Journal of neurotrauma
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Journal of neurotrauma · Feb 2017
Cerebrospinal fluid CCL2 is an early-response biomarker for blast overpressure wave- induced neurotrauma in rats.
Chemokines and their receptors are of great interest within the milieu of immune responses elicited in the central nervous system in response to trauma. Chemokine (C-C motif)) ligand 2 (CCL2), which is also known as monocyte chemotactic protein-1, has been implicated in the pathogenesis of traumatic brain injury (TBI), brain ischemia, Alzheimer's disease, and other neurodegenerative diseases. In this study, we investigated the time course of CCL2 accumulation in cerebrospinal fluid (CSF) after exposures to single and repeated blast overpressures of varied intensities along with the neuropathological changes and motor deficits resulting from these blast conditions. ⋯ CCL2 levels in CSF and plasma were tightly correlated with levels of CCL2 messenger RNA in cerebellum, the brain region most consistently neuropathologically disrupted by blast. In view of the roles of CCL2 that have been implicated in multiple neurodegenerative disorders, it is likely that the sustained high levels of CCL2 and the increased expression of its main receptor, CCR2, in the brain after blast may similarly contribute to neurodegenerative processes after blast exposure. In addition, the markedly elevated concentration of CCL2 in CSF might be a candidate early-response biomarker for diagnosis and prognosis of blast-induced TBI.
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Journal of neurotrauma · Feb 2017
Functional Changes after Recombinant Human Growth Hormone Replacement in Patients with Traumatic Brain Injury and Abnormal Growth Hormone Secretion.
We explored the effects of recombinant human growth hormone (rhGH) replacement on physical and cognitive functioning in subjects with a moderate-to-severe traumatic brain injury (TBI) with abnormal growth hormone (GH) secretion. Fifteen individuals who sustained a TBI at least 12 months prior to study enrollment were identified as having abnormal GH secretion by glucagon stimulation testing (maximum GH response less than 8 ng/mL). Peak cardiorespiratory capacity, body composition, and muscle force testing were assessed at baseline and one year after rhGH replacement. ⋯ Skeletal muscle fatigue did not change but the perceptual rating of fatigue was reduced by ∼25% (p = 0.06). Cognitive performance did not change significantly over time, whereas self-reported symptoms related to depression and fatigue significantly improved. The observed changes suggest that rhGH replacement has a positive impact on cardiorespiratory fitness and a positive impact on perceptual fatigue in survivors of TBI with altered GH secretion.
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Journal of neurotrauma · Feb 2017
Neurosurgical treatment variation of traumatic brain injury - Evaluation of acute subdural hematoma management in Belgium and The Netherlands.
Several recent global traumatic brain injury (TBI) initiatives rely on practice variation in diagnostic and treatment methods to answer effectiveness questions. One of these scientific dilemmas, the surgical management of the traumatic acute subdural hematoma (ASDH) might be variable among countries, among centers within countries, and even among neurosurgeons within a center, and hence be amenable for a comparative effectiveness study. The aim of our questionnaire, therefore, was to explore variations in treatment for ASDH among neurosurgeons in similar centers in a densely populated geographical area. ⋯ Most pronounced was that 1 out of 7 (14%) neurosurgeons in one region chose a surgical strategy compared with 9 out of 10 (90%) in another region for the same scenario. In conclusion, variation exists in the neurosurgical management of TBI within an otherwise homogeneous setting. This variation supports the methodology of the international Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) initiative, and shaped the Dutch Neurotraumatology Quality Registry (Net-QuRe) initiative.
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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.