Articles: traumatic-brain-injuries.
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Brain Behav. Immun. · Nov 2016
NOX2 drives M1-like microglial/macrophage activation and neurodegeneration following experimental traumatic brain injury.
Following traumatic brain injury (TBI), activation of microglia and peripherally derived inflammatory macrophages occurs in association with tissue damage. This neuroinflammatory response may have beneficial or detrimental effects on neuronal survival, depending on the functional polarization of these cells along a continuum from M1-like to M2-like activation states. The mechanisms that regulate M1-like and M2-like activation after TBI are not well understood, but appear in part to reflect the redox state of the lesion microenvironment. ⋯ NOX2 deficiency also promotes M2-like activation after CCI, through increased IL-4Rα signaling in infiltrating macrophages, suggesting that NOX2 acts as a critical switch between M1- and M2-like activation states after TBI. Administration of gp91ds-tat to wild-type CCI mice starting at 24h post-injury reduces deficits in cognitive function and increased M2-like activation in the hippocampus. Collectively, our data indicate that increased NOX2 activity after TBI drives M1-like activation that contributes to inflammatory-mediated neurodegeneration, and that inhibiting this pathway provides neuroprotection, in part by altering M1-/M2-like balance towards the M2-like neuroinflammatory response.
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Review Meta Analysis
Risk of Delayed Intracranial Hemorrhage in Anticoagulated Patients with Mild Traumatic Brain Injury: Systematic Review and Meta-Analysis.
Delayed intracranial hemorrhage is a potential complication of head trauma in anticoagulated patients. ⋯ The present study is the first published meta-analysis estimating the risk of delayed intracranial hemorrhage 24 h after head trauma in patients anticoagulated with vitamin K antagonist and normal initial CT scan. In most situations, a repeat CT scan in the emergency department 24 h later is not necessary if the first CT scan is normal. Special care may be required for patients with serious mechanism of injury, patients showing signs of neurologic deterioration, and patients presenting with excessive anticoagulation or receiving antiplatelet co-medication.
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Neurorehabil Neural Repair · Nov 2016
Multicenter StudyCOMT and ANKK1 Genetics Interact With Depression to Influence Behavior Following Severe TBI: An Initial Assessment.
Genetic variations in the dopamine (DA) system are associated with cortical-striatal behavior in multiple populations. This study assessed associations of functional polymorphisms in the ankyrin repeat and kinase domain (ANKK1; Taq1a) and catechol-O-methyltransferase (COMT; Val158Met) genes with behavioral dysfunction following traumatic brain injury (TBI). ⋯ In the context of depression, Val158Met and Taq1a polymorphisms are individually associated with behavioral dysfunction 12 months following severe TBI, with preliminary evidence suggesting cumulative, or perhaps epistatic, effects of COMT and ANKK1 on behavioral dysfunction.
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Traumatic atlanto-occipital dislocation (AOD) is an ominous injury with high mortality and morbidity in trauma patients. Improved survival has been observed with advancements in pre-hospital and hospital care. Furthermore, high quality imaging studies are accessible at most trauma centers; these are crucial for prompt diagnosis of AOD. ⋯ We found that patients with TBI are eight times more likely to die than patients without TBI. A high degree of suspicion for AOD during pre-hospital care, as well as, prompt diagnosis and management in the trauma center play a key role in the treatment of this devastating injury. The relationship between survival and factors such as TBI and SCI should be further explored.