Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Oct 2014
Experimental Traumatic Brain Injury Alters Ethanol Consumption and Sensitivity.
Altered alcohol consumption patterns after traumatic brain injury (TBI) can lead to significant impairments in TBI recovery. Few preclinical models have been used to examine alcohol use across distinct phases of the post-injury period, leaving mechanistic questions unanswered. To address this, the aim of this study was to describe the histological and behavioral outcomes of a noncontusive closed-head TBI in the mouse, after which sensitivity to and consumption of alcohol were quantified, in addition to dopaminergic signaling markers. ⋯ Intake across 7 days of consumption was significantly reduced in TBI mice compared with sham controls, paralleling the reduction in alcohol consumption observed clinically in the initial post-injury period. These data demonstrate that TBI increases sensitivity to ethanol-induced sedation and affects downstream signaling mediators of striatal dopaminergic neurotransmission while altering ethanol consumption. Examining TBI effects on ethanol responsitivity will improve our understanding of alcohol use post-TBI in humans.
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Journal of neurotrauma · Oct 2014
Comparative StudyPredicting outcome after traumatic brain injury: development of prognostic scores based on the IMPACT and the APACHE II.
Prediction models are important tools for heterogeneity adjustment in clinical trials and for the evaluation of quality of delivered care to patients with traumatic brain injury (TBI). We sought to improve the predictive performance of the IMPACT (International Mission for Prognosis and Analysis of Clinical Trials) prognostic model by combining it with the APACHE II (Acute Physiology and Chronic Health Evaluation II) for 6-month outcome prediction in patients with TBI treated in the intensive care unit. A total of 890 patients with TBI admitted to a large urban level 1 trauma center in 2009-2012 comprised the study population. ⋯ Internal validation using split-sample and resample bootstrap techniques yielded equivalent results, indicating low grade of overestimation. Our findings show that by combining the APACHE II with the IMPACT, improved 6-month outcome predictive performance is achieved. This may be applicable for heterogeneity adjustment in forthcoming TBI studies.
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Journal of neurotrauma · Oct 2014
The Parkland Protocol's Modified Berne-Norwood Criteria Predict Two Tiers of Risk for TBI Progression.
As a basis for venous thromboembolism (VTE) prophylaxis after traumatic brain injury (TBI), we have previously published an algorithm known as the Parkland Protocol. Patients are classified by risk for spontaneous progression of hemorrhage with chemoprophylaxis regimens tailored to each tier. We sought to validate this schema. ⋯ Tukey's post-hoc test showed the low-risk progression rate to be significantly different than both the moderate- and high-risk arms; no difference was noted between the moderate- and high-risk arms themselves. These criteria are a valid tool for classifying TBI patients into two categories of risk for spontaneous progression. This supports tailored chemoprophylaxis regimens for each arm.
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Hairy and enhancer of split 1 (Hes1), a downstream target of Notch signaling, has long been recognized as crucial in inhibiting neuronal differentiation. However, the role of Hes1 following traumatic brain injury (TBI) in adult neurogenesis in the mouse dentate gyrus (DG) remains partially understood. Here, we investigate the role of Hes1 in regulating neurogenesis in the DG of the adult hippocampus after TBI by up- or downregulating Hes1 expression. ⋯ Second, downregulation of Hes1 via RNA interference (RNAi) results in a significant increase in neuronal production and promotes the differentiation of NPCs into mature neurons in the DG, as assessed by BrdU and NeuN double staining. Furthermore, a Morris water maze (MWM) test clearly confirmed that the knockdown of Hes1 improves the spatial learning and memory capacity of adult mice following injury. Taken together, these observations suggest that Hes1 represents a negative regulator of adult neurogenesis post-TBI and that the precise space-time regulation of Hes1 expression in the DG may promote the recovery of neural function following TBI.