Journal of neurotrauma
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Journal of neurotrauma · May 2010
Attitude and opinion of neurosurgeons concerning protective bicycle-helmet use.
Wearing protective helmets decreases the risk of incurring traumatic brain injury (TBI) in bicycle accidents. In 2007, the German Neurosurgical Society advocated compulsory use of bicycle helmets. Although neurosurgeons are the specialists who primarily treat patients with TBI in Europe, the distribution of helmet users among neurosurgeons (NS), as well as factors that influence the decision to wear helmets and whether professional knowledge or experience in TBI influences the use or attitude concerning bicycle helmets, remains unclear. ⋯ With respect to compulsory helmet use, NS are also split in half. Experience with TBI and trauma education has effects. However, education alone does not suffice in promoting the use of bicycle helmets.
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Journal of neurotrauma · May 2010
Sensory stimulation prior to spinal cord injury induces post-injury dysesthesia in mice.
Chronic pain and dysesthesias are debilitating conditions that can arise following spinal cord injury (SCI). Research studies frequently employ rodent models of SCI to better understand the underlying mechanisms and develop better treatments for these phenomena. While evoked withdrawal tests can assess hypersensitivity in these SCI models, there is little consensus over how to evaluate spontaneous sensory abnormalities that are seen in clinical SCI subjects. ⋯ Mice subjected to either stimulus paradigm showed increased OG compared with unstimulated or uninjured mice. Histological analysis showed no difference in spinal cord lesion size due to sensory stimulation, or between mice that overgroomed or did not overgroom. The relationship between prior stimulation and contusion injury in mice that display OG indicates a critical interaction that may underlie one facet of spontaneous neuropathic symptoms after SCI.
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Journal of neurotrauma · May 2010
Finite element analysis of controlled cortical impact-induced cell loss.
The controlled cortical impact (CCI) model has been extensively used to study region-specific patterns of neuronal injury and cell death after a focal traumatic brain injury. Although external parameters such as impact velocity and depth of penetration have been defined in this injury model, little is known about the intracranial mechanical responses within cortical and subcortical brain regions where neuronal loss is prevalent. At present, one of the best methods to determine the internal responses of the brain is finite element (FE) modeling. ⋯ A linear relationship was found between the percentage of the neuronal loss observed in vivo and the FE model-predicted maximum principal strain (R(2) = 0.602). Interestingly, the FE model also predicted some risk of injury in the cerebellum, located remote from the point of impact, with a 25% neuronal loss for the "severe" impact condition. More research is needed to examine other regions that do not have histological data for comparison with FE model predictions before this injury mechanism and the associated injury threshold can be fully established.
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Journal of neurotrauma · May 2010
The effect of epidermal growth factor in the injured brain after trauma in rats.
Epidermal growth factor (EGF) is a known mitogen for neural stem and progenitor cells (NS/NPCs) in the central nervous system (CNS). In vitro, EGF maintains NS/NPCs in the proliferative state, whereas in the normal rodent brain it promotes their proliferation and migration in the subventricular zone (SVZ). Additionally, EGF administration can augment neuronal replacement in the ischemic-injured adult striatum. ⋯ Furthermore, we found that the EGF-induced proliferative population differentiated preferentially toward astroglial phenotype. Nevertheless, animals treated with EGF showed significant improvement in cognitive function, which was accompanied by reduced hippocampal neuronal cell loss. Collectively, the data from this study demonstrate that EGF exerts a neuroprotective rather than neurogenic effect in protecting the brain from injury.