Journal of neurotrauma
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Journal of neurotrauma · Aug 2009
Traumatic brain injury and intestinal dysfunction: uncovering the neuro-enteric axis.
Traumatic brain injury (TBI) can lead to several physiologic complications including gastrointestinal dysfunction. Specifically, TBI can induce an increase in intestinal permeability, which may lead to bacterial translocation, sepsis, and eventually multi-system organ failure. However, the exact mechanism of increased intestinal permeability following TBI is unknown. ⋯ Expression of ZO-1 was decreased by 49% relative to sham animals (p < 0.02), whereas expression of occludin was decreased by 73% relative to sham animals (p < 0.001). An increase in intestinal permeability corresponds with decreased expression of tight junction proteins ZO-1 and occludin following TBI. Expression of intestinal tight junction proteins may be an important factor in gastrointestinal dysfunction following brain injury.
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Journal of neurotrauma · Aug 2009
Integrated imaging approach with MEG and DTI to detect mild traumatic brain injury in military and civilian patients.
Traumatic brain injury (TBI) is a leading cause of sustained impairment in military and civilian populations. However, mild (and some moderate) TBI can be difficult to diagnose due to lack of obvious external injuries and because the injuries are often not visible on conventional acute MRI or CT. ⋯ The present study used a neuroimaging approach integrating findings of magnetoencephalography (MEG) and diffusion tensor imaging (DTI), evaluating their utility in diagnosing mild TBI in 10 subjects in whom conventional CT and MRI showed no visible lesions in 9. The results show: (1) the integrated approach with MEG and DTI is more sensitive than conventional CT and MRI in detecting subtle neuronal injury in mild TBI; (2) MEG slow waves in mild TBI patients originate from cortical gray matter areas that experience de-afferentation due to axonal injuries in the white matter fibers with reduced fractional anisotropy; (3) findings from the integrated imaging approach are consistent with post-concussive symptoms; (4) in some cases, abnormal MEG delta waves were observed in subjects without obvious DTI abnormality, indicating that MEG may be more sensitive than DTI in diagnosing mild TBI.
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Journal of neurotrauma · Aug 2009
Low-level blasts raise intracranial pressure and impair cognitive function in rats.
Brain injury after high-level blast has been established both clinically and experimentally. Less is known about the effects on the brain of exposure to low to moderate blast levels, such as those encountered by military personnel during the firing of weapons. This study investigates if exposure to occupational levels of low-level blasts affect intracranial pressure and cognitive performance. ⋯ After exposure to 10 or 30 kPa and re-testing 2 days later, the latency was increased by over 100%. The results show that exposure of rats to blast levels as low as 10 kPa affects both ICP and cognitive function. Though species differences do not allow direct extrapolation to humans, these findings do pose the question as to whether the thresholds for brain injury might be lower than those of other organs used to set training standards for blast exposure.
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Journal of neurotrauma · Aug 2009
Temporal and spatial dynamics of peroxynitrite-induced oxidative damage after spinal cord contusion injury.
The reactive nitrogen species peroxynitrite (PN) has been suggested to be an important mediator of the secondary oxidative damage that occurs following acute spinal cord injury (SCI). The PN decomposition products nitrogen dioxide (*NO(2)), hydroxyl radical (*OH), and carbonate radical (*CO(3)) are highly reactive with cellular lipids and proteins. In this immunohistochemical study, we examined the temporal (3, 24, and 72 h, and 1 and 2 weeks) and spatial relationships of PN-mediated oxidative damage in the contusion-injured rat thoracic spinal cord (IH device, 200 kdyn, T10) using 3-nitrotyrosine (3-NT), a marker for protein nitration by PN-derived *NO(2) and 4-hydroxynonenal (4-HNE), an indicator of lipid peroxidation (LP) initiated by any of the PN radicals. ⋯ At all time points except 3 h, there was no significant difference in the mean rostral or caudal extent of 3-NT and 4-HNE staining. By 1, and more so at 2 weeks, the longitudinal extent of the oxidative damage staining was greatly decreased. The spatial and temporal overlap of 3-NT and 4-HNE staining supports the concept that PN is involved in both damage produced by lipid peroxidation and protein nitration, and that antioxidant agents that target PN or PN-derived radicals should be effective neuroprotectants for acute SCI if administered during the first post-injury hours.
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Journal of neurotrauma · Aug 2009
Conditional knockout of brain-derived neurotrophic factor in the hippocampus increases death of adult-born immature neurons following traumatic brain injury.
It has been reported that the hippocampus is particularly vulnerable to traumatic brain injury (TBI), the consequence of which results in hippocampal-dependent cognitive impairment. In the previous study we found that adult-born immature neurons in the hippocampal dentate gyrus are the most vulnerable cell type to moderate TBI insult. ⋯ The results showed that the amount of adult-born immature neuron death in the hippocampal dentate gyrus significantly increased in the BDNF conditional knockout mice. This result suggests that BDNF is involved in regulating the survival of adult-born immature neurons in the hippocampus following TBI, and potentially might be a useful target for preventing the adult-born immature neurons from death following TBI.