Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Feb 2017
Electrophysiological and pathological characterization of the period of heightened vulnerability to repetitive injury in an in vitro stretch model.
Clinical studies suggest that repeat exposures to mild traumatic brain injury (mTBI) or concussion, such as sports-related mTBI, result in verbal, memory, and motor deficits that can progressively worsen and take longer for recovery with each additional concussion. Pre-clinical studies suggest that mild mechanical injury of the brain can initiate a period of heightened vulnerability during which the brain is more susceptible to a subsequent mild injury. It is unknown how long this period of heightened vulnerability lasts and, as a result, appropriate return-to-play guidelines for athletes who have sustained sports-related mTBI could be better clarified. ⋯ Cell loss, dendrite damage, and nitrite production were not significantly increased when the inter-injury interval was increased to 72 h; however, LTP deficits and astrogliosis persisted. An interval of 144 h was sufficient to prevent the detrimental effects of repetitive stretch. Improved understanding of the brain's response to repetitive mTBI in vitro may aid in translational studies, informing rest periods for the injured athlete.
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Journal of neurotrauma · Feb 2017
ReviewReview: CNS Injury and NADPH Oxidase: Oxidative Stress and Therapeutic Targets.
Injury to the central nervous system (CNS) includes both traumatic brain and spinal cord injury (TBI and SCI, respectively). These injuries, which are heterogeneous and, therefore, difficult to treat, result in long-lasting functional, cognitive, and behavioral deficits. Severity of injury is determined by multiple factors, and is largely mediated by the activity of the CNS inflammatory system, including the primary CNS immune cells, microglia. ⋯ ROS play a central role in inflammation, contributing to cytokine translation and release, microglial polarization and activation, and clearance of damaged tissue. NOX has been suggested as a potential therapeutic target in CNS trauma, as inhibition of this enzyme family modulates inflammatory cell response and ROS production. The purpose of this review is to understand how the different NOX enzymes function and what role they play in the scope of CNS trauma.
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Journal of neurotrauma · Feb 2017
Apolipoprotein E Mimetic Peptide Increases Cerebral Glucose Uptake by Relieving Blood Brain Barrier Disruption Following Controlled Cortical Impact in Mice: An 18F-fluorodeoxyglucose PET/CT Study.
Traumatic brain injury (TBI) disrupts the blood-brain barrier (BBB) and reduces cerebral glucose uptake. Vascular endothelial growth factor (VEGF) is believed to play a key role in TBI, and COG1410 has demonstrated neuroprotective activity in several models of TBI. However, the effects of COG1410 on VEGF and glucose metabolism following TBI are unknown. ⋯ The results showed that controlled cortical impact (CCI)-induced vestibulomotor deficits were accompanied by increases in brain edema and the expression of VEGF, with a decrease in cerebral glucose uptake. COG1410 treatment significantly improved vestibulomotor deficits and glucose uptake and produced decreases in VEGF in the pericontusion and ipsilateral hemisphere of injury, as well as in brain edema and neuronal degeneration compared with the control group. These data support that COG1410 may have potential as an effective drug therapy for TBI.
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Journal of neurotrauma · Feb 2017
Recovery of white matter following paediatric traumatic brain injury depends on injury severity.
Previous studies in pediatric traumatic brain injury (TBI) have been variable in describing the effects of injury severity on white-matter development. The present study used diffusion tensor imaging to investigate prospective sub-acute and longitudinal relationships between early clinical indicators of injury severity, diffusion metrics, and neuropsychological outcomes. Pediatric patients with TBI underwent magnetic resonance imaging (MRI) (n = 78, mean [M] = 10.56, standard deviation [SD] = 2.21 years) at the sub-acute stage after injury (M = 5.55, SD = 3.05 weeks), and typically developing children were also included and imaged (n = 30, M = 10.60, SD = 2.88 years). ⋯ Patients with more severe TBI also exhibited poorer information processing speed at 6-months post-injury, which in turn correlated with their diffusion metrics. These findings highlight that the severity of the injury not only has an impact on white-matter microstructure, it also impacts its recovery over time. Moreover, findings suggest that sub-acute microstructural changes may represent a useful prognostic marker to identify children at elevated risk for longer term deficits.
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The use of forced-swim, rat-validated cognition tests in mouse models of traumatic brain injury (TBI) raises methodological concerns; such models are vulnerable to a number of confounding factors including impaired motor function and stress-induced non-compliance (failure to swim). This study evaluated the ability of a Radial Water Tread (RWT) maze, designed specifically for mice, that requires no swimming to distinguish mice with controlled cortical impact (CCI) induced TBI and Sham controls. ⋯ The Radial Water Tread maze capitalizes on the natural tendency of mice to avoid open areas in favor of hugging the edges of an apparatus (thigmotaxis), and replaces a forced-swim model with water shallow enough that the animal is not required to swim, but aversive enough to motivate escape. Our findings indicate the RWT task is a sensitive species-appropriate behavioral test for evaluating spatial memory impairment in a mouse model of TBI.