Articles: traumatic-brain-injuries.
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The impact acceleration (I/A) model of traumatic brain injury (TBI) was developed to reliably induce diffuse traumatic axonal injury in rats in the absence of skull fractures and parenchymal focal lesions. This model replicates a pathophysiology that is commonly observed in humans with diffuse axonal injury (DAI) caused by acceleration-deceleration forces. Such injuries are typical consequences of motor vehicle accidents and falls, which do not necessarily require a direct impact to the closed skull. ⋯ Furthermore, the trauma device is inexpensive and readily manufactured in any laboratory, and the induction of injury is rapid (~45 min per animal from weighing to post-injury recovery) allowing multiple animal experiments per day. In this chapter, we describe in detail the methodology and materials required to produce the rat model of I/A in the laboratory. We also review current adaptations to the model to alter injury severity, discuss frequent complications and technical issues encountered using this model, and provide recommendations to ensure technically sound injury induction.
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Observational Study
Prospective evaluation of early propranolol after traumatic brain injury.
Although beta-adrenergic receptor blockade may improve outcomes after traumatic brain injury (TBI), its early use is not routine. We hypothesize that judicious early low-dose propranolol after TBI (EPAT) will improve outcomes without altering bradycardia or hypotensive events. ⋯ Although bradycardia and hypotensive events occur early after TBI, low-dose intravenous propranolol does not increase their number or severity. Early use of propranolol after TBI appears to be safe and may be associated with decreased ICU and hospital LOS.
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Traumatic brain injury (TBI) is the leading cause of death and disability for people under 45 years of age. Clinical TBI is often the result of disparate forces resulting in heterogeneous injuries. Preclinical modeling of TBI is a vital tool for studying the complex cascade of metabolic, cellular, and molecular post-TBI events collectively termed secondary injury. ⋯ This chapter details the most widely used models of preclinical TBI, including the controlled cortical impact, fluid percussion, blast, and closed head models. Each of these models replicates particular critical aspects of clinical TBI. Prior to selecting a preclinical TBI model, it is important to address what aspect of human TBI is being sought to evaluate.
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Brain injury : [BI] · Jan 2016
Voxel-based statistical analysis of brain metabolism in patients with growth hormone deficiency after traumatic brain injury.
The aim of this study was to investigate the regional cerebral metabolism related to growth hormone deficiency (GHD) after traumatic brain injury (TBI) using F-18 fluorodeoxyglucose positron emission tomography (F-18 FDG PET) images. ⋯ The findings are suggestive of the brain region influenced by GHD. These cortical areas are involved in regulation of intellectual function, executive function and working memory.
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NeuroImage. Clinical · Jan 2016
Brain volume loss contributes to arousal and empathy dysregulation following severe traumatic brain injury.
Severe traumatic brain injury (TBI) often leads to deficits in physiological arousal and empathy, which are thought to be linked. This study examined whether injury-related brain volume loss in key limbic system structures is associated with these deficits. Twenty-four adults with TBI and 24 matched Controls underwent MRI scans to establish grey matter volumes in the amygdala, thalamus, and hippocampus. ⋯ Regional brain volumes were differentially correlated to arousal and self-report empathy. Importantly, lower volume in pertinent brain structures correlated with lower empathy, for participants with and without TBI. Overall we provide new insights into empathic processes after TBI and their relationship to brain volume loss.