Articles: traumatic-brain-injuries.
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Since the introduction of all-terrain vehicles (ATV) to the United States in 1971, injuries and mortalities related to their use have increased significantly. Furthermore, these vehicles have become larger and more powerful. As there are no helmet requirements or limitations on engine-size in the State of Alabama, we hypothesised that larger engine size would correlate with an increased incidence of traumatic brain injury (TBI) in patients following an ATV crash. ⋯ Patients on an ATV with an engine size of 350 cc or greater were more likely to have a TBI. The use of a helmet was rarely present in this cohort. Legislative efforts to implement rider protection laws for ATVs are warranted.
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Journal of neurotrauma · Apr 2015
Group-wise evaluation and comparison of white matter fiber strain and maximum principal strain in sports-related concussion.
Sports-related concussion is a major public health problem in the United States and yet its biomechanical mechanisms remain unclear. In vitro studies demonstrate axonal elongation as a potential injury mechanism; however, current response-based injury predictors (e.g., maximum principal strain, ε(ep)) typically do not incorporate axonal orientations. We investigated the significance of white matter (WM) fiber orientation in strain estimation and compared fiber strain (ε(n)) with ε(ep) for 11 athletes with a clinical diagnosis of concussion. ⋯ For example, an average of 3.2% vs. 29.8% of WM was predicted above an optimal threshold of 0.18 established from an in vivo animal study using ε(n) and ε(ep), respectively, with an average Dice coefficient of 0.14. The distribution of WM regions with high ε(n) was consistent with typical heterogeneous patterns of WM disruptions in diffuse axonal injury, and the group-wise extent at the optimal threshold matched well with the percentage of WM voxels experiencing significant longitudinal changes of fractional anisotropy and mean diffusivity (3.2% and 3.44%, respectively) found from a separate independent study. These results suggest the significance of incorporating WM microstructural anisotropy in future brain injury studies.
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In this study, rats were put into traumatic brain injury-induced coma and treated with median nerve electrical stimulation. We explored the wake-promoting effect, and possible mechanisms, of median nerve electrical stimulation. ⋯ In addition, after the OX1R antagonist, SB334867, was injected into the brain of rats after traumatic brain injury, fewer rats were restored to consciousness, and orexin-A and OXIR expression in the prefrontal cortex was downregulated. Our findings indicate that median nerve electrical stimulation induced an up-regulation of orexin-A and OX1R expression in the prefrontal cortex of traumatic brain injury-induced coma rats, which may be a potential mechanism involved in the wake-promoting effects of median nerve electrical stimulation.
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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.