Journal of neurotrauma
-
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.
-
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.
-
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.
-
Journal of neurotrauma · Jul 2014
Using the Olfactory System as an in vivo Model to Study Traumatic Brain Injury and Repair.
Loss of olfactory function is an early indicator of traumatic brain injury (TBI). The regenerative capacity and well-defined neural maps of the mammalian olfactory system enable investigations into the degeneration and recovery of neural circuits after injury. Here, we introduce a unique olfactory-based model of TBI that reproduces many hallmarks associated with human brain trauma. ⋯ Behavioral experiments measured 4 days after impact also demonstrated loss of olfactory function, yet following a 30-day recovery period, we observed a significant improvement in olfactory function and partial recovery of olfactory circuitry, despite the persistence of TBI markers. Interestingly, by using the M71-IRES-tauLacZ reporter line to track OSN organization, we further determined that inducing neural activity during the recovery period with intense odor conditioning did not enhance the recovery process. Together, these data establish the mouse olfactory system as a new model to study TBI, serving as a platform to understand neural disruption and the potential for circuit restoration.
-
Journal of neurotrauma · Jul 2014
Cost-effectiveness analysis (CEA) of an early-initiated, continuous chain of rehabilitation after severe traumatic brain injury.
The aim of this study is to estimate the long-term cost-effectiveness of two different rehabilitation trajectories after severe traumatic brain injury (sTBI). A decision tree model compared hospitalization costs, health effects, and incremental cost-effectiveness ratios (ICER) of a continuous chain versus a broken chain of rehabilitation. The expected costs were estimated by the reimbursement system using diagnosis-related group and based on point estimates of the Disability Rating Scale (DRS); the health effects were measured by means of area under the curve (AUC). ⋯ By replacing the broken chain with the continuous chain, NOK 37.000 could be saved and 4.06 DRS points gained. By means of probabilistic sensitivity analysis, the majority of ICER estimates (67% of the Monte Carlo simulations) indicated that a continuous chain of rehabilitation was less costly and more effective. These findings indicate that the trajectory of continuous rehabilitation represents a dominant strategy in that it reduces costs and improves outcomes after sTBI under reasonable assumptions.