Articles: traumatic-brain-injuries.
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Int J Crit Illn Inj Sci · Apr 2015
Cardiac dysfunction following brain death after severe pediatric traumatic brain injury: A preliminary study of 32 children.
Cardiac dysfunction after brain death has been described in a variety of brain injury paradigms but is not well understood after severe pediatric traumatic brain injury (TBI). Cardiac dysfunction may have implications for organ donation in this patient population. ⋯ The incidence of cardiac dysfunction is higher among pediatric severe TBI patients with a diagnosis of brain death, as compared to patients without brain death. This finding may have implications for cardiac organ donation from this population and deserves further study.
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Brain Trauma Foundation (BTF) guidelines recommend intracranial pressure (ICP) monitoring for traumatic brain injury (TBI) patients with a Glasgow Coma Scale score of 8 or less with an abnormal head computed tomography, or a normal head computed tomography scan with systolic blood pressure ≤90 mm Hg, posturing, or in patients of age ≥40. The benefits of these guidelines on outcome remain unproven. We hypothesized that adherence to BTF guidelines for ICP monitoring does not improve outcomes in patients with TBI. ⋯ Our data suggest that there is a subset of patients meeting BTF criteria for ICP monitoring that do well without ICP monitoring. This finding should provoke reevaluation of the indication and utility of ICP monitoring in TBI patients.
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Journal of neurotrauma · Apr 2015
Inhibition of injury-induced cell proliferation in the dentate gyrus of the hippocampus impairs spontaneous cognitive recovery following traumatic brain injury.
Neurogenesis persists throughout life in the neurogenic regions of the mature mammalian brain, and this response is enhanced after traumatic brain injury (TBI). In the hippocampus, adult neurogenesis plays an important role in hippocampal-dependent learning and memory functions and is thought to contribute to the spontaneous cognitive recovery observed after TBI. Utilizing an antimitotic agent, arabinofuranosyl cytidine (Ara-C), the current study investigated the direct association of injury-induced hippocampal neurogenesis with cognitive recovery. ⋯ We found that a 7-day infusion of Ara-C significantly reduced the total number of BrdU(+) and DCX(+) cells in the dentate gyrus (DG) in both hemispheres. Moreover, inhibition of the injury-induced cell proliferative response in the DG completely abolished the innate cognitive recovery on MWM performance at 56-60 days postinjury. These results support the causal relationship of injury-induced hippocampal neurogenesis on cognitive functional recovery and suggest the importance of this endogenous repair mechanism on restoration of hippocampal function.
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To study the effect of simvastatin on neurological functional recovery after traumatic brain injuries (TBI) and the possible molecular mechanisms, we evaluated simvastatin-induced proliferation and differentiation of neural stem cells (NSCs) in vitro and in vivo and possible involvement of Notch-1 signaling in this process. ⋯ Simvastatin treatment enhanced neurological functional recovery after TBI possibly via activation of Notch signaling and increasing neurogenesis in the injured area.
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Proc. Natl. Acad. Sci. U.S.A. · Mar 2015
HDAC inhibition prevents white matter injury by modulating microglia/macrophage polarization through the GSK3β/PTEN/Akt axis.
Severe traumatic brain injury (TBI) elicits destruction of both gray and white matter, which is exacerbated by secondary proinflammatory responses. Although white matter injury (WMI) is strongly correlated with poor neurological status, the maintenance of white matter integrity is poorly understood, and no current therapies protect both gray and white matter. One candidate approach that may fulfill this role is inhibition of class I/II histone deacetylases (HDACs). ⋯ These findings are consistent with recent findings that microglial phenotypic switching modulates white matter repair and axonal remyelination and highlight a previously unexplored role for HDAC activity in this process. Furthermore, the functions of GSK3β may be more subtle than previously thought, in that GSK3β can modulate microglial functions via the PTEN/PI3K/Akt signaling pathway and preserve white matter homeostasis. Thus, inhibition of HDACs in microglia is a potential future therapy in TBI and other neurological conditions with white matter destruction.