown. Our previous study has shown aquaporin-4 (AQP4 plays an important role in brain edema elimination following ICH. Meanwhile, there is close relationship between VEGF and AQP4. In this study, we aimed to test effects of VEGF on brain edema following ICH and examine whether they were AQP4 dependent. Recombinant human VEGF165 (rhVEGF165 was injected intracerebroventricularly 1 d after ICH induced by microinjecting autologous whole blood into striatum. We detected perihemotomal AQP4 protein expression, then examined the effects of rhVEGF165 on perihemotomal brain edema at 1 d, 3 d, and 7 d after injection in wild type (AQP4(+/+ and AQP4 knock-out (AQP4(-/- mice. Furthermore, we assessed the possible signal transduction pathways activated by VEGF to regulate AQP4 expression via astrocyte cultures. We found perihemotomal AQP4 protein expression was highly increased by rhVEGF165. RhVEGF165 alleviated perihemotomal brain edema in AQP4(+/+ mice at each time point, but had no effect on AQP4(-/- mice. Perihemotomal EB extravasation was increased by rhVEGF165 in AQP4(-/- mice, but not AQP4(+/+ mice. RhVEGF165 reduced neurological deficits and increased Nissl's staining cells surrounding hemotoma in both types of mice and these effects were related to AQP4. RhVEGF165 up-regulated phospharylation of C-Jun amino-terminal kinase (p-JNK and extracellular signal-regulated kinase (p-ERK and AQP4 protein in cultured astrocytes. The latter was inhibited by JNK and ERK inhibitors. In conclusion, VEGF reduces neurological deficits, brain edema, and neuronal death surrounding hemotoma but has no influence on BBB permeability. These effects are closely related to AQP4 up-regulation, possibly through activating JNK and ERK pathways. The current study may present new insights to

  20. Integrating Traumatic Brain Injury Model Systems Data into the Federal Interagency Traumatic Brain Injury Research Informatics Systems

    Science.gov (United States)

    2016-10-01

    Research Informatics Systems PRINCIPAL INVESTIGATOR: Cynthia Harrison-Felix, PhD CONTRACTING ORGANIZATION: Craig Hospital Englewood, CO 80113...Traumatic Brain Injury Research Informatics Systems 5a. CONTRACT NUMBER 5b. GRANT NUMBER W81XWH-14-1-0564 5c. PROGRAM ELEMENT NUMBER 6. AUTHOR(S...Research (FITBIR) Informatics System. Local IRB approval and HRPO approval has been obtained for the TBI Model System (TBIMS) National Data and

  1. Art Therapy for Individuals with Traumatic Brain Injury: A Comprehensive Neurorehabilitation-Informed Approach to Treatment

    Science.gov (United States)

    Kline, Tori

    2016-01-01

    I describe an approach to art therapy treatment for survivors of traumatic brain injury developed at a rehabilitation facility for adults that serves inpatient, outpatient, and long-term residential clients. This approach is based on a review of the literature on traumatic brain injury, comprehensive neurorehabilitation, brain plasticity, and art…

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

    Science.gov (United States)

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

    2013-01-01

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

  3. Systematic review of depression in mild traumatic brain injury: study protocol

    OpenAIRE

    Lepage, Chris; Yuan, Tina; Leon, Stephanie; Marshall, Shawn; Labelle, Patrick; Ferland, Mark

    2016-01-01

    Background Of the over 1 million reported cases of traumatic brain injuries reported annually in the USA, a sizeable proportion are characterized as mild. Although it is generally well-accepted that most people who suffer a mild traumatic brain injury recover within 1 to 3?months, a proportion of individuals continue to experience physiological, psychological, and emotional symptoms beyond the expected window of recovery. Depression is commonly reported following mild traumatic brain injury; ...

  4. Lycium barbarum Extracts Protect the Brain from Blood-Brain Barrier Disruption and Cerebral Edema in Experimental Stroke

    Science.gov (United States)

    Yang, Di; Li, Suk-Yee; Yeung, Chung-Man; Chang, Raymond Chuen-Chung; So, Kwok-Fai; Wong, David; Lo, Amy C. Y.

    2012-01-01

    Background and Purpose Ischemic stroke is a destructive cerebrovascular disease and a leading cause of death. Yet, no ideal neuroprotective agents are available, leaving prevention an attractive alternative. The extracts from the fruits of Lycium barbarum (LBP), a Chinese anti-aging medicine and food supplement, showed neuroprotective function in the retina when given prophylactically. We aim to evaluate the protective effects of LBP pre-treatment in an experimental stroke model. Methods C57BL/6N male mice were first fed with either vehicle (PBS) or LBP (1 or 10 mg/kg) daily for 7 days. Mice were then subjected to 2-hour transient middle cerebral artery occlusion (MCAO) by the intraluminal method followed by 22-hour reperfusion upon filament removal. Mice were evaluated for neurological deficits just before sacrifice. Brains were harvested for infarct size estimation, water content measurement, immunohistochemical analysis, and Western blot experiments. Evans blue (EB) extravasation was determined to assess blood-brain barrier (BBB) disruption after MCAO. Results LBP pre-treatment significantly improved neurological deficits as well as decreased infarct size, hemispheric swelling, and water content. Fewer apoptotic cells were identified in LBP-treated brains by TUNEL assay. Reduced EB extravasation, fewer IgG-leaky vessels, and up-regulation of occludin expression were also observed in LBP-treated brains. Moreover, immunoreactivity for aquaporin-4 and glial fibrillary acidic protein were significantly decreased in LBP-treated brains. Conclusions Seven-day oral LBP pre-treatment effectively improved neurological deficits, decreased infarct size and cerebral edema as well as protected the brain from BBB disruption, aquaporin-4 up-regulation, and glial activation. The present study suggests that LBP may be used as a prophylactic neuroprotectant in patients at high risk for ischemic stroke. PMID:22438957

  5. Use Case Analysis: The Ambulatory EEG in Navy Medicine for Traumatic Brain Injuries

    Science.gov (United States)

    2016-12-01

    brain), brain tumors, encephalopathy (a disease that causes brain dysfunction), memory problems, sleep disorders, strokes, and dementia (Zehtabchi...useful in diagnosing epilepsy, multiple sclerosis, brain abscesses, brain tumors, mild traumatic brain injury, and hypertensive encephalopathy ...Bebek, N., Baykan, B., & Gokyigit, A. (2016). Appraisal of epileptic pain as a rare symptom of seizures. Epilepsy & Behavior, 55, 101–107. Pinho, F

  6. Misconceptions about traumatic brain injuries among South African university students

    Directory of Open Access Journals (Sweden)

    Chrisma Pretorius

    2013-08-01

    Full Text Available Objective. To investigate the incidence and type of misconceptions about traumatic brain injuries (TBIs harboured by university students.  Method. A convenience sample of 705 university students were recruited and data were collected using an electronic survey. The link to the survey was sent via e-mail to all registered students at Stellenbosch University. The participants had to complete the Common Misconceptions about Traumatic Brain Injury (CM-TBI questionnaire.  Results. The findings of this study suggest that the students subscribe to misconceptions from each of the 7 categories of misconceptions about TBIs. The mean percentages of misconceptions about TBIs were calculated and the amnesia (mean 49.7% and unconsciousness (mean 46.1% categories were identified as the categories about which the respondents had the most misconceptions, while the mean percentages of misconceptions were lower for the categories of recovery (mean 27.6%, rehabilitation (mean 26.56%, prevention (mean 20.8%, brain injury sequelae (mean 18.7% and brain damage (mean 8.4%.  Conclusion. Generally, these findings appear to be in keeping with previous literature, which suggests that misconceptions about TBIs are common among the general population. This study’s identification of these misconceptions could help create awareness, provide a focus for information provision, and contribute to the development of educational intervention programmes tailored for the South African context.

  7. Rates of symptom reporting following traumatic brain injury.

    Science.gov (United States)

    Dikmen, Sureyya; Machamer, Joan; Fann, Jesse R; Temkin, Nancy R

    2010-05-01

    This study examines rates of reporting of new or worse post-traumatic symptoms for patients with a broad range of injury severity at 1 month and 1 year after traumatic brain injury (TBI), as compared with those whose injury spared the head, and assesses variables related to symptom reporting at 1 year post-injury. Seven hundred thirty two TBI subjects and 120 general trauma comparison (TC) subjects provided new or worse symptom information at 1 month and/or 1 year post-injury. Symptom reporting at 1 year post-injury was compared in subgroups based on basic demographics, preexisting conditions, and severity of brain injury. The TBI group reported significantly more symptoms at 1 month and 1 year after injury than TCs (each p < .001). Although symptom endorsement declined from 1 month to 1 year, 53% of people with TBI and 24% of TC continued to report 3 or more symptoms at 1 year post-injury. Symptom reporting in the TBI group was significantly related to age, gender, preinjury alcohol abuse, pre-injury psychiatric history, and severity of TBI. Symptom reporting is common following a traumatic injury and continues to be experienced by a substantial number of TBI subjects of all severity levels at 1 year post-injury.

  8. Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion.

    Science.gov (United States)

    Kaiser, Melanie; Penk, Anja; Franke, Heike; Krügel, Ute; Nörenberg, Wolfgang; Huster, Daniel; Schaefer, Michael

    2016-09-01

    Effective therapeutic measures against the development of brain edema, a life-threatening complication of cerebral ischemia, are necessary to improve the functional outcome for the patient. Here, we identified a beneficial role of purinergic receptor P2X7 activation in acute ischemic stroke. Involvement of P2X7 in the development of neurological deficits, infarct size, brain edema, and glial responses after ischemic cerebral infarction has been analyzed. Neurologic evaluation, magnetic resonance imaging, and immunofluorescence assays were used to characterize the receptor's effect on the disease progress during 72 h after transient middle cerebral artery occlusion (tMCAO). Sham-operated animals were included in all experiments for control purposes. We found P2X7-deficient mice to develop a more prominent brain edema with a trend towards more severe neurological deficits 24 h after tMCAO. Infarct sizes, T2 times, and apparent diffusion coefficients did not differ significantly between wild-type and P2X7(-/-) animals. Our results show a characteristic spatial distribution of reactive glia cells with strongly attenuated microglia activation in P2X7(-/-) mice 72 h after tMCAO. Our data indicate that P2X7 exerts a role in limiting the early edema formation, possibly by modulating glial responses, and supports later microglia activation.

  9. THE EFFECT OF FLUOROCARBON ARTIFICIAL BLOOD (FC-34 IN ACUTE VASOGENIC BRAIN EDEMA

    Directory of Open Access Journals (Sweden)

    M NEEMATBAKHSH

    2000-03-01

    Full Text Available Background. Oxygen transport to tissue after an acute ischemia is strongly important. Fluorocarbon liquids are able to facilitated the oxygen transport. An animal experiment was designed to study the effect of FC-34 in acute brain ischemia. Methods. The left common carotid arteries were ligated in three groups of anesthetized animals for 30 minutes to obtain acute brain edema. The animals were subjected to received 15 ml/kg saline (group 1, 10% monitol (group 2 or FC-43 (group 3. All animals were recovered, and they monitored for two weeks. The electrolytes, BUN, and creatinine were measured before (all animals and after two weeks (survived animals. Pathological investigation was obtained by light and electron microscope via pathological process. Findings. The group 1 animals were died during first five days, but one and four animals were survived by two weeks in groups 2 & 3 respectively (P < 0.05. The pathological determinations indicate less cellular damages in group 3. No significant differences were detected in potassium, calcium, BUN, and creatinine before and after the experiment. Conclusion. The particle size and oxygen solubility in FC-43 is the major factors for better oxygen transport in ischem

  10. [Mechanism of potassium channel in hypoxia-ischemic brain edema: experiment with neonatal rat astrocyte].

    Science.gov (United States)

    Fu, Xue-mei; Xiang, Long; Liao, Da-qing; Feng, Zhi-chun; Mu, De-zhi

    2008-11-04

    To investigate the mechanism of potassium channel in brain edema caused by hypoxia-ischemia (HI). Astrocytes were obtained from 3-day-old SD rats, cultured, and randomly divided into 2 groups: normoxia group, cultured under normoxic condition, and hypoxic-ischemic group, cultured under hypoxic-ischemic condition. The cell volume was measured by radiologic method. Patch-clamp technique was used to observe the electric physiological properties of the voltage-gated potassium channels (Kv) in a whole cell configuration, and the change of voltage-gated potassium channel current (IKv) was recorded in cultured neonatal rat astrocyte during HI. Aquaporin 4 (AQP4) expression vector was constructed from pSUPER vector and transfected into the astrocytes (AQP4 RNAi) to construct AQP4 knockdown (AQP4-/-) cells. cellular volume was determined using [3H]-3-O-methyl-D-glucose uptake in both AQP4-/- and AQP4+/+ cells under the condition of HI. Real time PCR and Western blotting were used to detect the mRNA and protein expression of AQP4. The percentages of the AQP4+/+ and AQP4-/- astrocyte volumes in the condition of HI for 0.5, 1, 2, and 4 h were 104+/-7, 109+/-6, 126+/-12, and 152+/-9 times, and 97+/-7, 105+/-9, 109+/-7, and 132+/-6 times as those of their corresponding control groups (all Pastrocytes significantly increased during HI and the degrees of edema mediated by AQP4 knockdown at different time points were all significantly milder (all Pastrocytes via aquaporin-4 and then cell swelling.

  11. Neuropsychological and neuroimaging findings in traumatic brain injury and post-traumatic stress disorder.

    Science.gov (United States)

    Brenner, Lisa A

    2011-01-01

    Advances in imaging technology, coupled with military personnel returning home from Iraq and Afghanistan with traumatic brain injury (TBI) and/or post-traumatic stress disorder (PTSD), have increased interest in the neuropsychology and neurobiology of these two conditions. There has been a particular focus on differential diagnosis. This paper provides an overview of findings regarding the neuropsychological and neurobiological underpinnings of TBI and for PTSD. A specific focus is on assessment using neuropsychological measures and imaging techniques. Challenges associated with the assessment of individuals with one or both conditions are also discussed. Although use of neuropsychological and neuroimaging test results may assist with diagnosis and treatment planning, further work is needed to identify objective biomarkers for each condition. Such advances would be expected to facilitate differential diagnosis and implementation of best treatment practices.

  12. [Acoustic thermometry of the patient brain with traumatic brain injury].

    Science.gov (United States)

    Anosov, A A; Balashov, I S; Beliaev, R V; Vilkov, V A; Garskov, R V; Kazanskiĭ, A S; Mansfel'd, A D; Shcherbakov, M I

    2014-01-01

    Non-invasive deep brain acoustic thermometry is carried out for two patients at Burdenko Neurosurgery Institute. This method is based on the measurements of the own thermal acoustic radiation of the investigated object. These two patients have got the brain injury. Some of their skull bones are absent. Infrared thermometry was also used to measure the surface temperature of the forehead skin. On the basis of the experimental data the temperatures deep within the brain were reconstructed. The values for the two patients are equal to 37.3 0.7 and 37.0 0.3 degrees C.

  13. 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.

  14. Numerical impact simulation of gradually increased kinetic energy transfer has the potential to break up folded protein structures resulting in cytotoxic brain tissue edema.

    Science.gov (United States)

    von Holst, Hans; Li, Xiaogai

    2013-07-01

    Although the consequences of traumatic brain injury (TBI) and its treatment have been improved, there is still a substantial lack of understanding the mechanisms. Numerical simulation of the impact can throw further lights on site and mechanism of action. A finite element model of the human head and brain tissue was used to simulate TBI. The consequences of gradually increased kinetic energy transfer was analyzed by evaluating the impact intracranial pressure (ICP), strain level, and their potential influences on binding forces in folded protein structures. The gradually increased kinetic energy was found to have the potential to break apart bonds of Van der Waals in all impacts and hydrogen bonds at simulated impacts from 6 m/s and higher, thereby superseding the energy in folded protein structures. Further, impacts below 6 m/s showed none or very slight increase in impact ICP and strain levels, whereas impacts of 6 m/s or higher showed a gradual increase of the impact ICP and strain levels reaching over 1000 KPa and over 30%, respectively. The present simulation study shows that the free kinetic energy transfer, impact ICP, and strain levels all have the potential to initiate cytotoxic brain tissue edema by unfolding protein structures. The definition of mild, moderate, and severe TBI should thus be looked upon as the same condition and separated only by a gradual severity of impact.

  15. The possibility of application of spiral brain computed tomography to traumatic brain injury.

    Science.gov (United States)

    Lim, Daesung; Lee, Soo Hoon; Kim, Dong Hoon; Choi, Dae Seub; Hong, Hoon Pyo; Kang, Changwoo; Jeong, Jin Hee; Kim, Seong Chun; Kang, Tae-Sin

    2014-09-01

    The spiral computed tomography (CT) with the advantage of low radiation dose, shorter test time required, and its multidimensional reconstruction is accepted as an essential diagnostic method for evaluating the degree of injury in severe trauma patients and establishment of therapeutic plans. However, conventional sequential CT is preferred for the evaluation of traumatic brain injury (TBI) over spiral CT due to image noise and artifact. We aimed to compare the diagnostic power of spiral facial CT for TBI to that of conventional sequential brain CT. We evaluated retrospectively the images of 315 traumatized patients who underwent both brain CT and facial CT simultaneously. The hemorrhagic traumatic brain injuries such as epidural hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, and contusional hemorrhage were evaluated in both images. Statistics were performed using Cohen's κ to compare the agreement between 2 imaging modalities and sensitivity, specificity, positive predictive value, and negative predictive value of spiral facial CT to conventional sequential brain CT. Almost perfect agreement was noted regarding hemorrhagic traumatic brain injuries between spiral facial CT and conventional sequential brain CT (Cohen's κ coefficient, 0.912). To conventional sequential brain CT, sensitivity, specificity, positive predictive value, and negative predictive value of spiral facial CT were 92.2%, 98.1%, 95.9%, and 96.3%, respectively. In TBI, the diagnostic power of spiral facial CT was equal to that of conventional sequential brain CT. Therefore, expanded spiral facial CT covering whole frontal lobe can be applied to evaluate TBI in the future. Copyright © 2014 Elsevier Inc. All rights reserved.

  16. Atypical moral judgment following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Angelica Muresan

    2012-07-01

    Full Text Available Previous research has shown an association between emotions, particularly social emotions, and moral judgments. Some studies suggested an association between blunted emotion and the utilitarian moral judgments observed in patients with prefrontal lesions. In order to investigate how prefrontal brain damage affects moral judgment, we asked a sample of 29 TBI patients (12 females and 17 males and 41 healthy participants (16 females and 25 males to judge 22 hypothetical dilemmas split into three different categories (non-moral, impersonal and personal moral. The TBI group presented a higher proportion of affirmative (utilitarian responses for personal moral dilemmas when compared to controls, suggesting an atypical pattern of utilitarian judgements. We also found a negative association between the performance on recognition of social emotions and the proportion of affirmative responses on personal moral dilemmas. These results suggested that the preference for utilitarian responses in this type of dilemmas is accompanied by difficulties in social emotion recognition. Overall, our findings suggest that deontological moral judgments are associated with normal social emotion processing and that frontal lobe plays an important role in both emotion and moral judgment.

  17. The effects of Tanshinone IIA on blood-brain barrier and brain edema after transient middle cerebral artery occlusion in rats.

    Science.gov (United States)

    Tang, Chao; Xue, Hongli; Bai, Changlin; Fu, Rong; Wu, Anhua

    2010-12-01

    Disruption of blood-brain barrier (BBB) and edema formation play a key role in the development of neurological dysfunction after cerebral ischemia. In this study, the effects of Tanshinone IIA (Tan IIA), one of the active ingredients of Salvia miltiorrhiza root, on the BBB and brain edema after transient middle cerebral artery occlusion in rats were examined. Our study demonstrated that Tan IIA reduced brain infarct area, water content in the ischemic hemisphere. Furthermore, Tan IIA significantly decreased BBB permeability to Evans blue, suppressed the expression of intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-9 (MMP-9), inhibited the degradation of tight junction proteins zonula occludens-1 (ZO-1) and Occludin. These results demonstrated that Tan IIA was effective for attenuating the extent of brain edema formation in response to ischemia injury in rats, partly by Tan IIA's protective effect on the BBB. Our results may have implications in the treatment of brain edema in cerebral ischemia. Copyright © 2010 Elsevier GmbH. All rights reserved.

  18. Simvastatin attenuates the cerebral vascular endothelial inflammatory response in a rat traumatic brain injury.

    Science.gov (United States)

    Wang, Kuo-Wei; Chen, Han-Jung; Lu, Kang; Liliang, Po-Chou; Liang, Cheng-Loong; Tsai, Yu-Duan; Cho, Chung-Lung

    2014-01-01

    Traumatic brain injury (TBI) leads to important and deleterious inflammation, as evidenced by edema, cytokine production, induction of nitric oxide synthase, and leukocyte infiltration. After TBI, the activation of cerebral vascular endothelial cells plays a crucial role in the pathogenesis of inflammation. In this study, we hypothesized that the activation of cerebral vascular endothelial cells plays a crucial role in the pathogenesis of inflammation and outcome after TBI. It may represent a key cellular target for statin therapy. In our study, cortical contusions were induced, and the effect of continuous treatment of simvastatin on behavior and inflammation in adult rats following experimental TBI was evaluated. The treatment group received 15 mg/kg of simvastatin daily for 3 days. Neurological function was assessed with the grip test. The results showed that the non-treatment control group had a significantly greater increase in ICAM-1 expression from pre-injury to the post-injury 72 h time point as compared to the expression in treatment group. The treatment group had better neurological function as evidenced in a grip test performed from baseline to 72 h. The analysis of a western blot test and pathology also demonstrated reduced ICAM-1 expression and a smaller area of damage and tissue loss. Our findings suggest that simvastatin could attenuate the activation of cerebral vascular endothelial inflammatory response and decrease the loss of neurological function and brain tissue.

  19. 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.

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

    Science.gov (United States)

    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.

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

    Science.gov (United States)

    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...

  2. Mild traumatic brain injury: Graph-model characterization of brain networks for episodic memory

    NARCIS (Netherlands)

    Tsirka, V.; Simos, P.G.; Vakis, A.; Kanatsouli, K.; Vourkas, M.; Erimaki, S.; Pachou, E.; Stam, C.J.; Micheloyannis, S.

    2011-01-01

    Episodic memory is among the cognitive functions that can be affected in the acute phase following mild traumatic brain injury (MTBI). The present study used EEG recordings to evaluate global synchronization and network organization of rhythmic activity during the encoding and recognition phases of

  3. What predicts early volumetric edema increase following stereotactic radiosurgery for brain metastases?

    Science.gov (United States)

    Hanna, Andrew; Boggs, D Hunter; Kwok, Young; Simard, Marc; Regine, William F; Mehta, Minesh

    2016-04-01

    A volumetric analysis of pre- and post-radiosurgery (PreSRS and PostSRS) edema in patients with cerebral metastases was performed to determine factors of a predictive model assessing the risk of developing increased edema relatively early after SRS. One-hundred-fourteen metastases in 55 patients were analyzed. Selection for this analysis required an MRI ≤ 30 days before SRS and an MRI ≤ 100 days after SRS. Tumor volumes were calculated on PreSRS, SRS, and PostSRS T1-weighted postgadolinium images while edema volumes were calculating using PreSRS and PostSRS fluid-attenuated inversion recovery MR images. An increase in edema was defined as an increase in measurable edema of at least 5%. We developed and evaluated a model predicting the relative risk (RR) of increased edema after SRS. Peritumoral edema increased in 18% (21/114) of the analyzed lesions. Melanoma/renal histology, recursive partitioning analysis class III, and prior WBRT carried RRs of developing postSRS edema increase of 2.45, 2.48, and 3.16, respectively (all P values edema/tumor ratio predicted for a RR of 1.007/ratio unit, and steroid dose at time of SRS predicted for a RR of 0.89/mg (all P values edema after SRS was developed based from these data and may be useful in identifying patients who might benefit from prophylactic anti-edema therapies before, during, or after SRS. This model could be used as the basis of inclusion criteria for prospective trials investigating novel anti-edema therapies.

  4. Psychotherapy following traumatic brain injury: integrating theory and practice.

    Science.gov (United States)

    Coetzer, Rudi

    2007-01-01

    Psychotherapy is now an approach used within several models of neurorehabilitation. However, a core theoretical model to guide psychotherapeutic practice is lacking. This article attempts to illustrate how the Generic Model of Psychotherapy of Orlinsky and Howard, which emphasizes the common factors shared by many psychotherapies, can be applied in neurorehabilitation settings. A case report is presented to illustrate how this model can potentially inform psychotherapeutic practice. The use of a theoretical model to underpin psychotherapeutic interventions in neurorehabilitation settings has the potential to facilitate our understanding of the psychotherapeutic process following traumatic brain injury in this evolving area of professional practice.

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

    Directory of Open Access Journals (Sweden)

    FELIPE F eCASANUEVA

    2011-08-01

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

  6. Electron microscopic features of brain edema in rodent cerebral malaria in relation to glial fibrillary acidic protein expression.

    Science.gov (United States)

    Ampawong, Sumate; Chaisri, Urai; Viriyavejakul, Parnpen; Nontprasert, Apichart; Grau, Georges E; Pongponratn, Emsri

    2014-01-01

    The mechanisms leading to cerebral malaria (CM) are not completely understood. Brain edema has been suggested as having an important role in experimental CM. In this study, CBA/CaH mice were infected with Plasmodium berghei ANKA blood-stage and when typical symptoms of CM developed on day 7, brain tissues were processed for electron-microscopic and immunohistochemical studies. The study demonstrated ultrastructural hallmarks of cerebral edema by perivascular edema and astroglial dilatation confirming existing evidence of vasogenic and cytogenic edema. This correlates closely with the clinical features of CM. An adaptive response of astrocytic activity, represented by increasing glial fibrillary acidic protein (GFAP) expression in the perivascular area and increasing numbers of large astrocyte clusters were predominately found in the CM mice. The presence of multivesicular and lamellar bodies indicates the severity of cerebral damage in experimental CM. Congestion of the microvessels with occluded white blood cells (WBCs), parasitized red blood cells (PRBCs) and platelets is also a crucial covariate role for CM pathogenesis.

  7. Neuroprotective Effects of Exercise on Brain Edema and Neurological Movement Disorders Following the Cerebral Ischemia and Reperfusion in Rats.

    Science.gov (United States)

    Shamsaei, Nabi; Erfani, Soheila; Fereidoni, Masoud; Shahbazi, Ali

    2017-01-01

    Cerebral ischemia and reperfusion causes physiological and biochemical changes in the neuronal cells that will eventually lead to cell damage. Evidence indicates that exercise reduces the ischemia and reperfusion-induced brain damages in animal models of stroke. In the present study, the effect of exercise preconditioning on brain edema and neurological movement disorders following the cerebral ischemia and reperfusion in rats was investigated. Twenty-one adult male wistar rats (weighing 260-300 g) were randomly divided into three groups: sham operated, exercise plus ischemia, and ischemia group (7 rats per group). The rats in exercise group were trained to run on a treadmill 5 days a week for 4 weeks. Transient focal cerebral ischemia and reperfusion were induced by middle cerebral artery occlusion (MCAO) for 60 minutes, followed by reperfusion for 23 hours. After 24 hours ischemia, movement disorders were tested by a special neurological examination. Also, cerebral edema was assessed by determining the brain water content. The results showed that pre-ischemic exercise significantly reduced brain edema (Pedema and movement disorders. Thus, it could be considered as a useful strategy for prevention of ischemic injuries, especially in people at risk.

  8. Quantitation of brain edema and localisation of aquaporin 4 expression in relation to susceptibility to experimental cerebral malaria.

    Science.gov (United States)

    Ampawong, Sumate; Combes, Valéry; Hunt, Nicholas H; Radford, Jane; Chan-Ling, Tailoi; Pongponratn, Emsri; Grau, Georges E R

    2011-08-15

    The pathogenic mechanisms underlying the occurrence of cerebral malaria (CM) are still incompletely understood but, clearly, cerebral complications may result from concomitant microvessel obstruction and inflammation. The extent to which brain edema contributes to pathology has not been investigated. Using the model of P. berghei ANKA infection, we compared brain microvessel morphology of CM-susceptible and CM-resistant mice. By quantitative planimetry, we provide evidence that CM is characterized by enlarged perivascular spaces (PVS). We show a dramatic aquaporin 4 (AQP4) upregulation, selectively at the level of astrocytic foot processes, in both CM and non-CM disease, but significantly more pronounced in mice with malarial-induced neurological syndrome. This suggests that a threshold of AQP4 expression is needed to lead to neurovascular pathology, a view that is supported by significantly higher levels in mice with clinically overt CM. Numbers of intravascular leukocytes significantly correlated with both PVS enlargement and AQP4 overexpression. Thus, brain edema could be a contributing factor in CM pathogenesis and AQP4, specifically in its astrocytic location, a key molecule in this mechanism. Since experimental CM is associated with substantial brain edema, it models paediatric CM better than the adult syndrome and it is tempting to evaluate AQP4 in the former context. If AQP4 changes are confirmed in human CM, it may represent a novel target for therapeutic intervention.

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

    NARCIS (Netherlands)

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

    2011-01-01

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

  10. Factors influencing intracranial pressure monitoring guideline compliance and outcome after severe traumatic brain injury.

    NARCIS (Netherlands)

    Biersteker, H.A.; Andriessen, T.M.J.C.; Horn, J.; Franschman, G.; Naalt, J. van der; Hoedemaekers, C.W.E.; Lingsma, H.F.; Haitsma, I.; Vos, P.E.

    2012-01-01

    OBJECTIVE: To determine adherence to Brain Trauma Foundation guidelines for intracranial pressure monitoring after severe traumatic brain injury, to investigate if characteristics of patients treated according to guidelines (ICP+) differ from those who were not (ICP-), and whether guideline

  11. Factors influencing intracranial pressure monitoring guideline compliance and outcome after severe traumatic brain injury

    NARCIS (Netherlands)

    Biersteker, Heleen A. R.; Andriessen, Teuntje M. J. C.; Horn, Janneke; Franschman, Gaby; van der Naalt, Joukje; Hoedemaekers, Cornelia W. E.; Lingsma, Hester F.; Haitsma, Iain; Vos, Pieter E.

    2012-01-01

    Objective: To determine adherence to Brain Trauma Foundation guidelines for intracranial pressure monitoring after severe traumatic brain injury, to investigate if characteristics of patients treated according to guidelines (ICP+) differ from those who were not (ICP-), and whether guideline

  12. Factors influencing intracranial pressure monitoring guideline compliance and outcome after severe traumatic brain injury

    NARCIS (Netherlands)

    Biersteker, Heleen A. R.; Andriessen, Teuntje M. J. C.; Horn, Janneke; Franschman, Gaby; van der Naalt, Joukje; Hoedemaekers, Cornelia W. E.; Lingsma, Hester F.; Haitsma, Iain; Vos, Pieter E.

    Objective: To determine adherence to Brain Trauma Foundation guidelines for intracranial pressure monitoring after severe traumatic brain injury, to investigate if characteristics of patients treated according to guidelines (ICP+) differ from those who were not (ICP-), and whether guideline

  13. Radionuclidr diagnosis of brain tumors, brain inflammatory and traumatic lesions

    International Nuclear Information System (INIS)

    Badmaev, K.N.; Mel'kishev, V.F.; Dement'ev, E.V.; Svetlova, N.L.

    1982-01-01

    A complex of problems of radionuclide diagnosis of central nervous system diseases including tumors, traumas, vascular lessons, inflammatory processes is considered. The principles, technique and results of radionuclide xintigraphy of a tumor, depending on its localization are given. Radioindication of brain tumours in the operation is given

  14. Relationship between alternation of cerebral blood flow and formation of brain edema around the hematoma after experimental intracerebral hemorrhage

    International Nuclear Information System (INIS)

    Zhou Jian; Gao Peiyi; Li Xiaoguang

    2005-01-01

    Objective: To investigate the mechanism of brain edema formation around the hematoma and the relationship between the formation of brain edema and the changes of regional cerebral blood flow after intracerebral hemorrhage (ICH) in rats, and to provide experimental basis for the clinical treatment of ICH . Methods: Seventy male Sprague-Dawley rats were randomly divided into ICH groups and sham-operated groups. ICH was produced by microinjection of 40 ul fresh autologous blood or saline into the right caudatum. Dynamic CT perfusion imaging was performed, and the parameters of regional cerebral blood flow (rCBF), regional cerebral blood volume (rCBV), and mean transit time (MTT) around the hematoma were calculated respectively. Then the rats were sacrificed, and the water content, sodium, potassium, and calcium concentrations were measured respectively. The correlative study between the water content and rCBF and rCBV were carried out. Results:The gradient of perihematomal hypoperfusion was revealed on CT perfusion maps in ICH groups. The alternation of rCBF around the hematomas were fluctuated, and rCBF reduction was most pronounced at 1 hour afer ICH, then the rCBF gradually returned, reaching the peaks at 6 hours and 24 hours after ICH, respectively. In the meantime, rCBV reduction around the hematoma was most pronounced at 1 hour after ICH. Then the rCBV gradually increased, and reaching the peak at 24 hours. The water contents were gradually increased in the ipsilateral basal ganglia in the animals sacrificed at 6, 24, and 72 hours. The accumulation of water was at its peak at 24 hours, and remained in the animals sacrificed at the 72 hours. The perihemorrhagic water contents correlated significantly with rCBV surrounding hematomas, r=0.372 (one-tailed), P<0.05. Conclusion: The perihemorrhagic brain edema results from the common effects of the blood-brain-barrier disruption, cytotoxic edema, and the accumulation of osmotically active substances. The r

  15. Traumatic Brain Injury. Fact Sheet = Lesion Cerebral Traumatica (TBI). Hojas Informativas Sobre Discapacidades.

    Science.gov (United States)

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

    This fact sheet, written in both English and Spanish, offers general information about traumatic brain injury. Information includes a definition, incidence, individual characteristics, and educational implications. The signs of traumatic brain injury are listed and include physical disabilities, difficulties with thinking, and social, behavioral,…

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

    Science.gov (United States)

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

    2012-01-01

    Fifty-one patients with mild (n = 14), moderate (n = 10) and severe traumatic brain injury (n = 27) received early rehabilitation. Level of consciousness was evaluated using the Glasgow Coma Score. Functional level was determined using the Glasgow Outcome Score, whilst mobility was evaluated using the Mobility Scale for Acute Stroke. Activities of daily living were assessed using the Barthel Index. Following Bobath neurodevelopmental therapy, the level of consciousness was significantly improved in patients with moderate and severe traumatic brain injury, but was not greatly influenced in patients with mild traumatic brain injury. Mobility and functional level were significantly improved in patients with mild, moderate and severe traumatic brain injury. Gait recovery was more obvious in patients with mild traumatic brain injury than in patients with moderate and severe traumatic brain injury. Activities of daily living showed an improvement but this was insignificant except for patients with severe traumatic brain injury. Nevertheless, complete recovery was not acquired at discharge. Multiple regression analysis showed that gait and Glasgow Coma Scale scores can be considered predictors of functional outcomes following traumatic brain injury. PMID:25624828

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

    Science.gov (United States)

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

    2012-09-05

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

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

    NARCIS (Netherlands)

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

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

  19. Minocycline and N-acetylcysteine: A Synergistic Drug Combination to Treat Traumatic Brain Injury

    Science.gov (United States)

    2013-10-01

    TBI (“Multidrug treatment of traumatic brain injury”, PT073028) from the Fiscal Year 2007 CDMRP program for Psychological Health/Traumatic Brain...ncbi.nlm.nih.gov/pubmed/20166806). Inman, C.F., et al., 2005. Validation of computer-assisted, pixel-based analysis of multiple- colour immunofluorescence

  20. Outcome of severe traumatic brain injury at a critical care unit: a ...

    African Journals Online (AJOL)

    Outcome of severe traumatic brain injury at a critical care unit: a review of 87 patients. ... OBJECTIVE: To determine the outcome of severe traumatic brain injury and to document the factors influencing mortality. DESIGN: A six months prospective study. ... intracerebral mass lesions and blood sugar greater than 10mmol / L.

  1. 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)....

  2. Traumatic Brain Injury: A Guide for Caregivers of Service Members and Veterans

    Science.gov (United States)

    2010-01-01

    care planning, hospice care , and financial assistance from the National Hospice and Palliative ...development of “…coordinated, uniform, and consistent training curricula to be used in training family members in the provision of care and assistance to...members and former members of the Armed Forces with traumatic brain injuries.” This curriculum , Traumatic Brain Injury: A Guide for Caregivers

  3. Astrocytic Disruption in Traumatic Brain Injury and Alzheimer’s Disease

    Science.gov (United States)

    2014-10-01

    and physiology of hippocampal astrocytes . 15. SUBJECT TERMS Traumatic brain injury, Alzheimer’s disease, astrocytes , reactive astrocytosis, neuronal...neuronal pathologies seen in TBI and AD. Although astrocyte reactivity serves to protect neurons, some normal astrocytic functions including lactate...work. KEYWORDS: Traumatic brain injury, Alzheimer’s disease, astrocytes , reactive astrocytosis, neuronal excitability, monocarboxylate transporters

  4. Facilitated assessment of tissue loss following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Anders eHånell

    2012-03-01

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

  5. Mild traumatic brain injury: Impairment and disability assessment caveats.

    Science.gov (United States)

    Zasler, Nathan D; Martelli, Michael F

    2003-01-01

    Mild traumatic brain injury (MTBI) accounts for approximately 80% of all brain injuries, and persistent sequelae can impede physical, emotional, social, marital, vocational, and avocational functioning. Evaluation of impairment and disability following MTBI typically can involve such contexts as social security disability application, personal injury litigation, worker's compensation claims, disability insurance policy application, other health care insurance policy coverage issues, and the determination of vocational and occupational competencies and limitations. MTBI is still poorly understood and impairment and disability assessment in MTBI can present a significant diagnostic challenge. There are currently no ideal systems for rating impairment and disability for MTBI residua. As a result, medicolegal examiners and clinicians must necessarily familiarise themselves with the variety of disability and impairment evaluation protocols and understand their limitations. The current paper reviews recommended procedures and potential obstacles and confounding issues.

  6. Neuropsychological assessment of executive functions following pediatric traumatic brain injury.

    Science.gov (United States)

    Gaines, K Drorit; Soper, Henry V

    2018-01-01

    Assessment of executive functions in the adult is best captured at the stage where full maturation of brain development occurs. Assessment of executive functions of children, however, is considerably more complicated. First, assessment of executive functioning in children represents a snapshot of these developing functions at a particular time linked stage, which may have implications for further development. Second, neuropsychological measures available to assess executive functions in children are limited in number and scope and may not be sensitive to the gradual developmental changes. The present article provides an overview of the salient neurodevelopmental stages of executive functioning and discusses the utilization of recently developed neuropsychological measures to assess these stages. Comments on clinical implications of these findings regarding Traumatic Brain Injury will be provided.

  7. Traumatic Brain Injury and NADPH Oxidase: A Deep Relationship

    Directory of Open Access Journals (Sweden)

    Cristina Angeloni

    2015-01-01

    Full Text Available Traumatic brain injury (TBI represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox, ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS, have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after TBI, suggesting Nox critical role in the onset and development of this pathology. In this review, we summarize the current evidence about the role of Nox enzymes in the pathophysiology of TBI.

  8. The Pattern of Brain Microhemorrhages After Severe Lung Failure Resembles the One Seen in High-Altitude Cerebral Edema.

    Science.gov (United States)

    Riech, Sebastian; Kallenberg, Kai; Moerer, Onnen; Hellen, Peter; Bärtsch, Peter; Quintel, Michael; Knauth, Michael

    2015-09-01

    After suffering from severe acute respiratory distress syndrome, several patients show generalized brain alterations and atrophy. A distinctive morphologic pattern of cerebral injury, however, has not been found so far. We present the history of three patients who survived severe acute respiratory distress syndrome. In these patients, MRI of the brain showed multiple microhemorrhages predominantly in the splenium of the corpus callosum. An identical pattern of microhemorrhages has previously been described in mountaineers who suffered from high-altitude cerebral edema. This report demonstrates that patients after treatment for acute respiratory distress syndrome and high-altitude cerebral edema show congruent cerebral injuries. Further investigation into the similarities of the causative conditions and neurologic consequences might reveal underlying pathophysiologic mechanisms and clinical implications of this observation.

  9. Neural mechanisms underlying neurooptometric rehabilitation following traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Hudac CM

    2012-01-01

    Full Text Available Caitlin M Hudac1, Srinivas Kota1, James L Nedrow2, Dennis L Molfese1,31Department of Psychology, University of Nebraska-Lincoln, 2Oculi Vision Rehabilitation, 3Center for Brain, Biology, and Behavior, University of Nebraska-Lincoln, Lincoln, NEAbstract: Mild to severe traumatic brain injuries have lasting effects on everyday functioning. Issues relating to sensory problems are often overlooked or not addressed until well after the onset of the injury. In particular, vision problems related to ambient vision and the magnocellular pathway often result in posttrauma vision syndrome or visual midline shift syndrome. Symptoms from these syndromes are not restricted to the visual domain. Patients commonly experience proprioceptive, kinesthetic, vestibular, cognitive, and language problems. Neurooptometric rehabilitation often entails the use of corrective lenses, prisms, and binasal occlusion to accommodate the unstable magnocellular system. However, little is known regarding the neural mechanisms engaged during neurooptometric rehabilitation, nor how these mechanisms impact other domains. Event-related potentials from noninvasive electrophysiological recordings can be used to assess rehabilitation progress in patients. In this case report, high-density visual event-related potentials were recorded from one patient with posttrauma vision syndrome and secondary visual midline shift syndrome during a pattern reversal task, both with and without prisms. Results indicate that two factors occurring during the end portion of the P148 component (168–256 milliseconds poststimulus onset map onto two separate neural systems that were engaged with and without neurooptometric rehabilitation. Without prisms, neural sources within somatosensory, language, and executive brain regions engage inefficient magnocellular system processing. However, when corrective prisms were worn, primary visual areas were appropriately engaged. The impact of using early

  10. Persistent post-traumatic headache vs. migraine: an MRI study demonstrating differences in brain structure.

    Science.gov (United States)

    Schwedt, Todd J; Chong, Catherine D; Peplinski, Jacob; Ross, Katherine; Berisha, Visar

    2017-08-22

    The majority of individuals with post-traumatic headache have symptoms that are indistinguishable from migraine. The overlap in symptoms amongst these individuals raises the question as to whether post-traumatic headache has a unique pathophysiology or if head trauma triggers migraine. The objective of this study was to compare brain structure in individuals with persistent post-traumatic headache (i.e. headache lasting at least 3 months following a traumatic brain injury) attributed to mild traumatic brain injury to that of individuals with migraine. Twenty-eight individuals with persistent post-traumatic headache attributed to mild traumatic brain injury and 28 individuals with migraine underwent brain magnetic resonance imaging on a 3 T scanner. Regional volumes, cortical thickness, surface area and curvature measurements were calculated from T1-weighted sequences and compared between subject groups using ANCOVA. MRI data from 28 healthy control subjects were used to interpret the differences in brain structure between migraine and persistent post-traumatic headache. Differences in regional volumes, cortical thickness, surface area and brain curvature were identified when comparing the group of individuals with persistent post-traumatic headache to the group with migraine. Structure was different between groups for regions within the right lateral orbitofrontal lobe, left caudal middle frontal lobe, left superior frontal lobe, left precuneus and right supramarginal gyrus (p comparing the migraine cohort to healthy controls. In conclusion, persistent post-traumatic headache and migraine are associated with differences in brain structure, perhaps suggesting differences in their underlying pathophysiology. Additional studies are needed to further delineate similarities and differences in brain structure and function that are associated with post-traumatic headache and migraine and to determine their specificity for each of the headache types.

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

    Directory of Open Access Journals (Sweden)

    Steven R Flanagan

    2008-10-01

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

  12. Risk Factors for Institutionalization After Traumatic Brain Injury Inpatient Rehabilitation.

    Science.gov (United States)

    Eum, Regina S; Brown, Allen W; Watanabe, Thomas K; Zasler, Nathan D; Goldstein, Richard; Seel, Ronald T; Roth, Elliot J; Zafonte, Ross D; Glenn, Mel B

    To create a profile of individuals with traumatic brain injury (TBI) who received inpatient rehabilitation and were discharged to an institutional setting using characteristics measured at rehabilitation discharge. The Traumatic Brain Injury Model Systems National Database is a prospective, multicenter, longitudinal database for people with moderate to severe TBI. We analyzed data for participants enrolled from January 2002 to June 2012 who had lived in a private residence before TBI. This cross-sectional study used logistic regression analyses to identify sociodemographic factors, lengths of stay, and cognitive and physical functioning levels that differentiated patients discharged to institutional versus private settings. Older age, living alone before TBI, and lower levels of function at rehabilitation discharge (independence in locomotion, bladder management, comprehension, and social interaction) were significantly associated with higher institutionalization rates and provided the best models identifying factors associated with institutionalization. Institutionalization was also associated with decreased independence in bed-chair-wheelchair transfers and increased duration of posttraumatic amnesia. Individuals institutionalized after inpatient rehabilitation for TBI were older, lived alone before injury, had longer posttraumatic amnesia durations, and were less independent in specific functional characteristics. Research evaluating the effect of increasing postdischarge support and improving treatment effectiveness in these functional areas is recommended.

  13. Brain volume loss contributes to arousal and empathy dysregulation following severe traumatic brain injury.

    Science.gov (United States)

    Rushby, Jacqueline A; McDonald, Skye; Fisher, Alana C; Kornfeld, Emma J; De Blasio, Frances M; Parks, Nicklas; Piguet, Olivier

    2016-01-01

    Severe traumatic brain injury (TBI) often leads to deficits in physiological arousal and empathy, which are thought to be linked. This study examined whether injury-related brain volume loss in key limbic system structures is associated with these deficits. Twenty-four adults with TBI and 24 matched Controls underwent MRI scans to establish grey matter volumes in the amygdala, thalamus, and hippocampus. EEG and skin conductance levels were recorded to index basal physiological arousal. Self-report emotional empathy levels were also assessed. The TBI group had reduced brain volumes, topographic alpha differences, and lower emotional empathy compared to Controls. Regional brain volumes were differentially correlated to arousal and self-report empathy. Importantly, lower volume in pertinent brain structures correlated with lower empathy, for participants with and without TBI. Overall we provide new insights into empathic processes after TBI and their relationship to brain volume loss.

  14. Effects of Repetitive Transcranial Magnetic Stimulation on Behavioral Recovery during Early Stage of Traumatic Brain Injury in Rats.

    Science.gov (United States)

    Yoon, Kyung Jae; Lee, Yong-Taek; Chung, Pil-Wook; Lee, Yun Kyung; Kim, Dae Yul; Chun, Min Ho

    2015-10-01

    Repetitive transcranial magnetic stimulation (rTMS) is a promising technique that modulates neural networks. However, there were few studies evaluating the effects of rTMS in traumatic brain injury (TBI). Herein, we assessed the effectiveness of rTMS on behavioral recovery and metabolic changes using brain magnetic resonance spectroscopy (MRS) in a rat model of TBI. We also evaluated the safety of rTMS by measuring brain swelling with brain magnetic resonance imaging (MRI). Twenty male Sprague-Dawley rats underwent lateral fluid percussion and were randomly assigned to the sham (n=10) or the rTMS (n=10) group. rTMS was applied on the fourth day after TBI and consisted of 10 daily sessions for 2 weeks with 10 Hz frequency (total pulses=3,000). Although the rTMS group showed an anti-apoptotic effect around the peri-lesional area, functional improvements were not significantly different between the two groups. Additionally, rTMS did not modulate brain metabolites in MRS, nor was there any change of brain lesion or edema after magnetic stimulation. These data suggest that rTMS did not have beneficial effects on motor recovery during early stages of TBI, although an anti-apoptosis was observed in the peri-lesional area.

  15. 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.

  16. The use of antioxidants in the treatment of traumatic brain injury.

    Science.gov (United States)

    Venegoni, Whitney; Shen, Qiuhua; Thimmesch, Amanda R; Bell, Meredith; Hiebert, John B; Pierce, Janet D

    2017-06-01

    The aim of this study was to discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. One of the leading causes of death globally is traumatic brain injury, affecting individuals in all demographics. Traumatic brain injury is produced by an external blunt force or penetration resulting in alterations in brain function or pathology. Often, with a traumatic brain injury, secondary injury causes additional damage to the brain tissue that can have further impact on recovery and the quality of life. Secondary injury occurs when metabolic and physiologic processes alter after initial injury and includes increased release of toxic free radicals that cause damage to adjacent tissues and can eventually lead to neuronal necrosis. Although antioxidants in the tissues can reduce free radical damage, the magnitude of increased free radicals overwhelms the body's reduced defence mechanisms. Supplementing the body's natural supply of antioxidants, such as coenzyme Q10, can attenuate oxidative damage caused by reactive oxygen species. Discussion paper. Research literature published from 2011-2016 in PubMed, CINAHL and Cochrane. Prompt and accurate assessment of patients with traumatic brain injury by nurses is important to ensure optimal recovery and reduced lasting disability. Thus, it is imperative that nurses be knowledgeable about the secondary injury that occurs after a traumatic brain injury and aware of possible antioxidant treatments. The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury. © 2017 John Wiley & Sons Ltd.

  17. Experiences of giving and receiving care in traumatic brain injury: An integrative review.

    Science.gov (United States)

    Kivunja, Stephen; River, Jo; Gullick, Janice

    2018-04-01

    To synthesise the literature on the experiences of giving or receiving care for traumatic brain injury for people with traumatic brain injury, their family members and nurses in hospital and rehabilitation settings. Traumatic brain injury represents a major source of physical, social and economic burden. In the hospital setting, people with traumatic brain injury feel excluded from decision-making processes and perceive impatient care. Families describe inadequate information and support for psychological distress. Nurses find the care of people with traumatic brain injury challenging particularly when experiencing heavy workloads. To date, a contemporary synthesis of the literature on people with traumatic brain injury, family and nurse experiences of traumatic brain injury care has not been conducted. Integrative literature review. A systematic search strategy guided by the PRISMA statement was conducted in CINAHL, PubMed, Proquest, EMBASE and Google Scholar. Whittemore and Knafl's (Journal of Advanced Nursing, 52, 2005, 546) integrative review framework guided data reduction, data display, data comparison and conclusion verification. Across the three participant categories (people with traumatic brain injury/family members/nurses) and sixteen subcategories, six cross-cutting themes emerged: seeking personhood, navigating challenging behaviour, valuing skills and competence, struggling with changed family responsibilities, maintaining productive partnerships and reflecting on workplace culture. Traumatic brain injury creates changes in physical, cognitive and emotional function that challenge known ways of being in the world for people. This alters relationship dynamics within families and requires a specific skill set among nurses. Recommendations include the following: (i) formal inclusion of people with traumatic brain injury and families in care planning, (ii) routine risk screening for falls and challenging behaviour to ensure that controls are based on

  18. "In my before life": relationships, coping and post-traumatic growth in adolescent survivors of a traumatic brain injury.

    Science.gov (United States)

    Di Battista, Ashley; Godfrey, Celia; Soo, Cheryl; Catroppa, Cathy; Anderson, Vicki

    2014-11-01

    Explore the individual, adolescent phenomeno-logy of quality of life after traumatic brain injury. Adolescent survivors of traumatic brain injury. Qualitative interviews with 10 adolescents, mean age at assessment 17.09 years (SD 1.81). Mean time since injury 4.62 years (SD 2.89). Data were analysed using a primarily interpretative phenomenological analysis approach. Two major findings: (1) perceived quality of life was not automatically impacted by a traumatic brain injury, but when it was, the directionality of impact (positive, negative) varied depending on the life-domain; (2) changes in ability post-traumatic brain injury were attributed to the injury (more often cognitive and physical changes) or to a sense of normal maturation processes (72% and 28%, respectively). Attribution processing permeated themes of personal and social discrepancies, which also yielded themes of: altered family and relationships, roles, responsibilities, independence, coping and post-traumatic growth. All participants reported a happy life at the time of interview. The adolescents' appraisal of their identity from pre- to post-injury life was related to their current sense of well-being. Most notably was the sense of balance; participants addressed the negative and positive consequences of brain injury to qualify their sense of wellbeing.

  19. ECONOMIC LOSSES CAUSED BY TRAUMATIC BRAIN INJURY IN CHILDREN

    Directory of Open Access Journals (Sweden)

    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

  20. Predicting Intracranial Pressure and Brain Tissue Oxygen Crises in Patients With Severe Traumatic Brain Injury.

    Science.gov (United States)

    Myers, Risa B; Lazaridis, Christos; Jermaine, Christopher M; Robertson, Claudia S; Rusin, Craig G

    2016-09-01

    To develop computer algorithms that can recognize physiologic patterns in traumatic brain injury patients that occur in advance of intracranial pressure and partial brain tissue oxygenation crises. The automated early detection of crisis precursors can provide clinicians with time to intervene in order to prevent or mitigate secondary brain injury. A retrospective study was conducted from prospectively collected physiologic data. intracranial pressure, and partial brain tissue oxygenation crisis events were defined as intracranial pressure of greater than or equal to 20 mm Hg lasting at least 15 minutes and partial brain tissue oxygenation value of less than 10 mm Hg for at least 10 minutes, respectively. The physiologic data preceding each crisis event were used to identify precursors associated with crisis onset. Multivariate classification models were applied to recorded data in 30-minute epochs of time to predict crises between 15 and 360 minutes in the future. The neurosurgical unit of Ben Taub Hospital (Houston, TX). Our cohort consisted of 817 subjects with severe traumatic brain injury. Our algorithm can predict the onset of intracranial pressure crises with 30-minute advance warning with an area under the receiver operating characteristic curve of 0.86 using only intracranial pressure measurements and time since last crisis. An analogous algorithm can predict the start of partial brain tissue oxygenation crises with 30-minute advanced warning with an area under the receiver operating characteristic curve of 0.91. Our algorithms provide accurate and timely predictions of intracranial hypertension and tissue hypoxia crises in patients with severe traumatic brain injury. Almost all of the information needed to predict the onset of these events is contained within the signal of interest and the time since last crisis.

  1. Pharmacologic resuscitation for hemorrhagic shock combined with traumatic brain injury.

    Science.gov (United States)

    Jin, Guang; Duggan, Michael; Imam, Ayesha; Demoya, Marc A; Sillesen, Martin; Hwabejire, John; Jepsen, Cecilie H; Liu, Baoling; Mejaddam, Ali Y; Lu, Jennifer; Smith, William Michael; Velmahos, George C; Socrate, Simona; Alam, Hasan B

    2012-12-01

    We have previously demonstrated that valproic acid (VPA), a histone deacetylase inhibitor, can improve survival after hemorrhagic shock (HS), protect neurons from hypoxia-induced apoptosis, and attenuate the inflammatory response. We have also shown that administration of 6% hetastarch (Hextend [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. Yorkshire swine (42-50 kg) were instrumented to measure hemodynamic parameters, intracranial pressure, and brain tissue oxygenation. A custom-designed, computer-controlled cortical impact device was used to create a TBI through a 20-mm craniotomy: 15-mm cylindrical tip impactor at 4-m/s velocity, 100-millisecond dwell time, and 12-mm penetration depth. Volume-controlled hemorrhage was started (40% blood volume) concurrent with the TBI. After 2 hours of shock, animals were randomized to one of three resuscitation groups (n = 7 per group) as follows: (1) isotonic sodium chloride solution; (2) 6% hetastarch, Hex; and (3) Hex and VPA 300 mg/kg (Hex + VPA). Volumes of Hex matched the shed blood, whereas that of the isotonic sodium chloride solution was three times the volume. VPA treatment was started after an hour of shock. After 6 hours of postresuscitation monitoring, brains were sectioned into 5-mm slices and stained with 2, 3, 5-Triphenyltetrazolium chloride to quantify the lesion size (mm) and brain swelling (percent change compared with uninjured side). Levels of acetylated histone H3 were determined to quantify acetylation, and myeloperoxidase and interleukine-1β (IL-1β) levels were measured as markers of brain inflammation. Combination of 40% blood loss with cortical impact and a period of shock (2 hours) and resuscitation resulted in a highly reproducible brain injury. Lesion size and brain swelling in the Hex

  2. CT findings of traumatic primary brain-stem injury

    International Nuclear Information System (INIS)

    Hosaka, Yasuaki; Hatashita, Shizuo; Bandou, Kuniaki; Ueki, Yasuyuki; Abe, Kouzou; Koga, Nobunori; Sugimura, Jun; Sakakibara, Tokiwa; Takagi, Suguru

    1984-01-01

    A series of 27 consecutive patients with traumatic primary brain stem injuries was studied. They were diagnosed by means of clinical signs, neurological examination, and computerized tomography (CT). The CT findings of the brain-stem lesions were classified into 4 types: Type H, spotty, high-density; Type H and L, high- and low-densities; Type L, low-density; Type I, isodensity. The Glasgow coma scale (GCS), neurological findings on admission, CT findings (findings in the brain stem, obliteration of perimesencephalic cistern (PMC), and other findings), and the Glasgow outcome scale (GOS) were examined. In the 9 cases of Type H, there was a correlation between the GCS and the GOS, and the spotty, high-density lesions were localized mainly in the dorsal and/or ventral midbrain parenchyma, but these lesions did not show focal signs and symptoms. Without an obliteration of the PMC, Type-H patients did not always have a bad outcome. In the 4 cases of Type H and L, the 2 cases of Type L, and the 12 cases of Type I, there was an obliteration of the PMC. All of the these cases had a bad outcome (1 case of moderate disability, 3 cases of severe disability, and 14 cases of death). The mechanism producing a spotty, high-density area was discussed. The weaker impact (than the other types) and individual anatomical differences weresupposed to make for a spotty, high-density are in the brain stem. (author)

  3. Sex, Gender, and Traumatic Brain Injury: A Commentary.

    Science.gov (United States)

    Colantonio, Angela

    2016-02-01

    The goal of this supplemental issue is to address major knowledge, research, and clinical practice gaps regarding the limited focus on brain injury in girls and women as well as limited analysis of the effect of sex and gender in research on acquired brain injury. Integrating sex and gender in research is recognized as leading to better science and, ultimately, to better clinical practice. A sex and gender analytical approach to rehabilitation research is crucial to understanding traumatic brain injury and improving quality of life outcomes for survivors. Put another way, the lack of focus on sex and gender reduces the rigor of research design, the generalizability of study findings, and the effectiveness of clinical implementation and knowledge dissemination practices. The articles in this supplement examine sex and gender using a variety of methodological approaches and research contexts. Recommendations for future research on acquired brain injury that consciously incorporates sex and gender are made throughout this issue. This supplement is a product of the Girls and Women with ABI Task Force of the American Congress of Rehabilitation Medicine. Copyright © 2016 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.

  4. Treatment with the NK1 antagonist emend reduces blood brain barrier dysfunction and edema formation in an experimental model of brain tumors.

    Directory of Open Access Journals (Sweden)

    Elizabeth Harford-Wright

    Full Text Available The neuropeptide substance P (SP has been implicated in the disruption of the blood-brain barrier (BBB and development of cerebral edema in acute brain injury. Cerebral edema accumulates rapidly around brain tumors and has been linked to several tumor-associated deficits. Currently, the standard treatment for peritumoral edema is the corticosteroid dexamethasone, prolonged use of which is associated with a number of deleterious side effects. As SP is reported to increase in many cancer types, this study examined whether SP plays a role in the genesis of brain peritumoral edema. A-375 human melanoma cells were injected into the right striatum of male Balb/c nude mice to induce brain tumor growth, with culture medium injected in animals serving as controls. At 2, 3 or 4 weeks following tumor cell inoculation, non-treated animals were perfusion fixed for immunohistochemical detection of Albumin, SP and NK1 receptor. A further subgroup of animals was treated with a daily injection of the NK1 antagonist Emend (3 mg/kg, dexamethasone (8 mg/kg or saline vehicle at 3 weeks post-inoculation. Animals were sacrificed a week later to determine BBB permeability using Evan's Blue and brain water content. Non-treated animals demonstrated a significant increase in albumin, SP and NK1 receptor immunoreactivity in the peritumoral area as well as increased perivascular staining in the surrounding brain tissue. Brain water content and BBB permeability was significantly increased in tumor-inoculated animals when compared to controls (p<0.05. Treatment with Emend and dexamethasone reduced BBB permeability and brain water content when compared to vehicle-treated tumor-inoculated mice. The increase in peritumoral staining for both SP and the NK1 receptor, coupled with the reduction in brain water content and BBB permeability seen following treatment with the NK1 antagonist Emend, suggests that SP plays a role in the genesis of peritumoral edema, and thus warrants

  5. Treatment with the NK1 antagonist emend reduces blood brain barrier dysfunction and edema formation in an experimental model of brain tumors.

    Science.gov (United States)

    Harford-Wright, Elizabeth; Lewis, Kate M; Ghabriel, Mounir N; Vink, Robert

    2014-01-01

    The neuropeptide substance P (SP) has been implicated in the disruption of the blood-brain barrier (BBB) and development of cerebral edema in acute brain injury. Cerebral edema accumulates rapidly around brain tumors and has been linked to several tumor-associated deficits. Currently, the standard treatment for peritumoral edema is the corticosteroid dexamethasone, prolonged use of which is associated with a number of deleterious side effects. As SP is reported to increase in many cancer types, this study examined whether SP plays a role in the genesis of brain peritumoral edema. A-375 human melanoma cells were injected into the right striatum of male Balb/c nude mice to induce brain tumor growth, with culture medium injected in animals serving as controls. At 2, 3 or 4 weeks following tumor cell inoculation, non-treated animals were perfusion fixed for immunohistochemical detection of Albumin, SP and NK1 receptor. A further subgroup of animals was treated with a daily injection of the NK1 antagonist Emend (3 mg/kg), dexamethasone (8 mg/kg) or saline vehicle at 3 weeks post-inoculation. Animals were sacrificed a week later to determine BBB permeability using Evan's Blue and brain water content. Non-treated animals demonstrated a significant increase in albumin, SP and NK1 receptor immunoreactivity in the peritumoral area as well as increased perivascular staining in the surrounding brain tissue. Brain water content and BBB permeability was significantly increased in tumor-inoculated animals when compared to controls (p<0.05). Treatment with Emend and dexamethasone reduced BBB permeability and brain water content when compared to vehicle-treated tumor-inoculated mice. The increase in peritumoral staining for both SP and the NK1 receptor, coupled with the reduction in brain water content and BBB permeability seen following treatment with the NK1 antagonist Emend, suggests that SP plays a role in the genesis of peritumoral edema, and thus warrants further

  6. Measuring outcome in traumatic brain injury treatment trials: recommendations from the traumatic brain injury clinical trials network.

    Science.gov (United States)

    Bagiella, Emilia; Novack, Thomas A; Ansel, Beth; Diaz-Arrastia, Ramon; Dikmen, Sureyya; Hart, Tessa; Temkin, Nancy

    2010-01-01

    Traumatic brain injury (TBI) involves several aspects of a patient's condition, including physical, mental, emotional, cognitive, social, and functional changes. Therefore, a clinical trial with individuals with TBI should consider outcome measures that reflect their global status. We present the work of the National Institute of Child Health and Development-sponsored Traumatic Brain Injury Clinical Trials Network Outcome Measures subcommittee and its choice of outcome measures for a phase III clinical trial of patients with complicated mild to severe TBI. On the basis of theoretical and practical considerations, the subcommittee recommended the adoption of a core of 9 measures that cover 2 different areas of recovery: functional and cognitive. These measures are the Extended Glasgow Outcome Scale; the Controlled Oral Word Association Test; the Trail Making Test, Parts A and B; the California Verbal Learning Test-II; the Wechsler Adult Intelligence Scale-III Digit Span subtest; the Wechsler Adult Intelligence Scale-III Processing Speed Index; and the Stroop Color-Word Matching Test, Parts 1 and 2. The statistical methods proposed to analyze these measures using a global test procedure, along with research and methodological and regulatory issues involved with the use of multiple outcomes in a clinical trial, are discussed.

  7. Exacerbation of Acute Traumatic Brain Injury by Circulating Extracellular Vesicles.

    Science.gov (United States)

    Hazelton, Isla; Yates, Abi; Dale, Ashley; Roodselaar, Jay; Akbar, Naveed; Ruitenberg, Marc J; Anthony, Daniel C; Couch, Yvonne

    2018-02-15

    Inflammatory lesions in the brain activate a systemic acute-phase response (APR), which is dependent on the release of extracellular vesicles (EVs) into the circulation. The resulting APR is responsible for regulating leukocyte mobilization and subsequent recruitment to the brain. Factors that either exacerbate or inhibit the APR will also exacerbate or inhibit central nervous system (CNS) inflammation as a consequence and have the potential to influence ongoing secondary damage. Here, we were interested to discover how the circulating EV population changes after traumatic brain injury (TBI) and how manipulation of the circulating EV pool impacts on the outcome of TBI. We found the number of circulating EVs increased rapidly post-TBI, and this was accompanied by an increase in CNS and hepatic leukocyte recruitment. In an adoptive transfer study, we then evaluated the outcomes of TBI after administering EVs derived from either in vitro macrophage or endothelial cell lines stimulated with lipopolysaccharide (LPS), or from murine plasma from an LPS challenge using the air-pouch model. By manipulating the circulating EV population, we were able to demonstrate that each population of transferred EVs increased the APR. However, the characteristics of the response were dependent on the nature of the EVs; specifically, it was significantly increased when animals were challenged with macrophage-derived EVs, suggesting that the cellular origins of EVs may determine their function. Selectively targeting EVs from macrophage/monocyte populations is likely to be of value in reducing the impact of the systemic inflammatory response on the outcome of traumatic CNS injury.

  8. A pilot trial of l-carnitine in patients with traumatic brain injury: Effects on biomarkers of injury.

    Science.gov (United States)

    Mahmoodpoor, Ata; Shokouhi, Ghaffar; Hamishehkar, Hadi; Soleimanpour, Hassan; Sanaie, Sarvin; Porhomayon, Jahan; Rasouli, Fatemeh; Nader, Nader D

    2018-02-09

    To investigate the effects of l-Carnitine on neuron specific enolase (NSE) as a marker of inflammation in patients with traumatic brain injury (TBI). Forty patients with severe TBI were randomized into 2 groups. The (LCA-) group received standard treatment with placebo while the (LCA+) group received l-Carnitine 2g/day for one week. NSE was measured on days 1, 3 and 7 after the initiation of the study. Neurocognitive and neurobehavioral disorders were recorded on the first and third months. Neurocognitive function and NSE significantly improved within one week in both groups. Patient mortality was similar in LCA+ and LCA- groups (P value: 0.76). Brain edema was present in 7 patients in LCA+ group and 13 patients in LCA-group (P value: 0.044). While there was no difference in NSE levels between the two groups. Neurological function was preserved in the LCA+ group with an exception of attention deficit, which was frequent in the LCA+ group. We concluded that despite improvements in neurobehavioral function and the degree of cerebral edema, 7-days of treatment with l-Carnitine failed to reduce serum NSE levels or improve mortality rate at 90days in patients with TBI. Published by Elsevier Inc.

  9. Peritumoral edema of meningiomas and metastatic brain tumors: differences in diffusion characteristics evaluated with diffusion-tensor MR imaging

    International Nuclear Information System (INIS)

    Toh, Cheng-Hong; Wong, Alex M.-C; Wong, Ho-Fai; Wan, Yung-Liang; Wei, Kuo-Chen; Ng, Shu-Hang

    2007-01-01

    We prospectively compared the fractional anisotropy (FA) and mean diffusivity (MD) of the peritumoral edema of meningiomas and metastatic brain tumors with diffusion-tensor magnetic resonance (MR) imaging. The study protocol was approved by the local ethics committee, and written informed consent was obtained. Preoperative diffusion-tensor MR imaging was performed in 15 patients with meningiomas and 11 patients with metastatic brain tumors. Regions of interest (ROI) were placed in the peritumoral edema and normal-appearing white matter (NAWM) of the contralateral hemisphere to measure the FA and MD. The FA and MD ratios were calculated for each ROI in relation to the NAWM of the contralateral hemisphere. Changes in peritumoral MD and FA, in terms of primary values and ratios, were compared using a two-sample t-test; P -3 mm 2 /s) of the peritumoral edema for metastases and meningiomas, respectively, were 0.902 ± 0.057 and 0.820 ± 0.094, the mean MD ratios were 220.3 ± 22.6 and 193.1 ± 23.4, the mean FA values were 0.146 ± 0.026 and 0.199 ± 0.052, and the mean FA ratios were 32.3 ± 5.9 and 46.0 ± 12.1. All the values were significantly different between metastases and meningiomas (MD values P 0.016, MD ratios P = 0.006, FA values P = 0.005, FA ratios P = 0.002). The peritumoral edema of metastatic brain tumors and meningiomas show different MD and FA on diffusion-tensor MR imaging. (orig.)

  10. MRI findings of acute cerebral swelling and brain edema in the acute stage. A report of two cases

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    Oki, Hideo; Ueda, Shin; Matsumoto, Keizo; Kashihara, Michiharu; Furuichi, Masashi.

    1988-08-01

    We report two cases, one of acute cerebral swelling and the other with a major stroke, whose MRI has shown very interesting findings. Case 1, a 32-year-old male, was admitted to our service because of a lowering of his consciousness immediately after a head injury. On admission, the patient was semicomatous (E/sub 1/M/sub 2/V/sub 1/, with anisocoria (R > L). His plain skull X-ray was normal. A CT scan, however, demonstrated right isodensity hemispheric swelling associated with a subarachnoid hemorrhage in the right Sylvian fissure. A right carotid angiogram showed no vascular disorders. MR imaging of the spin density demonstrated a hyperintensitive thickening of the gray matter in the whole right hemisphere. Case 2, a 58-year-old female, was admitted because of a sudden onset of loss of consciousness, with right hemiparesis and dysarthria. On admission, her consciousness was semicomatous (E/sub 1/M/sub 3/V/sub 1/), and it deteriorated to a deep coma 1 hour later. A CT scan demonstrated a diffuse left hemispheric low density, with a finding of hemorrhagic infarction in the basal ganglia. MR imaging of the spin density showed a hyperintensitive thickening of the gray matter resembling that of Case 1. The findings of the spin-echo images of our two cases showed a hyperintensitive thickening of the gray matter in both. The hyperintensity and thickening of the gray matter apparently indicated a sort of hyperemia and brain edema. These findings led us to suspect that the hyperemia associated with acute cerebral swelling and ischemic brain edema of our two cases originated in the gray matter, although it has been considered that the pathogenesis of acute cerebral swelling is not known and that brain edema, especially vasogenic edema, will mostly develop in the white matter rather than in the gray matter.

  11. Investigations of primary blast-induced traumatic brain injury

    Science.gov (United States)

    Sawyer, T. W.; Josey, T.; Wang, Y.; Villanueva, M.; Ritzel, D. V.; Nelson, P.; Lee, J. J.

    2018-01-01

    The development of an advanced blast simulator (ABS) has enabled the reproducible generation of single-pulse shock waves that simulate free-field blast with high fidelity. Studies with rodents in the ABS demonstrated the necessity of head restraint during head-only exposures. When the head was not restrained, violent global head motion was induced by pressures that would not produce similar movement of a target the size and mass of a human head. This scaling artefact produced changes in brain function that were reminiscent of traumatic brain injury (TBI) due to impact-acceleration effects. Restraint of the rodent head eliminated these, but still produced subtle changes in brain biochemistry, showing that blast-induced pressure waves do cause brain deficits. Further experiments were carried out with rat brain cell aggregate cultures that enabled the conduct of studies without the gross movement encountered when using rodents. The suspension nature of this model was also exploited to minimize the boundary effects that complicate the interpretation of primary blast studies using surface cultures. Using this system, brain tissue was found not only to be sensitive to pressure changes, but also able to discriminate between the highly defined single-pulse shock waves produced by underwater blast and the complex pressure history exposures experienced by aggregates encased within a sphere and subjected to simulated air blast. The nature of blast-induced primary TBI requires a multidisciplinary research approach that addresses the fidelity of the blast insult, its accurate measurement and characterization, as well as the limitations of the biological models used.

  12. Vomiting With Head Trauma and Risk of Traumatic Brain Injury.

    Science.gov (United States)

    Borland, Meredith L; Dalziel, Stuart R; Phillips, Natalie; Dalton, Sarah; Lyttle, Mark D; Bressan, Silvia; Oakley, Ed; Hearps, Stephen J C; Kochar, Amit; Furyk, Jeremy; Cheek, John A; Neutze, Jocelyn; Babl, Franz E

    2018-04-01

    To determine the prevalence of traumatic brain injuries in children who vomit after head injury and identify variables from published clinical decision rules (CDRs) that predict increased risk. Secondary analysis of the Australasian Paediatric Head Injury Rule Study. Vomiting characteristics were assessed and correlated with CDR predictors and the presence of clinically important traumatic brain injury (ciTBI) or traumatic brain injury on computed tomography (TBI-CT). Isolated vomiting was defined as vomiting without other CDR predictors. Of the 19 920 children enrolled, 3389 (17.0%) had any vomiting, with 2446 (72.2%) >2 years of age. In 172 patients with ciTBI, 76 had vomiting (44.2%; 95% confidence interval [CI] 36.9%-51.7%), and in 285 with TBI-CT, 123 had vomiting (43.2%; 95% CI 37.5%-49.0%). With isolated vomiting, only 1 (0.3%; 95% CI 0.0%-0.9%) had ciTBI and 2 (0.6%; 95% CI 0.0%-1.4%) had TBI-CT. Predictors of increased risk of ciTBI with vomiting by using multivariate regression were as follows: signs of skull fracture (odds ratio [OR] 80.1; 95% CI 43.4-148.0), altered mental status (OR 2.4; 95% CI 1.0-5.5), headache (OR 2.3; 95% CI 1.3-4.1), and acting abnormally (OR 1.86; 95% CI 1.0-3.4). Additional features predicting TBI-CT were as follows: skull fracture (OR 112.96; 95% CI 66.76-191.14), nonaccidental injury concern (OR 6.75; 95% CI 1.54-29.69), headache (OR 2.55; 95% CI 1.52-4.27), and acting abnormally (OR 1.83; 95% CI 1.10-3.06). TBI-CT and ciTBI are uncommon in children presenting with head injury with isolated vomiting, and a management strategy of observation without immediate computed tomography appears appropriate. Copyright © 2018 by the American Academy of Pediatrics.

  13. Mild Traumatic Brain Injury: Longitudinal Study of Cognition, Functional Status, and Post-Traumatic Symptoms.

    Science.gov (United States)

    Dikmen, Sureyya; Machamer, Joan; Temkin, Nancy

    2017-04-15

    More than 75% of traumatic brain injuries (TBIs) seeking medical attention are mild, and outcome in that group is heterogeneous. Until sensitive and valid biomarkers are identified, methods are needed to classify mild TBI into more homogeneous subgroups. Four hundred twenty-one adults with mild TBI were divided into groups based on Glasgow Coma Scale (GCS) 13-15 without computed tomography (CT) abnormalities, GCS 15 with CT abnormalities, and GCS 13-14 with CT abnormalities, and were compared with 120 trauma controls on 1-month and 1-year outcomes. At 1 month post-injury, almost all neuropsychological variables differed significantly among the groups. Compared with trauma controls, the GCS 13-15 CT normal group showed no significant differences on any neuropsychological measure or Glasgow Outcome Scale (GOS). The GCS 15 CT abnormal group performed significantly worse on only a measure of episodic memory and learning (Selective Reminding Recall [SRCL]) and GOS, and the GCS 13-14 CT abnormal group performed significantly worse on most neuropsychological measures and GOS. At 1 year post-injury, except for an isolated difficulty on SRCL in the GCS 13-14 CT abnormal group, no differences were observed on any neuropsychological measures nor on GOS. Mean percent of total post-traumatic symptoms endorsed as new or worse and percent endorsing three or more symptoms differed significantly (p < 0.001), with each TBI subgroup reporting significantly more symptoms than the trauma controls at both 1 month and 1 year. In conclusion, this subgrouping improves granularity within mild TBI. While most neuropsychological and functional differences abate by 1 year, reporting three or more post-traumatic symptoms remain for about half of individuals.

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

    Science.gov (United States)

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

    2016-05-01

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

  15. Tongxinluo reduces brain edema and inhibits post-ischemic inflammation after middle cerebral artery occlusion in rats.

    Science.gov (United States)

    Cai, Min; Yu, Zhonghai; Wang, Lili; Song, Xiaoling; Zhang, Jingsi; Zhang, Zhennian; Zhang, Wen; Li, Wenwei; Xiang, Jun; Cai, Dingfang

    2016-04-02

    Tongxinluo (TXL), a widely used traditional Chinese medicine, has been proved multiple therapeutic effects in cerebral ischemic infraction. The purpose of this study was to investigate the protective effects of TXL on the brain edema and post-ischemic inflammatory response. Middle cerebral artery occlusion in the rat was used as the ischemia model. Rats were treated with TXL. In the first stage, the best dosage was chosen based on functional assessment and infarct size. In the second stage, rats were randomly divided into 5 groups: sham control (sham), ischemia and reperfusion (IR) 24h, TXL24h, I/R72h, TXL72h. TXL(1.6g/kg/day) administration was pre-performed for 3 days in TXL groups, and was post-performed for 24h (TXL24h group) or 72h (TXL72h group). Brain edema was measured by water content, MRI and AQP4 expression. Iba1, HMGB1, TLR4, NF-κB expression were examined by immunofluorescence staining or Western blot. TNF-α was determined by enzyme-linked immunosorbent assay. High dose (1.6g/kg/day) of TXL remarkably reduced neurological deficit scores and cerebral infarct area. Compared with those results of I/R24h group, pre-post treatment with TXL for 3 days decreased brain water content, down-regulated AQP4 expression, lowered relative signal intensity of T2WI, reduced lesion volume ratio, and inhibited the activation of microglia, HMGB1, TLR4, NF-κB and TNF-α. These results indicated that the TXL pre-post treatment for 3 days could be an effective therapy for brain ischemia by inhibiting the development of brain edema and post-ischemic inflammation. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  16. Role of the prostaglandin E2 EP1 receptor in traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Alexander V Glushakov

    Full Text Available Brain injuries promote upregulation of so-called proinflammatory prostaglandins, notably prostaglandin E2 (PGE2, leading to overactivation of a class of its cognate G-protein-coupled receptors, including EP1, which is considered a promising target for treatment of ischemic stroke. However, the role of the EP1 receptor is complex and depends on the type of brain injury. This study is focused on the investigation of the role of the EP1 receptor in a controlled cortical impact (CCI model, a preclinical model of traumatic brain injury (TBI. The therapeutic effects of post-treatments with a widely studied EP1 receptor antagonist, SC-51089, were examined in wildtype and EP1 receptor knockout C57BL/6 mice. Neurological deficit scores (NDS were assessed 24 and 48 h following CCI or sham surgery, and brain immunohistochemical pathology was assessed 48 h after surgery. In wildtype mice, CCI resulted in an obvious cortical lesion and localized hippocampal edema with an associated significant increase in NDS compared to sham-operated animals. Post-treatments with the selective EP1 receptor antagonist SC-51089 or genetic knockout of EP1 receptor had no significant effects on cortical lesions and hippocampal swelling or on the NDS 24 and 48 h after CCI. Immunohistochemistry studies revealed CCI-induced gliosis and microglial activation in selected ipsilateral brain regions that were not affected by SC-51089 or in the EP1 receptor-deleted mice. This study provides further clarification on the respective contribution of the EP1 receptor in TBI and suggests that, under this experimental paradigm, the EP1 receptor would have limited effects in modulating acute neurological and anatomical pathologies following contusive brain trauma. Findings from this protocol, in combination with previous studies demonstrating differential roles of EP1 receptor in ischemic, neurotoxic, and hemorrhagic conditions, provide scientific background and further clarification of

  17. Effect of Polyphenols on Oxidative Stress and Mitochondrial Dysfunction in Neuronal Death and Brain Edema in Cerebral Ischemia

    Directory of Open Access Journals (Sweden)

    Richard A. Anderson

    2011-11-01

    Full Text Available Polyphenols are natural substances with variable phenolic structures and are elevated in vegetables, fruits, grains, bark, roots, tea, and wine. There are over 8000 polyphenolic structures identified in plants, but edible plants contain only several hundred polyphenolic structures. In addition to their well-known antioxidant effects, select polyphenols also have insulin-potentiating, anti-inflammatory, anti-carcinogenic, anti-viral, anti-ulcer, and anti-apoptotic properties. One important consequence of ischemia is neuronal death and oxidative stress plays a key role in neuronal viability. In addition, neuronal death may be initiated by the activation of mitochondria-associated cell death pathways. Another consequence of ischemia that is possibly mediated by oxidative stress and mitochondrial dysfunction is glial swelling, a component of cytotoxic brain edema. The purpose of this article is to review the current literature on the contribution of oxidative stress and mitochondrial dysfunction to neuronal death, cell swelling, and brain edema in ischemia. A review of currently known mechanisms underlying neuronal death and edema/cell swelling will be undertaken and the potential of dietary polyphenols to reduce such neural damage will be critically reviewed.

  18. Clinical features of repetitive traumatic brain injury and chronic traumatic encephalopathy.

    Science.gov (United States)

    Montenigro, Philip H; Bernick, Charles; Cantu, Robert C

    2015-05-01

    Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by a distinct pattern of hyperphosphorylated tau (p-tau). Thought to be caused by repetitive concussive and subconcussive injuries, CTE is considered largely preventable. The majority of neuropathologically confirmed cases have occurred in professional contact sport athletes (eg, boxing, football). A recent post-mortem case series has magnified concerns for the public's health following its identification in six high school level athletes. CTE is diagnosed with certainty only following a post-mortem autopsy. Efforts to define the etiology and clinical progression during life are ongoing. The goal of this article is to characterize the clinical concepts associated with short- and long-term effects of repetitive traumatic brain injury, with a special emphasis on new clinical diagnostic criteria for CTE. Utilizing these new diagnostic criteria, two cases of neuropathologically confirmed CTE, one in a professional football player and one in a professional boxer, are reported. Differences in cerebellar pathology in CTE confirmed cases in boxing and football are discussed. © 2015 International Society of Neuropathology.

  19. Concepts and strategies for clinical management of blast-induced traumatic brain injury and posttraumatic stress disorder.

    Science.gov (United States)

    Chen, Yun; Huang, Wei; Constantini, Shlomi

    2013-01-01

    After exposure of the human body to blast, kinetic energy of the blast shock waves might be transferred into hydraulic energy in the cardiovascular system to cause a rapid physical movement or displacement of blood (a volumetric blood surge). The volumetric blood surge moves through blood vessels from the high-pressure body cavity to the low-pressure cranial cavity, causing damage to tiny cerebral blood vessels and the blood-brain barrier (BBB). Large-scale cerebrovascular insults and BBB damage that occur globally throughout the brain may be the main causes of non-impact, blast-induced brain injuries, including the spectrum of traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD). The volumetric blood surge may be a major contributor not only to blast-induced brain injuries resulting from physical trauma, but may also be the trigger to psychiatric disorders resulting from emotional and psychological trauma. Clinical imaging technologies, which are able to detect tiny cerebrovascular insults, changes in blood flow, and cerebral edema, may help diagnose both TBI and PTSD in the victims exposed to blasts. Potentially, prompt medical treatment aiming at prevention of secondary neuronal damage may slow down or even block the cascade of events that lead to progressive neuronal damage and subsequent long-term neurological and psychiatric impairment.

  20. Molecular mechanisms of cognitive dysfunction following traumatic brain injury.

    Science.gov (United States)

    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.

  1. Cerebral Infarction after Traumatic Brain Injury: Incidence and Risk Factors.

    Science.gov (United States)

    Bae, Dong-Hyeon; Choi, Kyu-Sun; Yi, Hyeong-Joong; Chun, Hyoung-Joon; Ko, Yong; Bak, Koang Hum

    2014-10-01

    Post-traumatic cerebral infarction (PTCI) is one of the most severe secondary insults after traumatic brain injury (TBI), and is known to be associated with poor outcome and high mortality rate. We assessed the practical incidence and risk factors for the development of PTCI. We conducted retrospective study on 986 consecutive patients with TBI from the period May 2005 to November 2012 at our institution. The definition of PTCI was made on non-enhanced CT scan based on a well-demarcated or fairly discernible region of low attenuation following specific vascular territory with normal initial CT. Clinical and radiological findings that related to patients' outcome were reviewed and statistically compared. PTCI was observed in 21 (2.1%) patients. Of various parameters, age (p=0.037), initial Glasgow coma scale score (paccident and PTCI, patterns of TBI and vascular territory of PTCI were not specific. The mortality rates were significantly higher in patients with PTCI than without PTCI. The development of PTCI is rare after TBI, but it usually results in serious outcome and high mortality. Early recognition for risks and aggressive managements is mandatory to prevent PTCI.

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

    Directory of Open Access Journals (Sweden)

    Michael E Hoffer

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

  3. A review of glutamate's role in traumatic brain injury mechanisms

    Science.gov (United States)

    Good, Cameron H.

    2013-05-01

    Glutamate is the primary excitatory neurotransmitter used by the central nervous system (CNS) for synaptic communication, and its extracellular concentration is tightly regulated by glutamate transporters located on nearby astrocytes. Both animal models and human clinical studies have demonstrated elevated glutamate levels immediately following a traumatic brain event, with the duration and severity of the rise corresponding to prognosis. This rise in extracellular glutamate likely results from a combination of excessive neurotransmitter release from damaged neurons and down regulation of uptake mechanisms in local astrocytes. The immediate results of a traumatic event can lead to necrotic tissue in severely injured regions, while prolonged increases in excitatory transmission can cause secondary excitotoxic injury through activation of delayed apoptotic pathways. Initial TBI animal studies utilized a variety of broad glutamate receptor antagonists to successfully combat secondary injury mechanisms, but unfortunately this same strategy has proven inconclusive in subsequent human trials due to deleterious side effects and heterogeneity of injuries. More recent treatment strategies have utilized specific glutamate receptor subunit antagonists in an effort to minimize side effects and have shown promising results. Future challenges will be detecting the concentration and kinetics of the glutamate rise following injury, determining which patient populations could benefit from antagonist treatment based on their extracellular glutamate concentrations and when drugs should be administered to maximize efficacy.

  4. Second language acquisition after traumatic brain injury: a case study.

    Science.gov (United States)

    Połczyńska-Fiszer, M; Mazaux, J M

    2008-01-01

    Post-traumatic language and memory impairment, as well as a subsequent recovery in monolinguals have been widely documented in the literature, yet little is known about learning the second language after a severe head trauma followed by coma, as well as the relationship of this process with cognitive recovery, psychological status and quality of life. The present study investigates the relationship of learning the second language (English) in the process of rehabilitation, with quality of life in a Polish female university student who, as a result of a car accident, suffered a major closed-head injury and was comatose for a month. The subject was enrolled in an English learning program nine months after the trauma. The experiment lasted six months and comprised monthly meetings. The patient improved the major components of the second language, including vocabulary. Within the 6 months, the subject was gradually capable of learning additional and more complex lexical items. Learning the second language after traumatic brain injury may positively influence emotional well-being, self-esteem, and, perhaps, recovery of quality of life. A long-term beneficial effect of learning L2 was a consequential improvement of the patient's memory.

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

    Science.gov (United States)

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

    2016-04-15

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

  6. Effect of Italy's motorcycle helmet law on traumatic brain injuries.

    Science.gov (United States)

    Servadei, F; Begliomini, C; Gardini, E; Giustini, M; Taggi, F; Kraus, J

    2003-09-01

    To evaluate the impact of a revised Italian motorcycle-moped-scooter helmet law on crash brain injuries. A pre-post law evaluation of helmet use and traumatic brain injury (TBI) occurrence from 1999 to 2001. Romagna region, northeastern Italy, with a 2000 resident population of 983 534 persons. Motorcycle-moped rider survey for helmet use compliance and all residents in the region admitted to the Division of Neurosurgery of the Maurizio Bufalini Hospital in Cesena, Italy for TBI. Helmet use compliance and change in TBI admissions and type(s) of brain lesions. Helmet use increased from an average of less than 20% to over 96%. A comparison of TBI incidence in the Romagna region shows that there was no significant variation before and after introduction of the revised helmet law, except for TBI admissions for motorcycle-moped crashes where a 66% decrease was observed. In the same area TBI admissions by age group showed that motorcycle mopeds riders aged 14-60 years sustained significantly fewer TBIs. The rate of TBI admissions to neurosurgery decreased by over 31% and epidural hematomas almost completely disappeared in crash injured moped riders. The revised Italian mandatory helmet law, with police enforcement, is an effective measure for TBI prevention at all ages.

  7. Traumatic brain injury impairs small-world topology.

    Science.gov (United States)

    Pandit, Anand S; Expert, Paul; Lambiotte, Renaud; Bonnelle, Valerie; Leech, Robert; Turkheimer, Federico E; Sharp, David J

    2013-05-14

    We test the hypothesis that brain networks associated with cognitive function shift away from a "small-world" organization following traumatic brain injury (TBI). We investigated 20 TBI patients and 21 age-matched controls. Resting-state functional MRI was used to study functional connectivity. Graph theoretical analysis was then applied to partial correlation matrices derived from these data. The presence of white matter damage was quantified using diffusion tensor imaging. Patients showed characteristic cognitive impairments as well as evidence of damage to white matter tracts. Compared to controls, the graph analysis showed reduced overall connectivity, longer average path lengths, and reduced network efficiency. A particular impact of TBI is seen on a major network hub, the posterior cingulate cortex. Taken together, these results confirm that a network critical to cognitive function shows a shift away from small-world characteristics. We provide evidence that key brain networks involved in supporting cognitive function become less small-world in their organization after TBI. This is likely to be the result of diffuse white matter damage, and may be an important factor in producing cognitive impairment after TBI.

  8. Functional brain study of chronic traumatic head injury

    International Nuclear Information System (INIS)

    Ceballos Alonso, Concepcion; Pelegrin Valero, Carmelo; Cordoba Diaz de Laspra, Elena

    2000-01-01

    Explosive aggressive behaviour is a significant clinical and medico-legal problem in patients suffering from head injury. However, experts in neuropsychiatry have proposed a specific category for this disorder: the o rganic aggressive syndrome: . The basic reason for proposing this diagnosis is that it describes the specificity of the violent conduct secondary to 'brain damage' with greater precision. Early diagnosis and treatment of the injury is critical. The impact of hnetium-99m-hexamethylpropuleneamine oxime (HMPAO) was examined for measuring brain damage in correlation to neuropsychological performance in patients with traumatic brain injury (TBI). We thus report the case of a twelve-year-old child with a history of CET, who presents with serious episodes of heteroaggressiveness and suggest the usefulness of single photon emission computerized tomography (SPECT) to establish the validity of this psychiatric diagnosis. The appearance of modern functional neuro-image techniques (SPECT) may help to increase the validity of clinical diagnoses in the field of psychiatry in general and of forensic psychiatry in particularly, as the related findings may be used as demarcation criteria to establish syndromic diagnoses (Au)

  9. Sleep disruption and the sequelae associated with traumatic brain injury.

    Science.gov (United States)

    Lucke-Wold, Brandon P; Smith, Kelly E; Nguyen, Linda; Turner, Ryan C; Logsdon, Aric F; Jackson, Garrett J; Huber, Jason D; Rosen, Charles L; Miller, Diane B

    2015-08-01

    Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. Published by Elsevier Ltd.

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

    Directory of Open Access Journals (Sweden)

    Keri Linda Carpenter

    2015-04-01

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

  11. Fatal traumatic brain injury with electrical weapon falls.

    Science.gov (United States)

    Kroll, Mark W; Adamec, Jiri; Wetli, Charles V; Williams, Howard E

    2016-10-01

    While generally reducing morbidity and mortality, electrical weapons have risks associated with their usage, including eye injuries and falls. With sufficient probe spread, an uncontrolled fall to the ground typically occurs along with the possibility of a fatal brain injury. We analyzed possible risk factors including running and elevated surfaces with established head-injury criteria to estimate the risk of brain injury. We searched for cases of arrest-related or in-custody death, with TASER(®) electrical weapon usage where fall-induced injuries might have contributed to the death. We found 24 cases meeting our initial inclusion criteria of a fatal fall involving electronic control. We then excluded 5 cases as intentional jumps, leaving 19 cases of forced falls. Autopsy reports and other records were analyzed to determine which of these deaths were from brain injury caused by the fall. We found 16 probable cases of fatal brain injuries induced by electronic control from electrical weapons. Out of 3 million field uses, this gives a risk of 5.3 ± 2.6 PPM which is higher than the theoretical risk of electrocution. The mean age was 46 ± 14 years which is significantly greater that the age of the typical ARD (36 ± 10). Probe shots to the subject's back may present a higher risk of a fatal fall. The use of electronic control presents a small but real risk of death from fatal traumatic brain injury. Increased age represents an independent risk factor for such fatalities. Copyright © 2016 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.

  12. The effect of butylphthalide on the brain edema, blood-brain barrier of rats after focal cerebral infarction and the expression of Rho A.

    Science.gov (United States)

    Hu, Jinyang; Wen, Qingping; Wu, Yue; Li, Baozhu; Gao, Peng

    2014-06-01

    The aim of this study was to explore the effect of butylphthalide on the brain edema, blood-brain barrier of rats of rats after focal cerebral infarction and the expression of Rho A. A total of 195 sprague-dawley male rats were randomly divided into control group, model group, and butylphthalide group (40 mg/kg, once a day, by gavage). The model was made by photochemical method. After surgery 3, 12, 24, 72, and 144 h, brain water content was done to see the effect of butylphthalide for the cerebral edema. Evans blue extravasation method was done to see the changes in blood-brain barrier immunohistochemistry, and Western blot was done to see the expression of Rho A around the infarction. Compared with the control group, the brain water content of model group and butylphthalide group rats was increased, the permeability of blood-brain barrier of model group and butylphthalide group rats was increased, and the Rho A protein of model group and butylphthalide group rats was increased. Compared with the model group, the brain water content of butylphthalide group rats was induced (73.67 ± 0.67 vs 74.14 ± 0.46; 74.89 ± 0.57 vs 75.61 ± 0.52; 77.49 ± 0.34 vs 79.33 ± 0.49; 76.31 ± 0.56 vs 78.01 ± 0.48; 72.36 ± 0.44 vs 73.12 ± 0.73; P edema, protect the blood-brain barrier, and decrease the expression of Rho A around the infarction.

  13. Neuropsychology of Neuroendocrine Dysregulation after Traumatic Brain Injury.

    Science.gov (United States)

    Zihl, Josef; Almeida, Osborne F X

    2015-05-20

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

  14. Neuropsychology of Neuroendocrine Dysregulation after Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Josef Zihl

    2015-05-01

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

  15. Supporting the literacy skills of adolescents with traumatic brain injury.

    Science.gov (United States)

    Krause, Miriam; Byom, Lindsey; Meulenbroek, Peter; Richards, Stephanie; O'Brien, Katy

    2015-02-01

    Traumatic brain injury (TBI) can affect developmental trajectories as well as language, attention, memory, executive functions, and other cognitive skills related to literacy. Literacy demands change through adolescence and into young adulthood, with academic literacy demands increasing and vocational literacy demands being introduced. Speech-language pathology services must evolve with the literacy needs of each client. This article discusses assessment and treatment approaches designed for adolescents with TBI and recommendations for adapting literacy interventions from the learning disabilities literature. Through proper assessment and intervention, speech-language pathologists can have a meaningful impact on the academic and vocational literacy needs of adolescents with TBI. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  16. Reverse Othello syndrome subsequent to traumatic brain injury.

    Science.gov (United States)

    Butler, P V

    2000-01-01

    Delusional syndromes that occur following head injury are frequently ascribed directly to the consequences of organic insult and seen as empty of psychological significance. The presence of an organic factor, however, does not necessarily indicate that delusional ideation is a direct product of that factor. In this article a detailed report is given of Reverse Othello syndrome (a delusional belief in the fidelity of a romantic partner) appearing in a 49-year-old male following extremely severe traumatic brain injury. This case report highlights the interaction and interpenetration of a complex array of biological, psychological, and social factors in the crystallization of a delusion system. It is argued, following Jaspers, that the emergence of erotically themed delusions following trauma may represent an active attempt to regain intrapsychic coherence and to confer meaning on otherwise catastrophic loss or emptiness.

  17. Misconceptions about traumatic brain injury among correctional health care professionals.

    Science.gov (United States)

    Yuhasz, James E

    2013-04-01

    This study explored the prevalence of misconceptions of traumatic brain injury (TBI) among a sample of correctional health care professionals. Prior research has identified a high prevalence of TBI among criminal offenders, and misconceptions about TBI exist among laypersons and nonexpert professionals. Participants (N = 155) completed a 25-item survey about the sequelae of TBI. Results were compared with previous studies. This sample performed significantly better than laypersons and commensurable to other nonexpert professionals. Misconceptions were higher on items related to loss of consciousness, memory, and recovery. Gender, prior familiarity to someone with a history of TBI, and prior training in TBI accounted for statistically fewer misconceptions. The findings support the need for continued training and increased awareness about TBI among inmates.

  18. Effect of Preferred Music on Agitation After Traumatic Brain Injury.

    Science.gov (United States)

    Park, Soohyun; Williams, Reg Arthur; Lee, Donghyun

    2016-04-01

    Agitation is a common behavioral problem after traumatic brain injury (TBI), which threatens the safety of patients and caregivers and disrupts the rehabilitation process. This study aimed to evaluate the effects of a preferred music intervention on the reduction of agitation in TBI patients and to compare the effects of preferred music with those of classical "relaxation" music. A single group, within-subjects, randomized crossover trial design was formed, consisting of 14 agitated patients with cognitive impairment after severe TBI. Patients listened to preferred music and classical "relaxation" music, with a wash-out period in between. Patients listening to the preferred music reported a significantly greater reduction in agitation compared with the effect seen during the classical "relaxation" music intervention (p = .046). These findings provide preliminary evidence that the preferred music intervention may be effective as an environmental therapeutic approach for reducing agitation after TBI. © The Author(s) 2015.

  19. Nursing Sensitive Outcomes After Severe Traumatic Brain Injury

    DEFF Research Database (Denmark)

    Odgaard, Lene; Aadal, Lena; Eskildsen, Marianne

    2018-01-01

    BACKGROUND: Complications such as infections and conditions after immobilization are frequent after severe traumatic brain injury (TBI) due to compromised bodily functions. Traditionally, bodily functions are core elements in nursing, and therefore nurses in the rehabilitation departments...... was to quantify complications during the first year after severe TBI. PARTICIPANTS: This study included patients 15 years or older who received subacute neurorehabilitation after severe TBI from 2011 to 2015 (N = 469). DESIGN: This is a register-based follow-up study using data from the Danish Head Trauma...... Database, a national clinical quality database aimed at monitoring and improving the quality of rehabilitation for patients with severe TBI. MAIN MEASURES: The following complications were assessed: urinary tract infection, pneumonia, pressure ulcers, joint contractures, and deep venous thrombosis...

  20. Psychosocial consequences of mild traumatic brain injury in children

    DEFF Research Database (Denmark)

    Keightley, Michelle L; Côté, Pierre; Rumney, Peter

    2014-01-01

    ,914 records were screened; 101 of these articles were deemed scientifically admissible, of which 6 investigated the psychosocial consequences of MTBI in children. DATA EXTRACTION: Two reviewers independently extracted data from accepted studies into evidence tables. DATA SYNTHESIS: We conducted a best......OBJECTIVE: To synthesize the best available evidence regarding psychosocial consequences of mild traumatic brain injury (MTBI) in children. DATA SOURCES: MEDLINE, Embase, CINAHL, PsycINFO, and SPORTDiscus were searched (2001-2012). Inclusion criteria included published peer-reviewed reports......-evidence synthesis by linking our conclusions to the evidence tables. Most accepted studies were exploratory rather than confirmatory. Preliminary evidence suggests that most children recover within 3 months post-MTBI. After 1 year, the prevalence of postconcussion symptoms and syndrome is similar between children...

  1. Guillain Barre Syndrome Following Traumatic Brain Injury: A Rare Case

    Directory of Open Access Journals (Sweden)

    Kirac Unal

    2016-06-01

    Full Text Available Introduction Guillain-Barre syndrome (GBS is an immune-mediated acute inflammatory disorder of the peripheral nervous system. Infectious agents were usually accused of playing a role in the etiology of GBS. Guillain-Barre syndrome has rarely been reported following subdural and subarachnoid hemorrhage after head trauma. Case Presentation We report on a 63-year-old male patient presenting GBS following Traumatic Brain Injury (TBI. Only five other similar cases are described in the literature. Conclusions Sudden onset of GBS symptoms following trauma may erroneously be assessed as secondary complications of the TBI and can lead to unnecessary procedures such as computerized tomography (CT scan and magnetic resonance imaging (MRI for a definitive diagnosis and may be a waste of time.

  2. Coping with traumatic brain injury: representative case studies.

    Science.gov (United States)

    Kwasnica, C M; Heinemann, A

    1994-04-01

    This case report compares the use of social supports and vulnerability to substance abuse for two rehabilitation clients after traumatic brain injury (TBI). Using a psychosocial assessment, the Motivational Structure Questionnaire, Adaptive Skills Battery, and Ways of Coping Checklist within a representative case method, we studied two individuals in depth to understand differences in postinjury drinking behaviors. We also examined differences in availability and use of social supports and how support was related to coping efforts. Finally, we illustrated goal-setting and the relationship between long-term planning and follow-through on goals. Social supports, adaptive problem-solving behaviors, and positive reappraisal of situations seem to be important elements in postinjury abstinence. Clinically, this research supports the need for fostering use of both social supports and substance use prevention and treatment services when working with both inpatient and outpatient TBI clients.

  3. Reverse phase protein microarray technology in traumatic brain injury.

    Science.gov (United States)

    Gyorgy, Andrea B; Walker, John; Wingo, Dan; Eidelman, Ofer; Pollard, Harvey B; Molnar, Andras; Agoston, Denes V

    2010-09-30

    Antibody based, high throughput proteomics technology represents an exciting new approach in understanding the pathobiologies of complex disorders such as cancer, stroke and traumatic brain injury. Reverse phase protein microarray (RPPA) can complement the classical methods based on mass spectrometry as a high throughput validation and quantification method. RPPA technology can address problematic issues, such as sample complexity, sensitivity, quantification, reproducibility and throughput, which are currently associated with mass spectrometry-based approaches. However, there are technical challenges, predominantly associated with the selection and use of antibodies, preparation and representation of samples and with analyzing and quantifying primary RPPA data. Here we present ways to identify and overcome some of the current issues associated with RPPA. We believe that using stringent quality controls, improved bioinformatics analysis and interpretation of primary RPPA data, this method will significantly contribute in generating new level of understanding about complex disorders at the level of systems biology. Published by Elsevier B.V.

  4. The association between adverse childhood experiences and adult traumatic brain injury/concussion: a scoping review.

    Science.gov (United States)

    Ma, Zechen; Bayley, Mark T; Perrier, Laure; Dhir, Priya; Dépatie, Lana; Comper, Paul; Ruttan, Lesley; Lay, Christine; Munce, Sarah E P

    2018-01-12

    Adverse childhood experiences are significant risk factors for physical and mental illnesses in adulthood. Traumatic brain injury/concussion is a challenging condition where pre-injury factors may affect recovery. The association between childhood adversity and traumatic brain injury/concussion has not been previously reviewed. The research question addressed is: What is known from the existing literature about the association between adverse childhood experiences and traumatic brain injury/concussion in adults? All original studies of any type published in English since 2007 on adverse childhood experiences and traumatic brain injury/concussion outcomes were included. The literature search was conducted in multiple electronic databases. Arksey and O'Malley and Levac et al.'s scoping review frameworks were used. Two reviewers independently completed screening and data abstraction. The review yielded six observational studies. Included studies were limited to incarcerated or homeless samples, and individuals at high-risk of or with mental illnesses. Across studies, methods for childhood adversity and traumatic brain injury/concussion assessment were heterogeneous. A positive association between adverse childhood experiences and traumatic brain injury occurrence was identified. The review highlights the importance of screening and treatment of adverse childhood experiences. Future research should extend to the general population and implications on injury recovery. Implications for rehabilitation Exposure to adverse childhood experiences is associated with increased risk of traumatic brain injury. Specific types of adverse childhood experiences associated with risk of traumatic brain injury include childhood physical abuse, psychological abuse, household member incarceration, and household member drug abuse. Clinicians and researchers should inquire about adverse childhood experiences in all people with traumatic brain injury as pre-injury health conditions can

  5. Comorbidity of Headache and Depression After Mild Traumatic Brain Injury.

    Science.gov (United States)

    Lucas, Sylvia; Smith, Brendon M; Temkin, Nancy; Bell, Kathleen R; Dikmen, Sureyya; Hoffman, Jeanne M

    2016-02-01

    To examine headache and depression over time in individuals who sustained mild traumatic brain injury (mTBI). Prevalence of headache and depression early after mTBI and at 1 year postinjury as well as the relationship between the two are evaluated. Headache is the most common physical symptom and depression is among the most common psychiatric diagnosis after traumatic brain injury regardless of severity. Headache and depression have been found to be two independent factors related to poor outcome after mTBI, yet there appears to be a paucity of research exploring the comorbidity of these two conditions after injury. Longitudinal survey design over 1 year of 212 participants with mTBI who were admitted to a Level 1 trauma center for observation or other system injuries. Depression was based on a score ≥10 on the Patient Health Questionnaire-9. Headache was based on participant report of new or worse-than-preinjury headache since hospitalization (baseline) or within the previous 3 months at 1 year postinjury. The prevalence of headache and depression at baseline was 64% (135/212) and 15% (31/212), respectively. The prevalence of headache and depression at 1 year was 68% (127/187) and 27% (50/187), respectively. The co-occurrence of headache and depression increased from 11% (23/212) at baseline to 25% (46/187) at 1 year. At 1 year, the risk ratio of individuals who had headache to be depressed was 5.43 (95% CI 2.05-14.40) compared to those without headache (P headache is consistently high over the first year after injury, rate of depression increased over the first year for those who were followed. Given the high rate of comorbidity, those with headache may develop depression over time. Evaluation for possible depression in those with headache after mTBI should be conducted to address both conditions over the year following injury. © 2016 American Headache Society.

  6. Dietary Virgin Olive Oil Reduces Blood Brain Barrier Permeability, Brain Edema, and Brain Injury in Rats Subjected to Ischemia-Reperfusion

    Directory of Open Access Journals (Sweden)

    Fatemeh Mohagheghi

    2010-01-01

    Full Text Available Recent studies suggest that dietary virgin olive oil (VOO reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in an in vivo study of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively. After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO. After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p < 0.05, and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p < 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls. Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.

  7. Regional mechanical properties of human brain tissue for computational models of traumatic brain injury.

    Science.gov (United States)

    Finan, John D; Sundaresh, Sowmya N; Elkin, Benjamin S; McKhann, Guy M; Morrison, Barclay

    2017-06-01

    To determine viscoelastic shear moduli, stress relaxation indentation tests were performed on samples of human brain tissue resected in the course of epilepsy surgery. Through the use of a 500µm diameter indenter, regional mechanical properties were measured in cortical grey and white matter and subregions of the hippocampus. All regions were highly viscoelastic. Cortical grey matter was significantly more compliant than the white matter or hippocampus which were similar in modulus. Although shear modulus was not correlated with the age of the donor, cortex from male donors was significantly stiffer than from female donors. The presented material properties will help to populate finite element models of the brain as they become more anatomically detailed. We present the first mechanical characterization of fresh, post-operative human brain tissue using an indentation loading mode. Indentation generates highly localized data, allowing structure-specific mechanical properties to be determined from small tissue samples resected during surgery. It also avoids pitfalls of cadaveric tissue and allows data to be collected before degenerative processes alter mechanical properties. To correctly predict traumatic brain injury, finite element models must calculate intracranial deformation during head impact. The functional consequences of injury depend on the anatomical structures injured. Therefore, morbidity depends on the distribution of deformation across structures. Accurate prediction of structure-specific deformation requires structure-specific mechanical properties. This data will facilitate deeper understanding of the physical mechanisms that lead to traumatic brain injury. Copyright © 2017 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.

  8. Misconceptions about traumatic brain injury among probation services.

    Science.gov (United States)

    O'Rourke, Conall; Linden, Mark A; Lohan, Maria

    2018-05-01

    The prevalence of traumatic brain injury (TBI) among offender populations is significantly higher than among the general population. Despite this, no study has yet assessed the knowledge of members of the probation service surrounding TBI. Knowledge was assessed among members of the Probation Board for Northern Ireland (PBNI) using a cross-sectional online version of the Common Misconceptions about TBI (CM-TBI) questionnaire. Mean total misconception scores, along with scores on four subdomains (recovery, sequelae, insight, and hidden injury) were calculated. Analysis of variance was used to explore differences in misconceptions based on the collected demographic information. The overall mean percentage of misconceptions for the group was 22.37%. The subdomain with the highest rate of misconceptions (38.21%) was insight into injury which covered misconceptions around offenders' self-awareness of injuries. Those who knew someone with a brain injury scored significantly higher in the CM-TBI total score, F(1,63) = 6.639, p = 0.012, the recovery subdomain, F(1,63) = 10.080, p = 0.002, and the insight subdomain, F(1,63) = 5.834, p = 0.019. Additionally, significant training deficits around TBI were observed among the probation service. This study is the first of its kind to examine the level of understanding around TBI within probation services. The findings reflect potential barriers to identification and rehabilitation of TBI for offenders coming into contact with the criminal justice system. A lack of identification coupled with misconceptions about TBI could lead to inaccurate court reporting with a subsequent impact on sentencing. Implications for Rehabilitation Despite being one of the first points of contact for offenders entering the criminal justice system, members of the probation service reported having no formal training on traumatic brain injury (TBI). The subdomain with the highest rate of misconceptions (insight into injury

  9. Effect of steroid on brain tumors and surround edemas : observation with regional cerebral blood volume (rCBV) maps of perfusion MRI

    International Nuclear Information System (INIS)

    Choi, Ju Youl; Sun, Joo Sung; Kim, Sun Yong; Kim, Ji Hyung; Suh, Jung Ho; Cho, Kyung Gi; Kim, Jang Sung

    2000-01-01

    To observe the hemodynamic change in brain tumors and peritumoral edemas after steroid treatment, and then investigate the clinical usefulness of perfusion MRI. We acquired conventional and perfusion MR images in 15 patients with various intracranial tumors (4 glioblastoma multiformes, 4 meningiomas, 3 metastatic tumors, 1 anaplastic ependymoma, 1 anaplastic astrocytoma, 1 hemangioblastoma, and 1 pilocytic astrocytoma). For perfusion MR imaging, a 1.5T unit employing the gradient-echo EPI technique was used, and further perfusion MR images were obtained 2-10 days after intravenous steroid therapy. After processing of the raw data, regional cerebral blood volume (rCBV) maps were reconstructed. The maps were visually evaluated by comparing relative perfusion in brain tumors and peritumoral edemas with that in contralateral white matter. Objective evaluations were performed by comparing the perfusion ratios of brain tumors and peritumoral edemas. Visual evaluations of rCBV maps, showed that in most brain tumors (67%, 10/15), perfusion was high before steroid treatment and showed in (80%, 12/15) decreased afterwards. Objective evaluation, showed that in all brain tumors, perfusion decreased. Visual evaluation of perfusion change in peritumoral edemas revealed change in only one case, but objective evaluation indicated that perfusion decreased significantly in all seven cases. rCBV maps acquired by perfusion MR imaging can provide hemodynamic information about brain tumors and peritumoral edemas. Such maps could prove helpful in the preoperative planning of brain tumor surgery and the monitoring of steroid effects during conservative treatment. (author)

  10. Acute traumatic brain-stem hemorrhage produced by sudden caudal displacement of the brain

    International Nuclear Information System (INIS)

    Mirvis, S.E.; Wolf, A.L.; Thompson, R.K.

    1990-01-01

    This paper determines in an experimental canine study and a clinical review, whether acute caudal displacement of the brain following blunt trauma produces hemorrhage in the rostral anterior midline of the brain stem by tethering the basilar to the fixed carotid arteries. In four dogs, a balloon catheter was suddenly inflated over the frontal lobe; in two, the carotid-basilar vascular connections were severed prior to balloon inflation. ICP was monitored during and after balloon inflation. Hemorrhage was verified by MR imaging and direct inspection of the fixed brain specimens. Admission CT scans demonstrating acute traumatic brain stem hemorrhage (TBH) in human patients were reviewed to determine the site of TBH, predominant site of impact, and neurologic outcome

  11. Specificity of Cognitive and Behavioral Complaints in Post-Traumatic Stress Disorder and Mild Traumatic Brain Injury

    Science.gov (United States)

    Pineau, Hélène; Marchand, André; Guay, Stéphane

    2015-01-01

    Characterization of cognitive and behavioral complaints is explored in Post-traumatic stress disorder (PTSD) and mild traumatic brain injury (MTBI) samples according to the severity of PTSD, depression and general anxiety conditions. Self-reported questionnaires on cognitive and behavioral changes are administered to PTSD, MTBI, MTBI/PTSD and control groups. Confounding variables are controlled. All groups report more complaints since the traumatic event. PTSD and MTBI/PTSD groups report more anxiety symptoms, depression and complaints compared to the MTBI group. Relatives of the PTSD group confirm most of the behavioral changes reported. Results suggest the utility of self-reported questionnaires to personalize cognitive and behavioral interventions in PTSD and MTBI to cope with the impacts of the traumatic event. PMID:25646994

  12. Specificity of Cognitive and Behavioral Complaints in Post-Traumatic Stress Disorder and Mild Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Hélène Pineau

    2015-01-01

    Full Text Available Characterization of cognitive and behavioral complaints is explored in Post-traumatic stress disorder (PTSD and mild traumatic brain injury (MTBI samples according to the severity of PTSD, depression and general anxiety conditions. Self-reported questionnaires on cognitive and behavioral changes are administered to PTSD, MTBI, MTBI/PTSD and control groups. Confounding variables are controlled. All groups report more complaints since the traumatic event. PTSD and MTBI/PTSD groups report more anxiety symptoms, depression and complaints compared to the MTBI group. Relatives of the PTSD group confirm most of the behavioral changes reported. Results suggest the utility of self-reported questionnaires to personalize cognitive and behavioral interventions in PTSD and MTBI to cope with the impacts of the traumatic event.

  13. Clinical review: Brain-body temperature differences in adults with severe traumatic brain injury

    Science.gov (United States)

    2013-01-01

    Surrogate or 'proxy' measures of brain temperature are used in the routine management of patients with brain damage. The prevailing view is that the brain is 'hotter' than the body. The polarity and magnitude of temperature differences between brain and body, however, remains unclear after severe traumatic brain injury (TBI). The focus of this systematic review is on the adult patient admitted to intensive/neurocritical care with a diagnosis of severe TBI (Glasgow Coma Scale score of less than 8). The review considered studies that measured brain temperature and core body temperature. Articles published in English from the years 1980 to 2012 were searched in databases, CINAHL, PubMed, Scopus, Web of Science, Science Direct, Ovid SP, Mednar and ProQuest Dissertations & Theses Database. For the review, publications of randomised controlled trials, non-randomised controlled trials, before and after studies, cohort studies, case-control studies and descriptive studies were considered for inclusion. Of 2,391 records identified via the search strategies, 37 were retrieved for detailed examination (including two via hand searching). Fifteen were reviewed and assessed for methodological quality. Eleven studies were included in the systematic review providing 15 brain-core body temperature comparisons. The direction of mean brain-body temperature differences was positive (brain higher than body temperature) and negative (brain lower than body temperature). Hypothermia is associated with large brain-body temperature differences. Brain temperature cannot be predicted reliably from core body temperature. Concurrent monitoring of brain and body temperature is recommended in patients where risk of temperature-related neuronal damage is a cause for clinical concern and when deliberate induction of below-normal body temperature is instituted. PMID:23680353

  14. Recommendations for diagnosing a mild traumatic brain injury: a National Academy of Neuropsychology education paper.

    Science.gov (United States)

    Ruff, Ronald M; Iverson, Grant L; Barth, Jeffrey T; Bush, Shane S; Broshek, Donna K

    2009-02-01

    A special interest group of the American Congress of Rehabilitation Medicine [ACRM; Mild Traumatic Brain Injury Committee. (1993). Definition of mild traumatic brain injury. Journal of Head Trauma Rehabilitation, 8 (3), 86-87.] was the first organized interdisciplinary group to advocate four specific criteria for the diagnosis of a mild traumatic brain injury (TBI). More recently, the World Health Organization (WHO) Collaborative Center Task Force on Mild Traumatic Brain Injury [Carroll, L. J., Cassidy, J. D., Holm, L., Kraus, J., & Coronado, V. G. (2004). Methodological issues and research recommendations for mild traumatic brain injury: the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. Journal of Rehabilitation Medicine, (Suppl. 43), 113-125.] conducted a comprehensive review of the definitions utilized in evidence-based studies with mild TBI patients. Based on this review, the WHO task force maintained the same four criteria but offered two modifications. The similarities and differences between these two definitions are discussed. The authors of the ACRM and the WHO definitions do not provide guidelines or specific recommendations for diagnosing the four criteria. Thus, we provide recommendations for assessing loss of consciousness, retrograde and post-traumatic amnesia, disorientation and confusion as well as clarification of the neurologic signs that can be indicative of a diagnosis of mild TBI. Finally, confounding factors mentioned in both definitions that should exclude a mild TBI diagnosis are summarized.

  15. Decreased light attenuation in cerebral cortex during cerebral edema detected using optical coherence tomography

    OpenAIRE

    Rodriguez, Carissa L. R.; Szu, Jenny I.; Eberle, Melissa M.; Wang, Yan; Hsu, Mike S.; Binder, Devin K.; Park, B. Hyle

    2014-01-01

    Abstract. Cerebral edema develops in response to a variety of conditions, including traumatic brain injury and stroke, and contributes to the poor prognosis associated with these injuries. This study examines the use of optical coherence tomography (OCT) for detecting cerebral edema in vivo. Three-dimensional imaging of an in vivo water intoxication model in mice was performed using a spectral-domain OCT system centered at 1300 nm. The change in attenuation coefficient was calculated and cere...

  16. Microglial-derived microparticles mediate neuroinflammation after traumatic brain injury.

    Science.gov (United States)

    Kumar, Alok; Stoica, Bogdan A; Loane, David J; Yang, Ming; Abulwerdi, Gelareh; Khan, Niaz; Kumar, Asit; Thom, Stephen R; Faden, Alan I

    2017-03-15

    Local and systemic inflammatory responses are initiated early after traumatic brain injury (TBI), and may play a key role in the secondary injury processes resulting in neuronal loss and neurological deficits. However, the mechanisms responsible for the rapid expansion of neuroinflammation and its long-term progression have yet to be elucidated. Here, we investigate the role of microparticles (MP), a member of the extracellular vesicle family, in the exchange of pro-inflammatory molecules between brain immune cells, as well as their transfer to the systemic circulation, as key pathways of inflammation propagation following brain trauma. Adult male C57BL/6 mice were subjected to controlled cortical impact TBI for 24 h, and enriched MP were isolated in the blood, while neuroinflammation was assessed in the TBI cortex. MP were characterized by flow cytometry, and MP content was assayed using gene and protein markers for pro-inflammatory mediators. Enriched MP co-cultured with BV2 or primary microglial cells were used for immune propagation assays. Enriched MP from BV2 microglia or CD11b-positive microglia from the TBI brain were stereotactically injected into the cortex of uninjured mice to evaluate MP-related seeding of neuroinflammation in vivo. As the neuroinflammatory response is developing in the brain after TBI, microglial-derived MP are released into the circulation. Circulating enriched MP from the TBI animals can activate microglia in vitro. Lipopolysaccharide stimulation increases MP release from microglia in vitro and enhances their content of pro-inflammatory mediators, interleukin-1β and microRNA-155. Enriched MP from activated microglia in vitro or CD11b-isolated microglia/macrophage from the TBI brain ex vivo are sufficient to initiate neuroinflammation following their injection into the cortex of naïve (uninjured) animals. These data provide further insights into the mechanisms underlying the development and dissemination of neuroinflammation after

  17. 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.

  18. Cystatin C Has a Dual Role in Post-Traumatic Brain Injury Recovery

    Directory of Open Access Journals (Sweden)

    Marina Martinez-Vargas

    2014-04-01

    Full Text Available Cathepsin B is one of the major lysosomal cysteine proteases involved in neuronal protein catabolism. This cathepsin is released after traumatic injury and increases neuronal death; however, release of cystatin C, a cathepsin inhibitor, appears to be a self-protective brain response. Here we describe the effect of cystatin C intracerebroventricular administration in rats prior to inducing a traumatic brain injury. We observed that cystatin C injection caused a dual response in post-traumatic brain injury recovery: higher doses (350 fmoles increased bleeding and mortality, whereas lower doses (3.5 to 35 fmoles decreased bleeding, neuronal damage and mortality. We also analyzed the expression of cathepsin B and cystatin C in the brains of control rats and of rats after a traumatic brain injury. Cathepsin B was detected in the brain stem, cerebellum, hippocampus and cerebral cortex of control rats. Cystatin C was localized to the choroid plexus, brain stem and cerebellum of control rats. Twenty-four hours after traumatic brain injury, we observed changes in both the expression and localization of both proteins in the cerebral cortex, hippocampus and brain stem. An early increase and intralysosomal expression of cystatin C after brain injury was associated with reduced neuronal damage.

  19. The AMPAR Antagonist Perampanel Attenuates Traumatic Brain Injury Through Anti-Oxidative and Anti-Inflammatory Activity.

    Science.gov (United States)

    Chen, Tao; Dai, Shu-Hui; Jiang, Zhi-Quan; Luo, Peng; Jiang, Xiao-Fan; Fei, Zhou; Gui, Song-Bai; Qi, Yi-Long

    2017-01-01

    Perampanel is a novel α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) antagonist, approved in over 35 countries as an adjunctive therapy for the treatment of seizures. Recently, it was found to exert protective effects against ischemic neuronal injury in vitro. In the present study, we investigated the potential protective effects of perampanel in a traumatic brain injury (TBI) model in rats. Oral administration with perampanel at a dose of 5 mg/kg exerted no major organ-related toxicities. We found that perampanel significantly attenuated TBI-induced brain edema, brain contusion volume, and gross motor dysfunction. The results of Morris water maze test demonstrated that perampanel treatment also improved cognitive function after TBI. These neuroprotective effects were accompanied by reduced neuronal apoptosis, as evidenced by decreased TUNEL-positive cells in brain sections. Moreover, perampanel markedly inhibited lipid peroxidation and obviously preserved the endogenous antioxidant system after TBI. In addition, enzyme-linked immunosorbent assay (ELISA) was performed at 4 and 24 h after TBI to evaluate the expression of inflammatory cytokines. The results showed that perampanel suppressed the expression of pro-inflammatory cytokines TNF-α and IL-1β, whereas increased the levels of anti-inflammatory cytokines IL-10 and TGF-β1. These data show that the orally active AMPAR antagonist perampanel affords protection against TBI-induced neuronal damage and neurological dysfunction through anti-oxidative and anti-inflammatory activity.

  20. Needs and Concerns of Male Combat Veterans with Mild Traumatic Brain Injury

    Science.gov (United States)

    2013-01-01

    if I had a bad headache, I’ll just take a couple of aspirin or something like that to try and make it go away . . . . Sometimes I just have to...The assessment and treatment of individuals with history of traumatic brain injury and post-traumatic stress disorder: A systematic review of the

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

    Science.gov (United States)

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

    2013-07-01

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

  2. Cognitive and psychosocial correlates of alexithymia following traumatic brain injury.

    Science.gov (United States)

    Henry, Julie D; Phillips, Louise H; Crawford, John R; Theodorou, Georgia; Summers, Fiona

    2006-01-01

    Changes in emotional and social behaviour are considered to be amongst the most common and debilitating consequences of traumatic brain injury (TBI). Little is known of the effects of TBI on alexithymia, which refers to impairment in aspects of understanding emotions. In the current study TBI patients (N=28) were compared with demographically matched healthy controls (N=31) on the Toronto Alexithymia Scale-20 (TAS-20), a measure that taps three distinct characteristics of the alexithymia concept; difficulty in identifying emotions, difficulty in describing emotions and externally oriented thinking. Patients and controls also completed measures of anxiety, depression, quality of life, and measures of fluency to assess executive function. Patients showed greater levels of alexithymia, in terms of difficulty identifying emotions and reduced introspection. Difficulty in identifying emotions was associated with poorer quality of life, even when depression and anxiety were controlled. Difficulty in identifying emotions was also uniquely associated with executive function deficits. Thus, although studies typically focus on aspects of cognitive change following head injury, these results lend support to Becerra et al.'s (Becerra, R., Amos, A., & Jongenelis, S. (2002). Organic alexithymia: a study of acquired emotional blindness. Brain Injury, 16, 633-645.) notion of an 'organic alexithymia', and suggest that more attention should be focused upon assessment of emotional change post-head injury.

  3. The influence of immunological stressors on traumatic brain injury.

    Science.gov (United States)

    Sun, Mujun; McDonald, Stuart J; Brady, Rhys D; O'Brien, Terence J; Shultz, Sandy R

    2018-03-01

    Traumatic brain injury (TBI) is a leading cause of death and disability worldwide, and typically involves a robust immune response. Although a great deal of preclinical research has been conducted to identify an effective treatment, all phase III clinical trials have been unsuccessful to date. These translational shortcomings are in part due to a failure to recognize and account for the heterogeneity of TBI, including how extracranial factors can influence the aftermath of TBI. For example, most preclinical studies have utilized isolated TBI models in young adult males, while clinical trials typically involve highly heterogeneous patient populations (e.g., different mechanisms of injury, a range of ages, presence of polytrauma or infection). This paper will review the current, albeit limited literature related to how TBI is affected by common concomitant immunological stressors. In particular, discussion will focus on whether extracranial trauma (i.e., polytrauma), infection, and age/immunosenescence can influence TBI pathophysiology, and thereby may result in a different brain injury than what would have occurred in an isolated TBI. It is concluded that these immunological stressors are all likely to be TBI modifiers that should be further studied and could impact translational treatment strategies. Copyright © 2018 Elsevier Inc. All rights reserved.

  4. Sexual behavior and its correlates after traumatic brain injury.

    Science.gov (United States)

    Turner, Daniel; Schöttle, Daniel; Krueger, Richard; Briken, Peer

    2015-03-01

    Traumatic brain injury (TBI) is one of the leading causes of permanent disability in young adults and is frequently accompanied by changes in sexual behaviors. Satisfying sexuality is an important factor for overall quality of life in people with disabilities. The purpose of this article is to review the studies evaluating the assessment, correlates and management of sexuality following TBI. The Brain Injury Questionnaire of Sexuality is the first validated questionnaire specifically developed for adults with TBI. A considerable amount of individuals with TBI show inappropriate sexual behaviors and sexual dysfunctions. Whereas inappropriate sexual behaviors are related to younger age, less social participation and more severe injuries, sexual dysfunctions show an association with higher fatigue, higher depression scores, less self-esteem and female sex. Healthcare professionals have suggested that because of discomfort at the individual or institutional level, sexual problems are often not sufficiently addressed and have suggested that a specialist should treat sexual problems. Although some important correlates of sexual problems could be identified, methodological differences across studies limit their comparability. Furthermore, there is an absence of evidence-based treatment strategies for addressing sexual problems. Therapeutic efforts should take into account the identified correlates of sexual problems following TBI.

  5. Position of probe determines prognostic information of brain tissue PO2 in severe traumatic brain injury.

    Science.gov (United States)

    Ponce, Lucido L; Pillai, Shibu; Cruz, Jovany; Li, Xiaoqi; Julia, H; Gopinath, Shankar; Robertson, Claudia S

    2012-06-01

    Monitoring brain tissue PO2 (PbtO2) is part of multimodality monitoring of patients with traumatic brain injury (TBI). However, PbtO2 measurement is a sampling of only a small area of tissue surrounding the sensor tip. To examine the effect of catheter location on the relationship between PbtO2 and neurological outcome. A total of 405 patients who had PbtO2 monitoring as part of standard management of severe traumatic brain injury were studied. The relationships between probe location and resulting PbtO2 and outcome were examined. When the probe was located in normal brain, PbtO2 averaged 30.8 ± 18.2 compared with 25.6 ± 14.8 mm Hg when placed in abnormal brain (P < .001). Factors related to neurological outcome in the best-fit logistic regression model were age, PbtO2 probe position, postresuscitation motor Glasgow Coma Scale score, and PbtO2 trend pattern. Although average PbtO2 was significantly related to outcome in univariate analyses, it was not significant in the final logistic model. However, the interaction between PbtO2 and probe position was statistically significant. When the PbtO2 probe was placed in abnormal brain, the average PbtO2 was higher in those with a favorable outcome, 28.8 ± 12.0 mm Hg, compared with those with an unfavorable outcome, 19.5 ± 13.7 mm Hg (P = .01). PbtO2 and outcome were not related when the probe was placed in normal-appearing brain. These results suggest that the location of the PbtO2 probe determines the PbtO2 values and the relationship of PbtO2 to neurological outcome.

  6. Posterior reversible encephalopathy syndrome (PRES, an acute neurological syndrome due to reversible multifactorial brain edema: a case report

    Directory of Open Access Journals (Sweden)

    Camilla Cicognani

    2013-04-01

    Full Text Available Background: The essential features of Posterior Reversible Encephalopathy Syndrome (PRES are headache, mental changes, seizures, visual symptoms and often arterial hypertension. Brain RMN typically shows cortico-sottocortical parieto-occipital edema, with a bilateral and symmetric distribution. PRES develops in clinical conditions as hypertensive encephalopathy, preeclampsia/ eclampsia, autoimmune diseases, after transplantation, infections and as an adverse effect of immunosuppressive drugs or chemotherapy. It usually completely reverses with treatment, although permanent sequelae are possible in case of delayed or missed diagnosis. Case report: We describe the case of a transsexual (M!F and tetraplegic patient, admitted for neck and low back pain. She suddenly developed headache, confusion, seizures and severe hypertension with normal blood tests. RMN showed multiple cortico-sottocortical areas of vasogenic and citotoxic edema in temporo-occipital, parietal, frontal, and cerebellar regions. Soon after the beginning of the antihypertensive therapy, clinical recovery was observed, as well as the disappearance of edema at RMN. Discussion and conclusions: Although PRES is usually associated with definite pathological conditions, it is not always the case, as was for the patient here described, who had no predisposing factors in her past clinical history, and presented hypertension only in the acute phase of the syndrome. Since, moreover, PRES usually presents with acute non specific features and it can be misdiagnosed with other serious diseases, the clinician will be helped by the knowledge of this syndrome to promptly start diagnostic workup and treatments, and avoid permanent neurological deficits.

  7. Cold Environment Exacerbates Brain Pathology and Oxidative Stress Following Traumatic Brain Injuries: Potential Therapeutic Effects of Nanowired Antioxidant Compound H-290/51.

    Science.gov (United States)

    Sharma, Aruna; Muresanu, Dafin F; Lafuente, José Vicente; Sjöquist, Per-Ove; Patnaik, Ranjana; Ryan Tian, Z; Ozkizilcik, Asya; Sharma, Hari S

    2018-01-01

    The possibility that traumatic brain injury (TBI) occurring in a cold environment exacerbates brain pathology and oxidative stress was examined in our rat model. TBI was inflicted by making a longitudinal incision into the right parietal cerebral cortex (2 mm deep and 4 mm long) in cold-acclimatized rats (5 °C for 3 h daily for 5 weeks) or animals at room temperature under Equithesin anesthesia. TBI in cold-exposed rats exhibited pronounced increase in brain lucigenin (LCG), luminol (LUM), and malondialdehyde (MDA) and marked pronounced decrease in glutathione (GTH) as compared to identical TBI at room temperature. The magnitude and intensity of BBB breakdown to radioiodine and Evans blue albumin, edema formation, and neuronal injuries were also exacerbated in cold-exposed rats after injury as compared to room temperature. Nanowired delivery of H-290/51 (50 mg/kg) 6 and 8 h after injury in cold-exposed group significantly thwarted brain pathology and oxidative stress whereas normal delivery of H-290/51 was neuroprotective after TBI at room temperature only. These observations are the first to demonstrate that (i) cold aggravates the pathophysiology of TBI possibly due to an enhanced production of oxidative stress, (ii) and in such conditions, nanodelivery of antioxidant compound has superior neuroprotective effects, not reported earlier.

  8. Effects of propranolol and clonidine on brain edema, blood-brain barrier permeability, and endothelial glycocalyx disruption after fluid percussion brain injury in the rat

    DEFF Research Database (Denmark)

    Genét, Gustav Folmer; Bentzer, Peter; Hansen, Morten Bagge

    2018-01-01

    ), vehicle (n = 16), or sham (n = 5) for 24 hours. Primary outcome was brain water content at 24 hours. Secondary outcomes were blood-brain barrier permeability and plasma levels of syndecan-1 (glycocalyx disruption), cell damage (histone-complexed DNA fragments), epinephrine, norepinephrine, and animal...... motor function. RESULTS: We found no difference in brain water content (mean ± SD) between propranolol (80.8 ± 0.3%; 95% confidence interval [CI], 80.7-81.0) and vehicle (81.1 ± 0.6%; 95% CI, 80.8-81.4) (p = 0.668) or between propranolol/clonidine (80.8 ± 0.3%; 95% CI, 80.7-81.0) and vehicle (p = 0...... beta-blockade with propranolol or the combination of propranolol and the alfa2-agonist clonidine on brain water content. The novel finding of an increase in plasma concentrations of epinephrine and syndecan-1 after propranolol treatment in traumatic brain injury is of unclear significance and should...

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

    NARCIS (Netherlands)

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

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

  10. Mild Traumatic Brain Injury in U.S. Soldiers Returning from Iraq

    National Research Council Canada - National Science Library

    Hoge, Charles W; McGurk, Dennis; Thomas, Jeffrey L; Cox, Anthony L; Engel, Charles C; Castro, Carl A

    2008-01-01

    .... Validated clinical instruments were used to compare soldiers reporting mild traumatic brain injury, defined as an injury with loss of consciousness or altered mental status (e.g., dazed or confused...

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

    DEFF Research Database (Denmark)

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

    2013-01-01

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

  12. An audit of traumatic brain injury (TBI) in a busy developing-world ...

    African Journals Online (AJOL)

    Guidelines_ · Management_2007w_bookmarks.pdf (accessed 8 May 2017). 8. Cushman JG, Agarwal N, Fabian T, et al. Practice management guidelines for the management of mild traumatic brain injury: The EAST Practice Management ...

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

    DEFF Research Database (Denmark)

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

    2012-01-01

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

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

    DEFF Research Database (Denmark)

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

    2007-01-01

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

  15. Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI)

    DEFF Research Database (Denmark)

    Maas, Andrew I R; Menon, David K; Steyerberg, Ewout W

    2015-01-01

    BACKGROUND: Current classification of traumatic brain injury (TBI) is suboptimal, and management is based on weak evidence, with little attempt to personalize treatment. A need exists for new precision medicine and stratified management approaches that incorporate emerging technologies. OBJECTIVE...

  16. Psychological outcome after severe traumatic brain injury in adolescents and young adults

    DEFF Research Database (Denmark)

    Doser, Karoline; Poulsen, Ingrid; Wuensch, Alexander

    2018-01-01

    OBJECTIVES: Young individuals surviving severe traumatic brain injury (TBI) frequently experience a wide range of cognitive, emotional and behavioural consequences. This cross-sectional follow-up study investigated psychological outcome of young survivors in the chronic phase, and whether...

  17. Severe traumatic brain injury in children: an evidence-based review of emergency department management [digest].

    Science.gov (United States)

    Morrissey, Kirsten; Fairbrother, Hilary; Vazquez, Michelle N

    2016-10-22

    More than 1.7 million traumatic brain injuries occur in adults and children each year in the United States, with approximately 30% occurring in children aged digest of Pediatric Emergency Medicine Practice].

  18. Neuropsychiatric Disturbances and Hypopituitarism After Traumatic Brain Injury in an Elderly Man

    Directory of Open Access Journals (Sweden)

    Yi-Cheng Chang

    2006-01-01

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

  19. Dementia resulting from traumatic brain injury: what is the pathology?

    Science.gov (United States)

    Shively, Sharon; Scher, Ann I; Perl, Daniel P; Diaz-Arrastia, Ramon

    2012-10-01

    Traumatic brain injury (TBI) is among the earliest illnesses described in human history and remains a major source of morbidity and mortality in the modern era. It is estimated that 2% of the US population lives with long-term disabilities due to a prior TBI, and incidence and prevalence rates are even higher in developing countries. One of the most feared long-term consequences of TBIs is dementia, as multiple epidemiologic studies show that experiencing a TBI in early or midlife is associated with an increased risk of dementia in late life. The best data indicate that moderate and severe TBIs increase risk of dementia between 2- and 4-fold. It is less clear whether mild TBIs such as brief concussions result in increased dementia risk, in part because mild head injuries are often not well documented and retrospective studies have recall bias. However, it has been observed for many years that multiple mild TBIs as experienced by professional boxers are associated with a high risk of chronic traumatic encephalopathy (CTE), a type of dementia with distinctive clinical and pathologic features. The recent recognition that CTE is common in retired professional football and hockey players has rekindled interest in this condition, as has the recognition that military personnel also experience high rates of mild TBIs and may have a similar syndrome. It is presently unknown whether dementia in TBI survivors is pathophysiologically similar to Alzheimer disease, CTE, or some other entity. Such information is critical for developing preventive and treatment strategies for a common cause of acquired dementia. Herein, we will review the epidemiologic data linking TBI and dementia, existing clinical and pathologic data, and will identify areas where future research is needed.

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

    Science.gov (United States)

    Bigler, Erin D

    2016-01-01

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

  1. Social Competence at Two Years after Childhood Traumatic Brain Injury.

    Science.gov (United States)

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

    2017-07-15

    Children with traumatic brain injury (TBI) are at risk for social impairment, but research has yet to document the trajectory of these skills post-injury and factors that may predict social problems. This study addressed these gaps in knowledge, reporting on findings from a prospective, longitudinal follow-up study that investigated social outcomes post-injury and explored factors contributing to these outcomes at two years post-injury. The sample included 113 children, 74 with TBI and 39 typically developing (TD) controls. TBI participants were recruited on presentation to the hospital. Parents rated pre-injury function at that time, and all children underwent magnetic resonance imaging (MRI). Participants were followed up at two years post-injury. Outcomes were social adjustment, social participation, social relationships, and social cognition. Predictors of social outcomes examined included brain lesion characteristics, child cognition (6 months post-TBI), and behavior and environmental factors (pre-injury and two years). Reduced social adjustment (p = 0.011) and social participation (p Poor social adjustment was predicted by externalizing behavior problems and younger age at injury. Reduced social participation was linked to internalizing behavior problems. Greater lesion volume, lower socioeconomic status, and family burden contributed to poorer social relationships, whereas age at injury predicted social cognition. Within the TBI group, 23% of children exhibited social impairments. Younger age at injury, greater pre-injury, and current behavior problems and family dysfunction, and poorer intelligence quotient (IQ), processing speed, and empathy were linked to impairment. Further follow-up is required to track social recovery and the influences of cognition, brain, and environment over time.

  2. 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.

  3. Neuroinflammatory responses to traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Paiva WS

    2015-03-01

    Full Text Available Wellingson Silva Paiva,1 Angelica Duarte Correia,2 Suely Kazue Marie2 1Division of Neurological Surgery, 2Laboratory of Medical Investigation 15, Department of Neurology, University of São Paulo Medical School, Sao Paulo, Brazil We read with great interest the recent study by Lozano et al1 published in the Neuropsychiatric Disease and Treatment. The recovery after traumatic brain injury (TBI is related to severity of the initial injury (primary injury and the presence of secondary injury.2 Evidences suggest that inflammation, oxidative stress, excitotoxicity, apoptosis, and neuroendocrine responses play an important role in the development of secondary brain injury.3 Therefore, an important part in the management of patients with TBI is trying to minimize the occurrence of deleterious secondary lesions. Lozano et al’s1 paper focused on the role of neuroinflammation in brain injury.Although some studies have described experimental drugs which may eventually have neuroprotective effects in patients with TBI,2–4 there is currently no approved pharmacological treatment for neuroinflammatory effects of the acute phase of the injury. The dissociation between experimental data with positive results and consecutive clinical trials with negative results leads to a dilemma for the treatment of patients with TBI. And, we agree with Lozano et al1 that further clarification of the neuroinflammatory mechanisms could be the basis for addressing the gap between bench and clinical results to provide better treatment and reduce death and sequelae of TBI.View original paper by Lozano and colleagues.

  4. An Epidemiologic Study of Traumatic Brain Injuries in Emergency Department

    Directory of Open Access Journals (Sweden)

    Vahid Monsef Kasmaei

    2014-09-01

    Full Text Available Introduction: Traumatic brain injuries (TBI are one of the most important causes of death in patients under the age of 25 years and is responsible for one third of total deaths caused by trauma. Therefore, knowing its epidemiologic pattern in different populations seems vital. Therefore, this study aims to examine the epidemiologic pattern of TBI in emergency department. Methods: In this cross-sectional study, the profiles of 1000 patients affected by TBI were selected using simple random sampling. The examined variables in this study included demographic, season, mechanism of injury, accompanying injuries, level of consciousness, hospitalization duration, computed tomography (CT scan results, needing surgery, admission to intensive care unit, and outcome of the patient. In the end, independent risk factors for the death of patients were determined. Results: 1000 patients suffering from were studied (81.8% male; mean age 38.5±21.7 years. The frequency of their referral to hospital in spring (31.4% was more (p<0.01. 45.9% of the patients had a level of consciousness less than 9 based on the Glasgow Coma Scale (GCS. Subdural (45.9% and epidural bleeding (23.7% were the most common findings in CT scans in this study (p<0.001. Finally, 233 (23.3% of the patients were dead. Over 60 years of age, falling and motorcycle accidents, intracranial hemorrhage accompanied by brain contusion, subdural bleeding, a GCS of less than 9, and the need to be admitted to intensive care unit were independent risk factors of death in TBI. Conclusion: Age Over 60 years, falling and motorcycle accidents, intracranial hemorrhage accompanied by brain contusion, subdural bleeding, a GCS of less than 9, and need to be admitted to intensive care unit were independent risk factors for the death in TBI patients.

  5. The brain in acute liver failure. A tortuous path from hyperammonemia to cerebral edema

    DEFF Research Database (Denmark)

    Bjerring, Peter Nissen; Eefsen, Martin; Hansen, Bent Adel

    2008-01-01

    Acute liver failure (ALF) is a condition with an unfavourable prognosis. Multiorgan failure and circulatory collapse are frequent causes of death, but cerebral edema and intracranial hypertension (ICH) are also common complications with a high risk of fatal outcome. The underlying pathogenesis has...

  6. Mycotic Aneurysm of External Carotid Artery following Traumatic Brain Injury: Case Report and Review of Literature

    OpenAIRE

    Khalili, Hosseinali; Derakhshan, Nima; Malekmohammadi, Zahed; Ghaffarpasand, Fariborz

    2014-01-01

    Mycotic aneurysm of external carotid artery is extremely rare. We herein report a case of external carotid artery (ECA) aneurysm following severe traumatic brain injury. A 24-year-old man with severe traumatic brain injury (TBI) following a car accident was referred to Rajaee Trauma Center Emergency Room affiliated to Shiraz University of Medical Sciences in Shiraz, Iran. He underwent ventriculostomy on arrival for intracerebral pressure (ICP) monitoring and for a second time due to hydroceph...

  7. Life satisfaction 6–15 years after a traumatic brain injury

    OpenAIRE

    Jacobsson, Lars; Lexell, Jan

    2013-01-01

    Objectives: To assess satisfaction with life as a whole and 10 domains of life satisfaction in Swedish individuals after a traumatic brain injury, to describe the relationship with demographic, social and injury related variables, and to compare the level of life satisfaction with a Swedish reference sample. Subjects: Fifty-one men and sixteen women, 6-15 years after a traumatic brain injury. Methods: Life Satisfaction Questionnaire (LiSat-11). Results: Many of the participants were, to some ...

  8. Motor Evoked Potentials of Trunk Muscles in Traumatic Brain Injury Patients

    OpenAIRE

    Seo, Min-Ho; Park, Sung-Hee; Ko, Myoung-Hwan; Seo, Jeong-Hwan

    2011-01-01

    Objective To evaluate the motor innervation of trunk muscles in traumatic brain injury patients. Method Twenty patients (12 men and 8 women) with traumatic brain injury were enrolled in this study. Their mean age was 41 years. Motor evoked potentials (MEPs) were performed on the motor cortex. Electromyographic activities were recorded from the bilateral rectus abdominis muscles, the external oblique abdominal muscles, and the 4th and 9th thoracic erector spinae muscles. The onset latency and ...

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

    DEFF Research Database (Denmark)

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

    2013-01-01

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

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

    LENUS (Irish Health Repository)

    Nichol, Alistair

    2015-02-08

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

  11. Mild Traumatic Brain Injury: Lessons Learned from Clinical, Sports, and Combat Concussions

    OpenAIRE

    Kelly, Judy C.; Amerson, Efland H.; Barth, Jeffrey T.

    2012-01-01

    Over the past forty years, a tremendous amount of information has been gained on the mechanisms and consequences of mild traumatic brain injuries. Using sports as a laboratory to study this phenomenon, a natural recovery curve emerged, along with standards for managing concussions and returning athletes back to play. Although advances have been made in this area, investigation into recovery and return to play continues. With the increase in combat-related traumatic brain injuries in the milit...

  12. The effect of pre-nutrition of hydroalcoholic extractof Origanum vulgare on brain edema and neurologic deficits in a rat stroke model

    Directory of Open Access Journals (Sweden)

    Meysam Foroozandeh

    2015-10-01

    Full Text Available Background and Aim: Stroke is one of the most important factors of mortality and disability in the world. Free radicals are produced following ischemic stroke and they play a central role in breaking the blood-brain barrier and  causing brain edema formation. The aim of the current study was to evaluate the effect of hydro- alcoholic extract of Origanum vulgare on brain edema and neurologic deficit in a rat stroke model. Materials and Methods: In thisexperimental study, 35 male Wistar rats were randomly divided into 5 equal groups.  The first  two groups (control and Sham received distilled water, while three treatment groups received oral Origanum vulgare extract for 30days (50,75and 100 mg/kgdaily, respectively.  Two hours after the last dose of Origanum vulgare extract,each main group underwent  a 60 min middle cerebral artery occlusion.  Then, the assessment of blood brain edema, and neurologic deficits analysis were done . Brain edema (brain water content was analyzed by One-Way ANOVA using LSD method and neurologic deficits analysis by means of Mann-Whitney U, and P<0.05 was taken as the significant level. Results: Origanum vulgare extract reduced brain edema in the experimental groups of 50 (82.49±0.47, 75 (80.89±0.63 and 100 mg/kg/day (80.80±0.66 compared to the control group (84.46±0.67. The neurologic deficit scores in the experimental groups of 75and 100mg/kg/day, compared with control group, but neurologic deficit scores did not affect the group receiving the dose 50 mg/kg. Conclusion:  The obtained data indicate that Origanum vulgar extract via reduction of brain edema and neurologic deficits scorescan have a protective effect on the stroke model.

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

    Directory of Open Access Journals (Sweden)

    Kevin F. Yee

    2016-01-01

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

  14. Motor performance in physically well-recovered men with traumatic brain injury.

    Science.gov (United States)

    Rinne, Marjo B; Pasanen, Matti E; Vartiainen, Matti V; Lehto, Tommi M; Sarajuuri, Jaana M; Alaranta, Hannu T

    2006-07-01

    The primary aim of this study was to compare the motor performance of physically well-recovered men with traumatic brain injury with that of healthy men. Cross-sectional study in a national rehabilitation centre. Static and dynamic balance, agility and rhythm co-ordination of men with traumatic brain injury (n=34) and healthy controls (n=36) were assessed. Between-group differences in dynamic balance and agility were analysed by analysis of covariance and differences in static balance and rhythm co-ordination by logistic regression analysis. Cut-off points for clinical screening were determined by receiver operating characteristics analyses. Men with traumatic brain injury had impaired balance and agility compared with healthy men and in a rhythm co-ordination test they had difficulties in starting and sustaining simultaneous rhythmical movements of hands and feet. In receiver operating characteristics analyses a running figure-of-eight test (agility), tandem walking forwards (dynamic balance) and rhythm co-ordination test with fast tempo were found the most sensitive and specific for distinguishing between men with traumatic brain injury and the healthy men. The impairments in motor performance of physically well-recovered patients with traumatic brain injury were obvious. The results of this study extend the knowledge of problems in motor performance among patients with traumatic brain injury and provide further information for clinical rehabilitation.

  15. Sleep Disorders Associated With Mild Traumatic Brain Injury Using Sport Concussion Assessment Tool 3.

    Science.gov (United States)

    Tkachenko, Nataliya; Singh, Kanwaljit; Hasanaj, Lisena; Serrano, Liliana; Kothare, Sanjeev V

    2016-04-01

    Sleep problems affect 30% to 80% of patients with mild traumatic brain injury. We assessed the prevalence of sleep disorders after mild traumatic brain injury and its correlation with other symptoms. Individuals with mild traumatic brain injury were assessed at the New York University Concussion Center during 2013-2014 with the Sports Concussion Assessment Tool, third edition, data following mild traumatic brain injury. The relationship between sleep problems (drowsiness, difficulty falling asleep, fatigue or low energy), psychiatric symptoms (sadness, nervousness or anxiousness), headache, and dizziness were analyzed by Spearman correlation and logistic regression using moderate to severe versus none to mild categorization. Ninety-three patients were retrospectively considered. The most common injury causes were falls (34.4%) and motor vehicle accidents (21.5%). There was a positive correlation between dizziness, headache, psychiatric problems (sadness, anxiety, irritability), and sleep problems (fatigue, drowsiness, and difficulty falling asleep) (P sleep symptoms (P Sleep symptoms became more severe with increased time interval from mild traumatic brain injury to Sport Concussion Assessment Tool 3 administration (odds ratio = 1.005, 1.006, and 1.008, P sleep disorders following mild traumatic brain injury and should be counseled and initiated with early interventions. Copyright © 2016 Elsevier Inc. All rights reserved.

  16. The prevalence of traumatic brain injury in the homeless community in a UK city.

    Science.gov (United States)

    Oddy, Michael; Moir, Jane Frances; Fortescue, Deborah; Chadwick, Sarah

    2012-01-01

    The main aim of the study was to investigate the prevalence of traumatic brain injury in a sample of homeless individuals. The researchers employed a cross-sectional survey design and contacted 12 organizations providing services for homeless individuals across a city in the UK. The sample included 100 homeless participants (75 males and 25 females) who met the inclusion criteria. A matched control group (n = 100) of individuals who were not homeless was also recruited. A questionnaire was administered to all participants to elicit information relating to history of possible traumatic brain injury. Results indicated that a significantly higher number of homeless participants (48%) reported a history of traumatic brain injury than control participants (21%). Of those homeless participants, 90% indicated they had sustained their first traumatic brain injury before they were homeless. These findings suggest that rates of traumatic brain injury are much higher among the homeless population than in the general population and that sustaining a traumatic brain injury may be a risk factor for homelessness.

  17. Predicting institutionalization after traumatic brain injury inpatient rehabilitation.

    Science.gov (United States)

    Eum, Regina S; Seel, Ronald T; Goldstein, Richard; Brown, Allen W; Watanabe, Thomas K; Zasler, Nathan D; Roth, Elliot J; Zafonte, Ross D; Glenn, Mel B

    2015-02-15

    Risk factors contributing to institutionalization after inpatient rehabilitation for people with traumatic brain injury (TBI) have not been well studied and need to be better understood to guide clinicians during rehabilitation. We aimed to develop a prognostic model that could be used at admission to inpatient rehabilitation facilities to predict discharge disposition. The model could be used to provide the interdisciplinary team with information regarding aspects of patients' functioning and/or their living situation that need particular attention during inpatient rehabilitation if institutionalization is to be avoided. The study population included 7219 patients with moderate-severe TBI in the Traumatic Brain Injury Model Systems (TBIMS) National Database enrolled from 2002-2012 who had not been institutionalized prior to injury. Based on institutionalization predictors in other populations, we hypothesized that among people who had lived at a private residence prior to injury, greater dependence in locomotion, bed-chair-wheelchair transfers, bladder and bowel continence, feeding, and comprehension at admission to inpatient rehabilitation programs would predict institutionalization at discharge. Logistic regression was used, with adjustment for demographic factors, proxy measures for TBI severity, and acute-care length-of-stay. C-statistic and predictiveness curves validated a five-variable model. Higher levels of independence in bladder management (adjusted odds ratio [OR], 0.88; 95% CI 0.83, 0.93), bed-chair-wheelchair transfers (OR, 0.81 [95% CI, 0.83-0.93]), and comprehension (OR, 0.78 [95% CI, 0.68, 0.89]) at admission were associated with lower risks of institutionalization on discharge. For every 10-year increment in age was associated with a 1.38 times higher risk for institutionalization (95% CI, 1.29, 1.48) and living alone was associated with a 2.34 times higher risk (95% CI, 1.86, 2.94). The c-statistic was 0.780. We conclude that this simple model

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

    Directory of Open Access Journals (Sweden)

    Simarjot K Dhaliwal

    2015-08-01

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

  19. Determinants of Glasgow outcome scale in patients with severe traumatic brain injury for better quality of life

    Science.gov (United States)

    Dharmajaya, R.; Sari, D. K.; Ganie, R. A.

    2018-03-01

    Primary and secondary brain injury may occur with severe traumatic brain injury. Secondary traumatic brain injury results in a more severe effect compared to primary traumatic brain injury. Therefore, prevention of secondary traumatic brain injury is necessary to obtain maximum therapeutic results and accurate determination of prognosis and better quality of life. This study aimed to determine accurate and noninvasive prognostic factors in patients with severe traumatic brain injury. It was a cohort study on 16 subjects. Intracranial pressure was monitored within the first 24 hours after traumatic brain injury. Examination of Brain-Derived Neurotrophic Factor (BDNF) and S100B protein were conducted four times. The severity of outcome was evaluated using Glasgow Outcome Scale (GOS) three months after traumatic brain injury. Intracranial pressure measurement performed 24 hours after traumatic brain injury, low S100B protein (6.16pg/ml) 48 hours after injury indicate good prognosis and were shown to be significant predictors (pquality of GOS. The conclusion is patient with a moderate increase in intracranial pressure Intracranial pressure S100B protein, being inexpensive and non-invasive, can substitute BDNF and intracranial pressure measurements as a tool for determining prognosis 120 hours following traumatic brain injury.

  20. Traumatic Brain Injury Profile of an Elderly Population in Puerto Rico.

    Science.gov (United States)

    Fernández-Abinader, Jose A; González-Colón, Karolyn; Feliciano, Caleb E; Mosquera-Soler, Ana María

    2017-12-01

    Describe the types of traumatic brain injury secondary to falls sustained by the members of an elderly population who received services at the Puerto Rico Medical Center and the demographic profile of that population. A group of 332 adults (60 years and over) assessed for traumatic brain injury secondary to falls suffered in 2013 were included in the analysis. The cases were retrieved from the computerized database of the Neurosurgery Section. We analyzed information such as age, gender, type of traumatic brain injury, mechanism of injury, and the performance of surgery (if applicable). Descriptive analysis was performed to derive a general profile of elderly adults who presented with traumatic brain injury secondary to falls. The sample consisted of 332 elderly adults: 73% were men and 27% were women. The mean age was 76.74 (SD=9.95) years: 75.67 (SD=9.78) for men and 79.13 (SD=10.02) for women. The most common traumatic brain injury was subdural hematoma (51%) and the mechanism of injury most prevalent was the groundlevel fall (83%). Other traumatic brain injuries included traumatic subarachnoid hemorrhages (14%), cerebral contusions (18%) and epidural hematomas (3%). Of all the cases, 52% had were managed surgically. The elderly population is growing and the risk of falls increases with advancing age. Recurrent falls are an important cause of morbidity, and mortality rates oscillate from 6 to 18%. Elderly patients have longer rehabilitation times, incur more expenses, and have greater levels of disability. This study provides a platform for future epidemiological studies to help develop strategies for the prevention of traumatic brain injury in older adults.

  1. Salidroside improves behavioral and histological outcomes and reduces apoptosis via PI3K/Akt signaling after experimental traumatic brain injury.

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    Szu-Fu Chen

    Full Text Available Traumatic brain injury (TBI induces a complex sequence of apopototic cascades that contribute to secondary tissue damage. The aim of this study was to investigate the effects of salidroside, a phenolic glycoside with potent anti-apoptotic properties, on behavioral and histological outcomes, brain edema, and apoptosis following experimental TBI and the possible involvement of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt signaling pathway.Mice subjected to controlled cortical impact injury received intraperitoneal salidroside (20, or 50 mg/kg or vehicle injection 10 min after injury. Behavioral studies, histology analysis and brain water content assessment were performed. Levels of PI3K/Akt signaling-related molecules, apoptosis-related proteins, cytochrome C (CytoC, and Smac/DIABLO were also analyzed. LY294002, a PI3K inhibitor, was administered to examine the mechanism of protection. The protective effect of salidroside was also investigated in primary cultured neurons subjected to stretch injury. Treatment with 20 mg/kg salidroside significantly improved functional recovery and reduced brain tissue damage up to post-injury day 28. Salidroside also significantly reduced neuronal death, apoptosis, and brain edema at day 1. These changes were associated with significant decreases in cleaved caspase-3, CytoC, and Smac/DIABLO at days 1 and 3. Salidroside increased phosphorylation of Akt on Ser473 and the mitochondrial Bcl-2/Bax ratio at day 1, and enhanced phosphorylation of Akt on Thr308 at day 3. This beneficial effect was abolished by pre-injection of LY294002. Moreover, delayed administration of salidroside at 3 or 6 h post-injury reduced neuronal damage at day 1. Salidroside treatment also decreased neuronal vulnerability to stretch-induced injury in vitro.Post-injury salidroside improved long-term behavioral and histological outcomes and reduced brain edema and apoptosis following TBI, at least partially via the PI3K/Akt signaling

  2. Wogonin improves histological and functional outcomes, and reduces activation of TLR4/NF-κB signaling after experimental traumatic brain injury.

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    Chien-Cheng Chen

    Full Text Available Traumatic brain injury (TBI initiates a neuroinflammatory cascade that contributes to neuronal damage and behavioral impairment. This study was undertaken to investigate the effects of wogonin, a flavonoid with potent anti-inflammatory properties, on functional and histological outcomes, brain edema, and toll-like receptor 4 (TLR4- and nuclear factor kappa B (NF-κB-related signaling pathways in mice following TBI.Mice subjected to controlled cortical impact injury were injected with wogonin (20, 40, or 50 mg·kg(-1 or vehicle 10 min after injury. Behavioral studies, histology analysis, and measurement of blood-brain barrier (BBB permeability and brain water content were carried out to assess the effects of wogonin. Levels of TLR4/NF-κB-related inflammatory mediators were also examined. Treatment with 40 mg·kg(-1 wogonin significantly improved functional recovery and reduced contusion volumes up to post-injury day 28. Wogonin also significantly reduced neuronal death, BBB permeability, and brain edema beginning at day 1. These changes were associated with a marked reduction in leukocyte infiltration, microglial activation, TLR4 expression, NF-κB translocation to nucleus and its DNA binding activity, matrix metalloproteinase-9 activity, and expression of inflammatory mediators, including interleukin-1β, interleukin-6, macrophage inflammatory protein-2, and cyclooxygenase-2.Our results show that post-injury wogonin treatment improved long-term functional and histological outcomes, reduced brain edema, and attenuated the TLR4/NF-κB-mediated inflammatory response in mouse TBI. The neuroprotective effects of wogonin may be related to modulation of the TLR4/NF-κB signaling pathway.

  3. Delayed traumatic hematomas of the brain: the early manifestations of CT

    International Nuclear Information System (INIS)

    Liu Shuyan; Tang Guangjian; Fu Jiazhen; Xu Bing; Yin Yanyu

    2002-01-01

    Objective: To study the CT manifestations of delayed traumatic hematomas of the brain and evaluate their diagnostic significance in predicting the delayed traumatic brain hematoma. Methods: The manifestations of initial CT studies and follow-up CT examinations of 31 delayed traumatic brain hematomas were analyzed. Another 50 CT studies of head trauma without delayed brain hematomas were included randomly as control. Results: The abnormal findings of CT studies of the 31 delayed traumatic brain hematomas included: (1) Decreased density of the local brain parenchyma and disappeared difference between gray and white matter of the same area in 18 cases; (2) Local subarachnoid space hemorrhage in 24 cases; (3) Slight mass effect of local brain parenchyma in 16 cases. (4) Subdural hematoma in 9 cases. The locations of the abnormalities were roughly the same with the delayed hematoma except one local subarachnoid space hemorrhage, which was in the opposite of the delayed hematoma. The appearing rate of those abnormal findings in the control group was low and the difference was statistically significant. Conclusion: The decrease of density of local brain parenchyma, the disappeared difference between the gray and white matter, local subarachnoid space hemorrhage, and local swollen of brain presented in the initial CT study of the patient with heat trauma should be taken as indicators of delayed hemorrhage of the same area of brain, and it is necessary to do follow-up CT studies to exclude it

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

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

    2013-09-15

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

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

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

    2013-01-01

    This study compared the difference in brain structure in 12 mine disaster survivors with chronic post-traumatic stress disorder, 7 cases of improved post-traumatic stress disorder symptoms, and 14 controls who experienced the same mine disaster but did not suffer post-traumatic stress disorder, using the voxel-based morphometry method. The correlation between differences in brain structure and post-traumatic stress disorder symptoms was also investigated. Results showed that the gray matter volume was the highest in the trauma control group, followed by the symptoms-improved group, and the lowest in the chronic post-traumatic stress disorder group. Compared with the symptoms-improved group, the gray matter volume in the lingual gyrus of the right occipital lobe was reduced in the chronic post-traumatic stress disorder group. Compared with the trauma control group, the gray matter volume in the right middle occipital gyrus and left middle frontal gyrus was reduced in the symptoms-improved group. Compared with the trauma control group, the gray matter volume in the left superior parietal lobule and right superior frontal gyrus was reduced in the chronic post-traumatic stress disorder group. The gray matter volume in the left superior parietal lobule was significantly positively correlated with the State-Trait Anxiety Inventory subscale score in the symptoms-improved group and chronic post-traumatic stress disorder group (r = 0.477, P = 0.039). Our findings indicate that (1) chronic post-traumatic stress disorder patients have gray matter structural damage in the prefrontal lobe, occipital lobe, and parietal lobe, (2) after post-traumatic stress, the disorder symptoms are improved and gray matter structural damage is reduced, but cannot recover to the trauma-control level, and (3) the superior parietal lobule is possibly associated with chronic post-traumatic stress disorder. Post-traumatic stress disorder patients exhibit gray matter abnormalities. PMID:25206550

  6. Genomic responses in rat cerebral cortex after traumatic brain injury

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    Mathiesen Tiit

    2005-11-01

    Full Text Available Abstract Background Traumatic brain injury (TBI initiates a complex sequence of destructive and neuroprotective cellular responses. The initial mechanical injury is followed by an extended time period of secondary brain damage. Due to the complicated pathological picture a better understanding of the molecular events occurring during this secondary phase of injury is needed. This study was aimed at analysing gene expression patterns following cerebral cortical contusion in rat using high throughput microarray technology with the goal of identifying genes involved in an early and in a more delayed phase of trauma, as genomic responses behind secondary mechanisms likely are time-dependent. Results Among the upregulated genes 1 day post injury, were transcription factors and genes involved in metabolism, e.g. STAT-3, C/EBP-δ and cytochrome p450. At 4 days post injury we observed increased gene expression of inflammatory factors, proteases and their inhibitors, like cathepsins, α-2-macroglobulin and C1q. Notably, genes with biological function clustered to immune response were significantly upregulated 4 days after injury, which was not found following 1 day. Osteopontin and one of its receptors, CD-44, were both upregulated showing a local mRNA- and immunoreactivity pattern in and around the injury site. Fewer genes had decreased expression both 1 and 4 days post injury and included genes implicated in transport, metabolism, signalling, and extra cellular matrix formation, e.g. vitronectin, neuroserpin and angiotensinogen. Conclusion The different patterns of gene expression, with little overlap in genes, 1 and 4 days post injury showed time dependence in genomic responses to trauma. An early induction of factors involved in transcription could lead to the later inflammatory response with strongly upregulated CD-44 and osteopontin expression. An increased knowledge of genes regulating the pathological mechanisms in trauma will help to find future

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

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    Jacky T Yeung

    2013-01-01

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

  8. 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.

  9. 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.

  10. Post-concussive complaints after mild traumatic brain injury associated with altered brain networks during working memory performance

    NARCIS (Netherlands)

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

    2016-01-01

    The aim was to investigate brain network function during working memory (WM) task performance in patients with uncomplicated mild traumatic brain injury (mTBI) in the sub-acute phase post-injury. We were particularly interested in differences between patients with (PCC-present) and without

  11. Volunteer work and psychological health following traumatic brain injury.

    Science.gov (United States)

    Ouellet, Marie-Christine; Morin, Charles M; Lavoie, André

    2009-01-01

    To compare the long-term psychological functioning of 3 groups of survivors of traumatic brain injury (TBI): (1) those who report being regularly active either by working or studying, (2) those who are not competitively employed but are active volunteers, and (3) those who report neither working, studying, nor volunteering. PARTICIPANTS AND PROCEDURE: Two hundred eight participants aged 16 years and older with minor to severe TBI were classified as (1) Working/Studying (N = 78), (2) Volunteering (N = 54), or (3) Nonactive (N = 76). Measures of psychological distress (anxiety, depression, cognitive disturbance, irritability/anger), fatigue, sleep disturbance, and perception of pain. Survivors of TBI who report being active through work, studies, or volunteering demonstrate a significantly higher level of psychological adjustment than persons who report no activity. Even among participants who are unable to return to work and are declared on long-term disability leave, those who report engaging in volunteer activities present significantly better psychological functioning than participants who are nonactive. Volunteering is associated with enhanced psychological well-being and should be encouraged following TBI.

  12. Neuropsychological differential diagnosis of mild traumatic brain injury.

    Science.gov (United States)

    Larrabee, Glenn J; Rohling, Martin L

    2013-01-01

    The diagnosis and evaluation of mild traumatic brain injury (mTBI) is reviewed from the perspective of meta-analyses of neuropsychological outcome, showing full recovery from a single, uncomplicated mTBI by 90 days post-trauma. Persons with history of complicated mTBI characterized by day-of-injury computed tomography or magnetic resonance imaging abnormalities, and those who have suffered prior mTBIs may or may not show evidence of complete recovery similar to that experienced by persons suffering a single, uncomplicated mTBI. Persistent post-concussion syndrome (PCS) is considered as a somatoform presentation, influenced by the non-specificity of PCS symptoms which commonly occur in non-TBI samples and co-vary as a function of general life stress, and psychological factors including symptom expectation, depression and anxiety. A model is presented for forensic evaluation of the individual mTBI case, which involves open-ended interview, followed by structured interview, record review, and detailed neuropsychological testing. Differential diagnosis includes consideration of other neurologic and psychiatric disorders, symptom expectation, diagnosis threat, developmental disorders, and malingering. Copyright © 2013 John Wiley & Sons, Ltd.

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

    Science.gov (United States)

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

    2017-01-01

    Abstract Cognitive impairment is a core clinical feature of traumatic brain injury (TBI). After TBI, cognition is a key determinant of post-injury productivity, outcome, and quality of life. As a final common pathway of diverse molecular and microstructural TBI mechanisms, cognition is an ideal endpoint in clinical trials involving many candidate drugs and nonpharmacological interventions. Cognition can be reliably measured with performance-based neuropsychological tests that have greater granularity than crude rating scales, such as the Glasgow Outcome Scale-Extended, which remain the standard for clinical trials. Remarkably, however, there is no well-defined, widely accepted, and validated cognition endpoint for TBI clinical trials. A single cognition endpoint that has excellent measurement precision across a wide functional range and is sensitive to the detection of small improvements (and declines) in cognitive functioning would enhance the power and precision of TBI clinical trials and accelerate drug development research. We outline methodologies for deriving a cognition composite score and a research program for validation. Finally, we discuss regulatory issues and the limitations of a cognition endpoint. PMID:27188248

  14. 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).

  15. Cognitive correlates of narrative impairment in moderate traumatic brain injury.

    Science.gov (United States)

    Marini, Andrea; Zettin, Marina; Galetto, Valentina

    2014-11-01

    Traumatic brain injuries (TBIs) are often associated with communicative deficits. The incoherent and impoverished language observed in non-aphasic individuals with severe TBI has been linked to a problem in the global organization of information at the text level. The present study aimed to analyze the features of narrative discourse impairment in a group of adults with moderate TBI (modTBI). 10 non-aphasic speakers with modTBI and 20 neurologically intact participants were recruited for the experiment. Their cognitive, linguistic and narrative skills were thoroughly assessed. The persons with modTBI exhibited normal phonological, lexical and grammatical skills. However, their narratives were characterized by lower levels of Lexical Informativeness and more errors of both Local and Global Coherence that, at times, made their narratives vague and ambiguous. Significant correlations were found between these narrative difficulties and the production of both perseverative and non-perseverative errors on the WCST. These disturbances confirm previous findings which suggest a deficit at the interface between cognitive and linguistic processing rather than a specific linguistic disturbance in these patients. Copyright © 2014 Elsevier Ltd. All rights reserved.

  16. Executive Functioning of Combat Mild Traumatic Brain Injury.

    Science.gov (United States)

    Gaines, Katy D; Soper, Henry V; Berenji, Gholam R

    2016-01-01

    This study investigates neuropsychological deficits in recently deployed veterans with mild traumatic brain injury (mTBI). Veterans discharged from 2007 to 2012 were recruited from Veterans Affairs clinics. Independent groups of participants with mTBI (n = 57) and those without TBI (n = 57) were administered the Beck Depression Inventory-II, Combat Exposure Scale, Word Memory Test, and the Self-Awareness of Deficits Interview. Neuropsychological instruments included the Rey-Osterrieth Complex Figure Test, Letter and Category Fluency, Trail-Making Test-Parts A and B, Christiansen H-abbreviated, Soper Neuropsychology Screen, Wechsler Memory Scale subtests Logical Memory I and II, and the Street Completion Test. The mTBI group performed significantly worse on all of the executive and nonexecutive measurements with the exception of Category Fluency, after controlling for age, depression effort, and combat exposure. Depression and combat exposure were greater for the mTBI group. The mTBI group scored poorer on effort, but only the Multiple Choice subtest was significant. The mTBI group had good awareness of their deficits.

  17. 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.

  18. Tracheostomy risk factors and outcomes after severe traumatic brain injury.

    Science.gov (United States)

    Humble, Stephen S; Wilson, Laura D; McKenna, John W; Leath, Taylor C; Song, Yanna; Davidson, Mario A; Ehrenfeld, Jesse M; Guillamondegui, Oscar D; Pandharipande, Pratik P; Patel, Mayur B

    2016-01-01

    To determine risk factors associated with tracheostomy placement after severe traumatic brain injury (TBI) and subsequent outcomes among those who did and did not receive a tracheostomy. This retrospective cohort study compared adult trauma patients with severe TBI (n = 583) who did and did not receive tracheostomy. A multivariable logistic regression model assessed the associations between age, sex, race, insurance status, admission GCS, AIS (Head, Face, Chest) and tracheostomy placement. Ordinal logistic regression models assessed tracheostomy's influence on ventilator days and ICU LOS. To limit immortal time bias, Cox proportional hazards models assessed mortality at 1, 3 and 12-months. In this multivariable model, younger age and private insurance were associated with increased probability of tracheostomy. AIS, ISS, GCS, race and sex were not risk factors for tracheostomy placement. Age showed a non-linear relationship with tracheostomy placement; likelihood peaked in the fourth decade and declined with age. Compared to uninsured patients, privately insured patients had an increased probability of receiving a tracheostomy (OR = 1.89 [95% CI = 1.09-3.23]). Mortality was higher in those without tracheostomy placement (HR = 4.92 [95% CI = 3.49-6.93]). Abbreviated injury scale-Head was an independent factor for time to death (HR = 2.53 [95% CI = 2.00-3.19]), but age, gender and insurance were not. Age and insurance status are independently associated with tracheostomy placement, but not with mortality after severe TBI. Tracheostomy placement is associated with increased survival after severe TBI.

  19. Counter-intuitive moral judgement following traumatic brain injury.

    Science.gov (United States)

    Rowley, Dane A; Rogish, Miles; Alexander, Timothy; Riggs, Kevin J

    2017-02-07

    Several neurological patient populations, including traumatic brain injury (TBI), appear to produce an abnormally 'utilitarian' pattern of judgements to moral dilemmas; they tend to make judgements that maximize the welfare of the majority, rather than deontological judgements based on the following of moral rules (e.g., do not harm others). However, this patient research has always used extreme dilemmas with highly valued moral rules (e.g., do not kill). Data from healthy participants, however, suggest that when a wider range of dilemmas are employed, involving less valued moral rules (e.g., do not lie), moral judgements demonstrate sensitivity to the psychological intuitiveness of the judgements, rather than their deontological or utilitarian content (Kahane et al., Social Cognitive and Affective Neuroscience, 7, 2011, 393). We sought the moral judgements of 30 TBI participants and 30 controls on moral dilemmas where content (utilitarian/deontological) and intuition (intuitive/counter-intuitive) were measured concurrently. Overall TBI participants made utilitarian judgements in equal proportions to controls; disproportionately favouring utilitarian judgements only when they were counter-intuitive, and deontological judgements only when they were counter-intuitive. These results speak against the view that TBI causes a specific utilitarian bias, suggesting instead that moral intuition is broadly disrupted following TBI. © 2017 The British Psychological Society.

  20. Prospective memory in pediatric traumatic brain injury: a preliminary study.

    Science.gov (United States)

    McCauley, Stephen R; Levin, Harvey S

    2004-01-01

    Prospective memory (PM) performance was investigated in a preliminary study of children and adolescents ages 10-19 in 3 groups: individuals with orthopedic injuries (not involving the head) requiring hospitalization (Ortho, N = 15), mild traumatic brain injury (TBI, N = 17), and severe TBI (N = 15). All participants with TBI were at least 5 years postinjury and participants in the Ortho group were at least 3 years postinjury. The PM task involved reporting words presented in blue during a category decision task in which words were presented in several different colors and participants were to determine which of two categories the word belonged. Participants were asked to make their choices as quickly as possible. After a 10- to 15-min intervening computer task in which all words were presented in black letters, a large proportion of participants with mild or severe TBI failed to indicate any blue words when they appeared. After a reminder to perform the PM task was given to all at the same point in the task, PM performance increased in the Ortho and Mild TBI groups, but remained comparably impaired in the Severe TBI group. Reaction time (RT) data indicated that mean RT was slower with increasing TBI severity. Further, there was a significant cost in RT for performing the PM task during the ongoing category decision task for all groups. The cost in terms of slowed RT increased with greater TBI severity.

  1. Robotic assessment of sensorimotor deficits after traumatic brain injury.

    Science.gov (United States)

    Debert, Chantel T; Herter, Troy M; Scott, Stephen H; Dukelow, Sean

    2012-06-01

    Robotic technology is commonly used to quantify aspects of typical sensorimotor function. We evaluated the feasibility of using robotic technology to assess visuomotor and position sense impairments following traumatic brain injury (TBI). We present results of robotic sensorimotor function testing in 12 subjects with TBI, who had a range of initial severities (9 severe, 2 moderate, 1 mild), and contrast these results with those of clinical tests. We also compared these with robotic test outcomes in persons without disability. For each subject with TBI, a review of the initial injury and neuroradiologic findings was conducted. Following this, each subject completed a number of standardized clinical measures (Fugl-Meyer Assessment, Purdue Peg Board, Montreal Cognitive Assessment, Rancho Los Amigos Scale), followed by two robotic tasks. A visually guided reaching task was performed to assess visuomotor control of the upper limb. An arm position-matching task was used to assess position sense. Robotic task performance in the subjects with TBI was compared with findings in a cohort of 170 person without disabilities. Subjects with TBI demonstrated a broad range of sensory and motor deficits on robotic testing. Notably, several subjects with TBI displayed significant deficits in one or both of the robotic tasks, despite normal scores on traditional clinical motor and cognitive assessment measures. The findings demonstrate the potential of robotic assessments for identifying deficits in visuomotor control and position sense following TBI. Improved identification of neurologic impairments following TBI may ultimately enhance rehabilitation.

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

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

    2008-07-01

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

  3. Imagining the future in children with severe traumatic brain injury.

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    Lah, Suncica; Gott, Chloe; Epps, Adrienne; Parry, Louise

    2018-03-22

    Imagining the future events is thought to rely on re-combination and integration of past episodic memory traces into future events. Future and past events contain episodic and non-episodic details. Children with severe traumatic brain injury (TBI) were found to have impaired recall of past episodic (but not semantic) event details. Here we examined whether severe TBI impairs construction of future events. Cross-sectional. Children with severe TBI (n = 14) and healthy controls (NC; n = 33) (i) completed tests of anterograde (narrative and relational) memory and executive skills, (ii) recalled past events and generated future events, and (iii) rated events' phenomenological qualities. Events were scored for episodic (internal) and non-episodic (external) details. The groups did not differ in generating details of future events although children with TBI recalled significantly fewer past internal (but not external) events' details relative to NCs. Moreover, the number of past internal details relative to future internal details was significantly higher in the NC group, but not in the TBI groups. Significant correlations between past and future were found for (i) episodic details in both groups, and (ii) semantic details in the NC group. The TBI group rated their events as being less significant than did the NC group. The groups did not differ on ratings of visual intensity and rehearsal. Children who have sustained severe TBI had impoverished recall of past, but not generation of future events. This unexpected dissociation between past and future event construction requires further research.

  4. Balance function and sensory integration after mild traumatic brain injury.

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    Lin, Li-Fong; Liou, Tsan-Hon; Hu, Chaur-Jong; Ma, Hon-Ping; Ou, Ju-Chi; Chiang, Yung-Hsiao; Chiu, Wen-Ta; Tsai, Shin-Han; Chu, Woei-Chyn

    2015-01-01

    This study examined the disparities in balance functions and sensory integration in patients with mild traumatic brain injuries (mTBIs) and healthy controls. One hundred and seven patients with mTBI and 107 age- and sex-matched controls were recruaited for this study. Symptoms of dizziness, balance functions and the ability to perform daily activities were assessed using the dizziness handicap inventory (DHI). This study also performed the postural-stability test and a modified clinical test of sensory integration by using the Biodex Stability System (BBS). DHI scores (functional, emotional, physical and total self-reported scores) were substantially increased in patients following an mTBI compared with the scores of the controls (p sensory-integration test index (eyes-open-firm-surface index) (p = 0.006) were substantially lower in patients with mTBI than in the controls. However, indices of two other postural-stability test indices (overall and medial-lateral) and three other sensory-integration tests indices (eyes-closed-firm-surface, eyes-open-foam-surface and eyes-closed-foam-surface) measured for the mTBI group did not differ from those of the control group. Activities of daily living, balance in postural stability and sensory integration were strongly impaired in patients with mTBI.

  5. Neurobehavioral Abnormalities Associated with Executive Dysfunction after Traumatic Brain Injury

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    Rodger Ll. Wood

    2017-10-01

    Full Text Available Objective: This article will address how anomalies of executive function after traumatic brain injury (TBI can translate into altered social behavior that has an impact on a person’s capacity to live safely and independently in the community.Method: Review of literature on executive and neurobehavioral function linked to cognitive ageing in neurologically healthy populations and late neurocognitive effects of serious TBI. Information was collated from internet searches involving MEDLINE, PubMed, PyscINFO and Google Scholar as well as the authors’ own catalogs.Conclusions: The conventional distinction between cognitive and emotional-behavioral sequelae of TBI is shown to be superficial in the light of increasing evidence that executive skills are critical for integrating and appraising environmental events in terms of cognitive, emotional and social significance. This is undertaken through multiple fronto-subcortical pathways within which it is possible to identify a predominantly dorsolateral network that subserves executive control of attention and cognition (so-called cold executive processes and orbito-frontal/ventro-medial pathways that underpin the hot executive skills that drive much of behavior in daily life. TBI frequently involves disruption to both sets of executive functions but research is increasingly demonstrating the role of hot executive deficits underpinning a wide range of neurobehavioral disorders that compromise relationships, functional independence and mental capacity in daily life.

  6. Detecting Mild Traumatic Brain Injury Using Resting State Magnetoencephalographic Connectivity.

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    Vasily A Vakorin

    2016-12-01

    Full Text Available Accurate means to detect mild traumatic brain injury (mTBI using objective and quantitative measures remain elusive. Conventional imaging typically detects no abnormalities despite post-concussive symptoms. In the present study, we recorded resting state magnetoencephalograms (MEG from adults with mTBI and controls. Atlas-guided reconstruction of resting state activity was performed for 90 cortical and subcortical regions, and calculation of inter-regional oscillatory phase synchrony at various frequencies was performed. We demonstrate that mTBI is associated with reduced network connectivity in the delta and gamma frequency range (>30 Hz, together with increased connectivity in the slower alpha band (8-12 Hz. A similar temporal pattern was associated with correlations between network connectivity and the length of time between the injury and the MEG scan. Using such resting state MEG network synchrony we were able to detect mTBI with 88% accuracy. Classification confidence was also correlated with clinical symptom severity scores. These results provide the first evidence that imaging of MEG network connectivity, in combination with machine learning, has the potential to accurately detect and determine the severity of mTBI.

  7. Incidence and treatment of visual dysfunction in traumatic brain injury.

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    Schlageter, K; Gray, B; Hall, K; Shaw, R; Sammet, R

    1993-01-01

    The incidence of visual dysfunction and effectiveness of visual exercises in acute traumatically brain injured inpatients in a rehabilitation programme were studied. Vision evaluation norms were established on 23 hospital staff. The evaluation was then administered to 51 inpatients within days after admission. An additional 21 patients were unable to participate, usually due to decreased cognition or agitation. Thirty of 51 (59%) scored impaired in one or more of the following: pursuits, saccades, ocular posturing, stereopsis, extra-ocular movements, and near/far eso-exotropia. For patients having dysfunction in pursuits or saccades, a 2-week baseline was followed by vision exercises. During the baseline interval patients were evaluated by an optometrist to verify therapists' findings. Six patients who participated in several weeks of treatment were evaluated at 2-week intervals by an independent rater. Progress is graphically illustrated. Conclusions were that the suitability of an inpatient vision programme, from our experience, is questionable. However, an initial evaluation proved valuable for informing staff of patients' visual status and for referral to an optometrist/ophthalmologist for further treatment.

  8. Traumatic brain injury amongst indigenous people: a systematic review.

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    Lakhani, Ali; Townsend, Clare; Bishara, Jason

    2017-01-01

    To identify the types of research focusing on Traumatic Brain Injury (TBI) amongst Indigenous people in order to (i) synthesise their findings and (ii) ascertain where research gaps exist. A systematic review using the PRISMA approach was employed. Eight databases were searched for peer-reviewed literature published at any date. Twenty-six studies met the inclusion criteria and were included in this review. The majority of studies focused on the prevalence or incidence of TBI amongst Indigenous people (n = 15). Twelve of these found Indigenous people had a higher prevalence or incidence of TBI compared to non-Indigenous people. Under-researched areas include (with number of articles identified in brackets): Indigenous level of injury or recovery (n = 2), neuropsychological assessment and TBI (n = 3), Indigenous perspectives of TBI (n = 2), Indigenous intervention for TBI (n = 1), and rehabilitation for TBI (n = 4). Published studies demonstrate that Indigenous people have a higher prevalence or incidence of TBI compared to non-Indigenous people. Limited studies explore culturally appropriate rehabilitation and intervention methods and Indigenous understandings of TBI. It is imperative that future research consider the nature and efficacy of culturally appropriate approaches and their contribution towards better outcomes for Indigenous people with TBI, and their families and communities.

  9. Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury

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    Kent Reifschneider

    2015-07-01

    Full Text Available Traumatic brain injuries (TBI are common occurrences in childhood, often resulting in long term, life altering consequences. Research into endocrine sequelae following injury has gained attention; however, there are few studies in children. This paper reviews the pathophysiology and current literature documenting risk for endocrine dysfunction in children suffering from TBI. Primary injury following TBI often results in disruption of the hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release, with implications for both acute management and survival. Secondary injuries, occurring hours to weeks after TBI, result in both temporary and permanent alterations in pituitary function. At five years after moderate to severe TBI, nearly 30% of children suffer from hypopituitarism. Growth hormone deficiency and disturbances in puberty are the most common; however, any part of the hypothalamic-pituitary axis can be affected. In addition, endocrine abnormalities can improve or worsen with time, having a significant impact on children’s quality of life both acutely and chronically. Since primary and secondary injuries from TBI commonly result in transient or permanent hypopituitarism, we conclude that survivors should undergo serial screening for possible endocrine disturbances. High indices of suspicion for life threatening endocrine deficiencies should be maintained during acute care. Additionally, survivors of TBI should undergo endocrine surveillance by 6–12 months after injury, and then yearly, to ensure early detection of deficiencies in hormonal production that can substantially influence growth, puberty and quality of life.

  10. Discourse macrolevel processing after severe pediatric traumatic brain injury.

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    Chapman, Sandra Bond; Sparks, Garen; Levin, Harvey S; Dennis, Maureen; Roncadin, Caroline; Zhang, Lifang; Song, James

    2004-01-01

    The purpose of this study was to determine if discourse macrolevel processing abilities differed between children with severe traumatic brain injury (TBI) at least 2 years postinjury and typically developing children. Twenty-three children had sustained a severe TBI either before the age of 8 (n = 10) or after the age of 8 (n = 13). The remaining 32 children composed a control group of typically developing peers. The groups' summaries and interpretive lesson statements were analyzed according to reduction and transformation of narrative text information. Compared to the control group, the TBI group condensed the original text information to a similar extent. However, the TBI group produced significantly less transformed information during their summaries, especially those children who sustained early injuries. The TBI and control groups did not significantly differ in their production of interpretive lesson statements. In terms of related skills, discourse macrolevel summarization ability was significantly related to problem solving but not to lexical or sentence level language skills or memory. Children who sustain a severe TBI early in childhood are at an increased risk for persisting deficits in higher level discourse abilities, results that have implications for academic success and therapeutic practices.

  11. Community integration after severe traumatic brain injury in adults.

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    Truelle, Jean-Luc; Fayol, Patrick; Montreuil, Michèle; Chevignard, Mathilde

    2010-12-01

    Despite being the main cause of death and disability in young adults, traumatic brain injury (TBI) is a rather neglected epidemic. Community integration of persons with TBI was, until recently, insufficiently informed by clinical research. To bridge the gap between rehabilitation and community re-entry, the first task is to assess the person, using TBI-specific outcome measures. The second task is to provide re-entry programs, the effectiveness of which is assessed by those measures, using well designed studies. There are very few such studies. However, there are some effective comprehensive programs and others which are specifically targeted dealing mainly with return to work, behavior, and family issues. The complex psychological and environmental components of the disability require individualized and often long-term care. For persons with severe TBI trying to achieve the best possible community integration a new semiology is required, not just limited to medical care, but also involving social and psychological care that is tailored to the needs of each individual and family, living within his/her environment. Currently, only a minority benefit from well validated programs.

  12. Deficits in analogical reasoning in adolescents with traumatic brain injury.

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    Krawczyk, Daniel C; Hanten, Gerri; Wilde, Elisabeth A; Li, Xiaoqi; Schnelle, Kathleen P; Merkley, Tricia L; Vasquez, Ana C; Cook, Lori G; McClelland, Michelle; Chapman, Sandra B; Levin, Harvey S

    2010-01-01

    Individuals with traumatic brain injury (TBI) exhibit deficits in executive control, which may impact their reasoning abilities. Analogical reasoning requires working memory and inhibitory abilities. In this study, we tested adolescents with moderate to severe TBI and typically developing (TD) controls on a set of picture analogy problems. Three factors were varied: complexity (number of relations in the problems), distraction (distractor item present or absent), and animacy (living or non-living items in the problems). We found that TD adolescents performed significantly better overall than TBI adolescents. There was also an age effect present in the TBI group where older participants performed better than younger ones. This age effect was not observed in the TD group. Performance was affected by complexity and distraction. Further, TBI participants exhibited lower performance with distractors present than TD participants. The reasoning deficits exhibited by the TBI participants were correlated with measures of executive function that required working memory updating, attention, and attentional screening. Using MRI-derived measures of cortical thickness, correlations were carried out between task accuracy and cortical thickness. The TD adolescents showed negative correlations between thickness and task accuracy in frontal and temporal regions consistent with cortical maturation in these regions. This study demonstrates that adolescent TBI results in impairments in analogical reasoning ability. Further, TBI youth have difficulty effectively screening out distraction, which may lead to failures in comprehension of the relations among items in visual scenes. Lastly, TBI youth fail to show robust cortical-behavior correlations as observed in TD individuals.