Journal of neurotrauma
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Journal of neurotrauma · Jul 2014
ReviewDiffusion Tensor Imaging Findings in Semi-Acute Mild Traumatic Brain Injury.
The past 10 years have seen a rapid increase in the use of diffusion tensor imaging to identify biomarkers of traumatic brain injury (TBI). Although the literature generally indicates decreased anisotropic diffusion at more chronic injury periods and in more severe injuries, considerable debate remains regarding the direction (i.e., increased or decreased) of anisotropic diffusion in the acute to semi-acute phase (here defined as less than 3 months post-injury) of mild TBI (mTBI). A systematic review of the literature was therefore performed to (1) determine the prevalence of different anisotropic diffusion findings (increased, decreased, bidirectional, or null) during the semi-acute injury phase of mTBI and to (2) identify clinical (e.g., age of injury, post-injury scan time, etc.) and experimental factors (e.g., number of unique directions, field strength) that may influence these findings. ⋯ Chi-squared analyses indicated that the total number of diffusion-weighted (DW) images was significantly associated with findings of either increased (DW ≥ 30) versus decreased (DW ≤ 25) anisotropic diffusion. Other clinical and experimental factors were not statistically significant for direction of anisotropic diffusion, but these results may have been limited by the relatively small number of studies within each domain (e.g., pediatric studies). In summary, current results indicate roughly equivalent number of studies reporting increased versus decreased anisotropic diffusion during semi-acute mTBI, with the number of unique diffusion images being statistically associated with the direction of findings.
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Journal of neurotrauma · Jul 2014
Real-time monitoring of changes in brain extracellular sodium and potassium concentrations and intracranial pressure after selective vasopressin-1a receptor (V1aR) inhibition following focal traumatic brain injury in rats.
Brain swelling and increased intracranial pressure (ICP) following traumatic brain injury (TBI) contribute to poor outcome. Vasopressin-1a receptors (V1aR) and aquaporin-4 (AQP4) regulate water transport and brain edema formation, perhaps in part by modulating cation fluxes. After focal TBI, V1aR inhibitors diminish V1aR and AQP4, reduce astrocytic swelling and brain edema. ⋯ Thus, selective V1aR inhibition allowed faster [Na(+)]e recovery and reduced ICP. By augmenting the [Na(+)]e recovery rate, SR49059 may reduce trauma-induced ionic imbalance, blunting cellular water influx and edema after TBI. These findings suggest SR49059 and V1aR inhibitors are potential tools for treating cellular edema post-TBI.
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Journal of neurotrauma · Jul 2014
Exposure of the thorax to a sublethal blast wave causes a hydrodynamic pulse that leads to perivenular inflammation in the brain.
Traumatic brain injury (TBI) caused by an explosive blast (blast-TBI) is postulated to result, in part, from transvascular transmission to the brain of a hydrodynamic pulse (a.k.a., volumetric blood surge, ballistic pressure wave, hydrostatic shock, or hydraulic shock) induced in major intrathoracic blood vessels. This mechanism of blast-TBI has not been demonstrated directly. We tested the hypothesis that a blast wave impacting the thorax would induce a hydrodynamic pulse that would cause pathological changes in the brain. ⋯ Immunolabeling 24 h after injury by TOBIA showed up-regulation of tumor necrosis factor alpha, ED-1, sulfonylurea receptor 1 (Sur1), and glial fibrillary acidic protein in veins or perivenular tissues and microvessels throughout the brain. The perivenular inflammatory effects induced by TOBIA were prevented by ligating the jugular vein and were reproduced using JOBIA. We conclude that blast injury to the thorax leads to perivenular inflammation, Sur1 up-regulation, and reactive astrocytosis resulting from the induction of a hydrodynamic pulse in the vasculature.
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Journal of neurotrauma · Jul 2014
Inhibition of Src Family Kinases Protects Hippocampal Neurons and Improves Cognitive Function after Traumatic Brain Injury.
Traumatic brain injury (TBI) is often associated with intracerebral and intraventricular hemorrhage. Thrombin is a neurotoxin generated at bleeding sites fater TBI and can lead to cell death and subsequent cognitive dysfunction via activation of Src family kinases (SFKs). ⋯ Systemic administration of the SFK inhibitor, PP2, immediately after moderate TBI blocks ROCK1 expression, protects hippocampal CA2/3 neurons, and improves spatial memory function. These data suggest the possibility that inhibiting SFKs after TBI might improve clinical outcomes.
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Journal of neurotrauma · Jul 2014
Transport mode to level I and II trauma centers and survival of pediatric patients with traumatic brain injury.
The use of helicopter emergency medical services (EMS) for pediatric trauma patients is an issue of debate. We investigated the association of helicopter transport with survival of pediatric patients with traumatic brain injury (TBI). We conducted a retrospective cohort study of pediatric patients with TBI who were transported to level I and II trauma centers and were registered in the National Trauma Data Bank (NTDB) between 2009 and 2011. ⋯ Multivariable logistic regression analysis demonstrated an association of helicopter transport with increased survival (OR, 2.35; 95% CI, 1.30-4.25; ARR 5.36%). This again persisted after propensity score matching (OR 2.56; 95% CI 1.28-5.11; ARR 6.14). Pediatric patients with TBI transported to level I and II trauma centers had improved survival in comparison with similar patients transported via ground EMS.