Journal of neurotrauma
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Journal of neurotrauma · Oct 2015
Increased network excitability due to altered synaptic inputs to neocortical layer V intact and axotomized pyramidal neurons after mild traumatic brain injury.
Mild traumatic brain injury (mTBI) can produce long lasting cognitive dysfunction. There is typically no cell death and only diffuse structural injury after mTBI. Thus, functional changes in intact neurons may contribute to symptoms. ⋯ The amplitude of this evoked negativity was significantly larger than controls over a series of stimulus intensities at both the 1 d and 2 d survival times. Interictal-like spikes never occurred in the field potential recordings from controls but were observed in 20-80% of stimulus presentations in injured cortex. Together, these results suggest an overall increase in network excitability and the production of particularly powerful (intact) neurons that have both increased intrinsic and synaptic excitability.
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Journal of neurotrauma · Oct 2015
Pro-Neurotrophin binding to p75 neurotrophin receptor (p75NTR) is essential for brain lesion formation and functional impairment after experimental traumatic brain injury.
Traumatic brain injury (TBI) initiates an excessive mediator release of e.g. neurotrophins, which promote neuronal survival, differentiation, and modulate synaptic plasticity. Paradoxically, mature forms of neurotrophins promote neuronal survival, whereas unprocessed forms of neurotrophins induce cell death through p75 neurotrophin receptor (p75NTR) signaling. p75NTR is widely expressed during synaptogenesis and is subsequently downregulated in adulthood. Repair mechanisms after acute cerebral insults can reactivate its expression. ⋯ Pharmacological inhibition of the p75NTR signaling reduced lesion volume by 18%. The present study presents first time evidence that genetic mutation of the neurotrophin interaction site of p75NTR strongly limits post-traumatic cell death. In addition, we revealed pharmacological targeting of the intracellular p75NTR cell death domain as a promising approach to limit acute brain damage.
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Journal of neurotrauma · Oct 2015
ReviewSleep-wake disturbances and fatigue following pediatric traumatic brain injury: a systematic review of the literature.
Sleep-wake disturbances (SWD) after traumatic brain injury (TBI) are frequently reported and can persist several years post-injury. The adult literature covering this topic is exhaustive; numerous robust studies using objective measures of sleep and advanced methodologies support the presence of SWD post-TBI. Despite being the leading cause of morbidity in children and adolescents, however, relatively few studies exist investigating SWD and symptoms of fatigue after pediatric TBI. ⋯ Moreover, no study targeted preschool children despite the fact that there is evidence regarding the critical importance of sleep for appropriate cognitive development, especially in high-order cognitive functioning. In sum, the results of the studies analyzed were consistent with the presence of SWD and fatigue after pediatric TBI, but there is a lack of information concerning this relationship in younger children. The use of more objective measures, such as actigraphy, could bring better insight to the impact of TBI on the quality of children's sleep.
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Journal of neurotrauma · Oct 2015
Head trauma with or without mild brain injury increases the risk of future traumatic death: A controlled prospective 15-year follow-up study.
Patients who have recovered from traumatic brain injury (TBI) show an increased risk of premature death. To investigate long-term mortality rates in a population admitted to the hospital for head injury (HI), we conducted a population-based prospective case-control, record-linkage study, All subjects who were living in Northern Ostrobothnia, and who were admitted to Oulu University Hospital in 1999 because of HI (n=737), and 2196 controls matched by age, gender, and residence randomly drawn from the population of Northern Ostrobothnia were included. Death rate and causes of death in HI subjects during 15 years of follow-up was compared with the general population controls. ⋯ The main founding was that even HI without TBI carries an increased risk of future traumatic death. The reason for this remains unknown and further studies are needed. To prevent such premature deaths, post-traumatic therapy should include an interview focusing on lifestyle factors.
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Journal of neurotrauma · Oct 2015
Matrix Metalloproteinase Expression in Contusional Traumatic Brain Injury: A Paired Microdialysis Study.
Matrix metalloproteinases (MMPs) are extracellular enzymes that have been implicated in the pathophysiology of blood-brain barrier (BBB) breakdown, contusion expansion, and vasogenic edema after traumatic brain injury (TBI). Specifically, in focal injury models, increased MMP-9 expression has been observed in pericontusional brain, and MMP-9 inhibitors reduce brain swelling and final lesion volume. The aim of this study was to examine whether there is a similarly localized increase of MMP concentrations in patients with contusional TBI. ⋯ Repeated-measures analysis of variance showed that MMP-9 concentrations were significantly higher in pericontusional brain (p=0.03) and within the first 72 h of injury, compared with later in the monitoring period (p=0.04). No significant differences were found for the other MMPs assayed. MMP-9 concentrations are increased in pericontusional brain early post-TBI and may represent a potential therapeutic target to reduce hemorrhagic progression and vasogenic edema.