Journal of neurotrauma
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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.
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Journal of neurotrauma · Apr 2010
Clinical TrialCerebrospinal fluid inflammatory cytokines and biomarkers of injury severity in acute human spinal cord injury.
There is an urgent need for both the scientific development and clinical validation of novel therapies for acute spinal cord injury (SCI). The scientific development of novel therapies would be facilitated by a better understanding of the acute pathophysiology of human SCI. Clinical validation of such therapies would be facilitated by the availability of biomarkers with which to stratify injury severity and predict neurological recovery. ⋯ Furthermore, segmental motor recovery at 6 months post injury was better predicted by these CSF proteins than with the patients' baseline ASIA grade. The pattern of expression over the first 3 to 4 days post injury of a number of inflammatory cytokines such as IL-6, IL-8, and MCP-1 provides invaluable information about the pathophysiology of human SCI. A prediction model that could use such biological data to stratify injury severity and predict neurological outcome may be extremely useful for facilitating the clinical validation of novel treatments in acute human SCI.
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Journal of neurotrauma · Apr 2010
Hyperoxic reperfusion after global cerebral ischemia promotes inflammation and long-term hippocampal neuronal death.
In this study we tested the hypothesis that long-term neuropathological outcome is worsened by hyperoxic compared to normoxic reperfusion in a rat global cerebral ischemia model. Adult male rats were anesthetized and subjected to bilateral carotid arterial occlusion plus bleeding hypotension for 10 min. The rats were randomized to one of four protocols: ischemia/normoxia (21% oxygen for 1 h), ischemia/hyperoxia (100% oxygen for 1 h), sham/normoxia, and sham/hyperoxia. ⋯ Behavioral deficits were also observed following hyperoxic, but not normoxic, reperfusion. We conclude that early post-ischemic hyperoxic reperfusion is followed by greater hippocampal neuronal death and cellular inflammatory reactions compared to normoxic reperfusion. The results of these long-term outcome studies, taken together with previously published results from short-term experiments performed with large animals, support the hypothesis that neurological outcome can be improved by avoiding hyperoxic resuscitation after global cerebral ischemia such as that which accompanies cardiac arrest.