Articles: traumatic-brain-injuries.
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Depressive symptoms occur in approximately half of trauma patients, negatively impacting on functional outcome and quality of life following severe head injury. Pontine noradrenaline has been shown to increase upon trauma and associated β-adrenergic receptor activation appears to consolidate memory formation of traumatic events. Blocking adrenergic activity reduces physiological stress responses during recall of traumatic memories and impairs memory, implying a potential therapeutic role of β-blockers. This study examines the effect of pre-admission β-blockade on post-traumatic depression. ⋯ β-blockade appears to act prophylactically and significantly reduces the risk of post-traumatic depression in patients suffering from isolated severe traumatic brain injuries. Further prospective randomized studies are warranted to validate this finding.
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Journal of neurotrauma · Jan 2017
TBI induces alterations in cortical glutamate uptake without a reduction in GLT-1 protein expression.
We hypothesize that the primary mechanism for removal of glutamate from the extracellular space is altered after traumatic brain injury (TBI). To evaluate this hypothesis, we initiated TBI in adult male rats using a 2.0 atm lateral fluid percussion injury (LFPI) model. In the ipsilateral cortex and hippocampus, we found no differences in expression of the primary glutamate transporter in the brain (GLT-1) 24 h after TBI. ⋯ Exploratory studies using an inhibitor of Akt suggest selective activation of kinases in LFPI versus controls. Ingenuity pathway analyses of implicated kinases from our network model found apoptosis and cell death pathways as top functions in acute LFPI. Taken together, our data suggest diminished activity of glutamate transporters in the prefrontal cortex, with no changes in protein expression of the primary glutamate transporter GLT-1, and global alterations in signaling networks that include serine-threonine kinases that are known modulators of glutamate transport activity.
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Observational Study
Management and outcome of traumatic brain injury patients at Muhimbili Orthopaedic Institute Dar es Salaam, Tanzania.
Traumatic brain Injuries represents a significant cause of morbidity and mortality worldwide and road traffic crashes accounts for a significant proportion of these injuries. However, access to neurosurgical care is poor in low income countries like Tanzania. The aim of this study was to assess the management and outcome of Traumatic brain injury patients at a tertiary level health facility in Tanzania. ⋯ Traumatic brain injury is a public health problem in Tanzania, mostly due to road traffic crashes. It is therefore important to reinforce preventive measures for road traffic crashes. There is also a need to develop and implement protocols for pre-hospital as well as in-hospital management of brain trauma in Tanzania.
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Journal of neurotrauma · Jan 2017
Comparative StudyStrong correlation of genome-wide expression after traumatic brain injury in vitro and in vivo implicates a role for SORLA.
The utility of in vitro models of traumatic brain injury (TBI) depends on their ability to recapitulate the in vivo TBI cascade. In this study, we used a genome-wide approach to compare changes in gene expression at several time points post-injury in both an in vitro model and an in vivo model of TBI. We found a total of 2073 differentially expressed genes in our in vitro model and 877 differentially expressed genes in our in vivo model when compared to noninjured controls. ⋯ We confirmed downregulation of SORLA expression in organotypic hippocampal slice cultures by immunohistochemistry and Western blotting and present preliminary data from human tissue that is consistent with these experimental results. Together, these data suggest that the in vitro model of TBI used in this study strongly recapitulates the in vivo TBI pathobiology and is well suited for future mechanistic or therapeutic studies. The data also suggest the possible involvement of SORLA in the post-traumatic cascade linking TBI to AD.
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This study examined whether a history of traumatic brain injury (TBI) is associated with earlier onset of Alzheimer disease (AD), independent of apolipoprotein ε4 status (Apoe4) and gender. ⋯ History of self-reported TBI can be associated with an earlier onset of AD-related cognitive decline, regardless of Apoe4 status and gender. TBI may be related to an underlying neurodegenerative process in AD, but the implications of age at time of injury, severity, and repetitive injuries remain unclear.