Journal of neurotrauma
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Journal of neurotrauma · Apr 2014
The VEGF concentration in chronic subdural hematoma fluid is related to CT appearance and exudation rate.
Chronic subdural hematoma (CSH) is characterized by a net increase of volume over time. Major underlying mechanisms appear to be hemorrhagic episodes and a continuous exudation, which may be studied using labeled proteins to yield an exudation rate in a given patient. We tested the hypothesis that the concentration of vascular endothelial growth factor (VEGF) in hematoma fluid correlates with the rate of exudation. ⋯ There was a statistically significant correlation between VEGF concentrations and exudation rates in the four classes of CT appearance (r=0.98). The current report is the first to suggest a pathophysiological link between the VEGF concentration and the exudation rate underlying the steady increase of hematoma volume and CT appearance. With this finding, the current report adds another piece of evidence in favor of the pathophysiological role of VEGF in the development of CSH, including mechanisms contributing to hematoma growth and CT appearance.
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Journal of neurotrauma · Apr 2014
Predictors of very long-term socio-cognitive function after pediatric traumatic brain injury (TBI): support for the vulnerability of the immature 'social brain.'
Emotion perception (EP) forms an integral part of social communication and is critical to attain developmentally appropriate goals. This skill, which emerges relatively early in development, is driven by increasing connectivity among regions of a distributed sociocognitive neural network and may be vulnerable to disruption from early-childhood traumatic brain injury (TBI). The present study aimed to evaluate the very-long-term effect of childhood TBI on EP, as well as examine the contribution of injury- and non-injury-related risk and resilience factors to variability in sociocognitive outcomes. ⋯ Survivors of severe childhood TBI were found to have significantly poorer emotion perception than controls and young adults with mild-to-moderate injuries. Further, poorer emotion perception was associated with reduced volume of the posterior corpus callosum, presence of frontal pathology, lower SES, and a less-intimate family environment. Our findings lend support to the vulnerability of the immature "social brain" network to early disruption and underscore the need for context-sensitive rehabilitation that optimizes early family environments to enhance recovery of EP skills after childhood TBI.
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Journal of neurotrauma · Apr 2014
Temporal course of changes in gene expression suggests a cytokine-related mechanism for long-term hippocampal alteration after controlled cortical impact.
Mild traumatic brain injury (mTBI) often has long-term effects on cognitive function and social behavior. Altered gene expression may be predictive of long-term psychological effects of mTBI, even when acute clinical effects are minimal or transient. Controlled cortical impact (CCI), which causes concussive, but nonpenetrant, trauma to underlying (non-cortical) brain, resulting in persistent changes in hippocampal synaptic function, was used as a model of mTBI. ⋯ Ccl2 and Ccl7 transcripts were up-regulated within 24 h after CCI, and their elevation subsided within 1 week of injury. Other transcriptional changes occurred later and were more stable, some persisting for at least 1 month, suggesting that short-term inflammatory responses trigger longer-term alteration in the expression of genes previously associated with injury, aging, and neuronal function in the brain. These transcriptional responses to mTBI may underlie long-term changes in excitatory and inhibitory neuronal imbalance in hippocampus, leading to long-term behavioral consequences of mTBI.
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Journal of neurotrauma · Apr 2014
Supplementary motor area activation is impaired in severe traumatic brain injury parkinsonism.
A high percentage of survivors of severe traumatic brain injury present diffuse axonal injury and extrapyramidal symptoms. The association between diffuse cerebral damage and parkinsonian symptoms is probably because of the interruption of nigro-striato-frontal pathways. While functional magnetic resonance imaging (fMRI) has been widely used to investigate parkinsonism in idiopathic Parkinson disease, little is known about functional brain modifications related to post-traumatic parkinsonism (PTP). ⋯ During the mime of action, which involved actual movement, the hypoactivation was localized to the motor network. Our results suggest that patients with PTP showed a cerebral reorganization for motor tasks in agreement with the cerebral reorganization observed in idiopathic Parkinson disease. For patients with PTP, supplementary motor area impairment seems to play a central role in parkinsonism, in line with the brain reorganization of action-related tasks.
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Journal of neurotrauma · Apr 2014
Increased expression of vascular endothelial growth factor (VEGF)attenuates contusion necrosis without influencing contusion edema after traumatic brain injury in rats.
To clarify the role of vascular endothelial growth factor (VEGF) in the formation of contusion edema and necrosis after traumatic brain injury, we examined the time course of changes in the VEGF expression (enzyme-linked immunosorbent assay), cerebrovascular permeability (extravasation of Evans blue), and water content (dry-wet weight method) of the contused brain tissue in a cortical impact injury model using rats. In addition, we tested the effects of administration of bevacizumab (VEGF monoclonal antibody) on changes in the cerebrovascular permeability and water content of the contused brain tissue, as well as the neurological deficits (rota rod test) and volume of contusion necrosis. Increased VEGF expression was maximal at 72 h after injury (p<0.003). ⋯ Administration of bevacizumab did not influence these changes in cerebrovascular permeability and water content, but led to a significant rise in the neurological deficits at 72 h-14 days (p<0.05 or 0.01) and the volume of contusion necrosis at 21 days (p<0.001) after injury. These findings suggest that increased expression of VEGF after injury does not contribute to the formation of contusion edema, but attenuates the formation of contusion necrosis. This is probably because of an increased angiogenesis and improved microcirculation in the areas surrounding the core of contusion.