Articles: traumatic-brain-injuries.
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There are currently no federally approved neuroprotective agents to treat traumatic brain injury. Progesterone, a hydrophobic steroid hormone, has been shown in recent studies to exhibit neuroprotective effects in controlled cortical impact rat models. Akt is a protein kinase known to play a role in cell signaling pathways that reduce edema, inflammation, apoptosis, and promote cell growth in the brain. ⋯ Traumatic brain injury caused a significant decrease in Akt phosphorylation compared to sham operation. However, mice treated with progesterone following traumatic brain injury had an increase in phosphorylation of Akt compared to traumatic brain injury vehicle. Our findings suggest that progesterone is a viable treatment option for activating neuroprotective pathways after traumatic brain injury.
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Traumatic brain injury (TBI) remains a significant public health problem and is a leading cause of death and disability in many countries. Durable treatments for neurological function deficits following TBI have been elusive, as there are currently no FDA-approved therapeutic modalities for mitigating the consequences of TBI. Neurostimulation strategies using various forms of electrical stimulation have recently been applied to treat functional deficits in animal models and clinical stroke trials. ⋯ There have been only a few studies using deep brain stimulation (DBS) in human TBI patients, and future studies are warranted to validate the feasibility of this technique in the clinical treatment of TBI. In this review, the authors summarize insights from studies employing neurostimulation techniques in the setting of brain injury. Moreover, they relate these findings to the future prospect of using DBS to ameliorate motor and cognitive deficits following TBI.
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Neurotrauma continues to be a significant cause of morbidity and mortality. Prevention of primary neurologic injury is a critical public health concern. ⋯ Critical care management of the patient with neurotrauma is focused on the prevention of secondary injuries. Much research is still needed for potential neuroprotection therapies.
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Premature mortality is a public health concern that can be quantified as years of potential life lost (YPLL). Studying premature mortality can help guide hospital initiatives and resource allocation. We investigated the categories of neurologic and neurosurgical conditions associated with in-hospital deaths that account for the highest YPLL and their trends over time. ⋯ The in-hospital mortality rate has been stable or decreasing for all of these diagnoses except TBI, which rose from 5.1% in 1988 to 7.8% in 2011. Using YPLL, we provide a framework to compare the burden of premature in-hospital mortality on patients with neurologic disorders, which may prove useful for informing decisions related to allocation of health resources or research funding. Considering premature mortality alone, increased efforts should be focused on TBI, particularly in and related to the hospital setting.
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TBI causes localized cerebral ischemia that, in turn, is accompanied by both changes in BBB permeability and recruitment of CD34(+) cells to the injured tissue. However, it remains unknown whether CD34(+) cell recruitment is linked to BBB permeability. This study is a preliminary investigation into possible correlations between CD34(+) cell recruitment and BBB permeability following TBI in a rat model. ⋯ The negative linear correlation between CD34(+) cell recruitment and BBB permeability following TBI provides a support for further study of CD34(+) cell transplantation for BBB repair after TBI.