Journal of neurotrauma
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Journal of neurotrauma · Jan 2017
Characterization of the ionic profile of the extracellular space of the injured and ischemic brain: A microdialysis study.
Traumatic brain injury (TBI) and ischemic stroke cause a variable disruption of ionic homeostasis and massive ionic fluxes with subsequent osmotic water movement across the cells that causes edema, brain swelling, and deformation of the damaged tissue. Although cerebral microdialysis (CMD) has been used to study the brain neurochemistry, the ionic profiles of brain interstitial space fluid have rarely been reported in humans. We studied the ionic profile in injured areas of the brain by using CMD. ⋯ In the traumatic core (TC), significantly higher levels of [Na+]o, [Cl-]o, and [K+]o were found. The main finding in the penumbra was a completely normal ionic profile for [Na+]o and [K+]o in 60% of the samples. ICP-MS coupled to ionic assays creates a powerful tool for a better understanding of the complex ionic disturbances that occur after severe TBI and ischemic stroke.
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Journal of neurotrauma · Jan 2017
Traumatic brain injury causes endothelial dysfunction in the systemic microcirculation through arginase-1-dependent uncoupling of endothelial nitric oxide synthase.
Endothelial dysfunction is a hallmark of many chronic diseases, including diabetes and long-term hypertension. We show that acute traumatic brain injury (TBI) leads to endothelial dysfunction in rat mesenteric arteries. Endothelial-dependent dilation was greatly diminished 24 h after TBI because of impaired nitric oxide (NO) production. ⋯ Moreover, evidence for increased reactive oxygen species production, a consequence of l-arginine starvation-dependent eNOS uncoupling, was detected in endothelium and plasma. Collectively, our findings demonstrate endothelial dysfunction in a remote vascular bed after TBI, manifesting as impaired endothelial-dependent vasodilation, with increased arginase activity, decreased generation of NO, and increased O2- production. We conclude that blood vessels have a "molecular memory" of neurotrauma, 24 h after injury, because of functional changes in vascular endothelial cells; these effects are pertinent to understanding the systemic inflammatory response that occurs after TBI even in the absence of polytrauma.
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Journal of neurotrauma · Jan 2017
TBI induces alterations in cortical glutamate uptake without a reduction in GLT-1 protein expression.
We hypothesize that the primary mechanism for removal of glutamate from the extracellular space is altered after traumatic brain injury (TBI). To evaluate this hypothesis, we initiated TBI in adult male rats using a 2.0 atm lateral fluid percussion injury (LFPI) model. In the ipsilateral cortex and hippocampus, we found no differences in expression of the primary glutamate transporter in the brain (GLT-1) 24 h after TBI. ⋯ Exploratory studies using an inhibitor of Akt suggest selective activation of kinases in LFPI versus controls. Ingenuity pathway analyses of implicated kinases from our network model found apoptosis and cell death pathways as top functions in acute LFPI. Taken together, our data suggest diminished activity of glutamate transporters in the prefrontal cortex, with no changes in protein expression of the primary glutamate transporter GLT-1, and global alterations in signaling networks that include serine-threonine kinases that are known modulators of glutamate transport activity.
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Journal of neurotrauma · Jan 2017
Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala Following Experimental Diffuse Traumatic Brain Injury.
In the pathophysiology of traumatic brain injury (TBI), the amygdala remains understudied, despite involvement in processing emotional and stressful stimuli associated with anxiety disorders, such as post-traumatic stress disorder (PTSD). Because the basolateral amygdala (BLA) integrates inputs from sensory and other limbic structures coordinating emotional learning and memory, injury-induced changes in circuitry may contribute to psychiatric sequelae of TBI. This study quantified temporal changes in dendritic complexity of BLA neurons after experimental diffuse TBI, modeled by midline fluid percussion injury. ⋯ However, the BLA was relatively spared from neuropathology, demonstrated by an absence of argyrophilic accumulation over time, in contrast to other brain regions. These data suggest an early and persistent enhancement of dendritic complexity within the BLA after a single diffuse TBI. Increased dendritic complexity would alter information processing into and through the amygdala, contributing to emotional symptoms post-TBI, including PTSD.
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Journal of neurotrauma · Jan 2017
Management and Outcomes of Isolated Tentorial and Parafalcine 'Smear' Subdural Hematomas at a Level-1 Trauma Center: Is high acuity care necessary?
Data suggest that patients who present to trauma centers with mild traumatic brain injury (TBI) are admitted to an excessively high level of care and undergo myriad, unnecessary repeat radiographic and laboratory tests that do not affect outcome. Surprisingly, a paucity of data exists regarding the management of isolated, traumatic, parafalcine, or tentorial acute subdural hematoma (aSDH). Therefore, a retrospective, cohort study was completed to analyze factors associated with outcomes in patients who present to a high-volume, urban, level 1 trauma center with isolated parafalcine or tentorial aSDH after closed head injury. ⋯ Depressed GCS, systemic injury, and being elderly were associated with poor discharge disposition; whereas being systemically injured, female, or elderly were associated with poor functional status at discharge. Although 94% of admitted patients underwent at least one repeat head computed tomography (CT) scan while hospitalized, not a single aSDH enlarged, including four patients on antiplatelet agents, anticoagulants, or both. Based on these data, young patients who present with GCS 13-15 without systemic injury following blunt trauma with an associated isolated parafalcine and tentorial aSDH may be safely admitted to a standard medical/surgical floor for observation.