Developmental neuroscience
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The objective of this study was to describe the incidence of impaired cerebral autoregulation and to describe the relationship between impaired cerebral autoregulation and outcome after severe pediatric traumatic brain injury (TBI). We prospectively examined cerebral autoregulation in 28 children
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Traumatic brain injury (TBI) is the leading cause of death and disability in children. Evidence-based guidelines for the management of this population are available; however, the data highlight significant deficiencies with few treatment standards or guidelines. Considering the limited availability of resources, it is necessary to define realistic goals. Attention should be given to injury prevention, developing standardized pediatric admission and outcome evaluations, increasing the utility and spectrum of physiological and biochemical testing, and defining the evolving role of imaging in TBI.
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Mitochondria play a central role in cerebral energy metabolism, intracellular calcium homeostasis and reactive oxygen species generation and detoxification. Following traumatic brain injury (TBI), the degree of mitochondrial injury or dysfunction can be an important determinant of cell survival or death. Literature would suggest that brain mitochondria from the developing brain are very different from those from mature animals. ⋯ This review will focus on four main areas of secondary injury after pediatric TBI, including excitotoxicity, oxidative stress, alterations in energy metabolism and cell death pathways. Specifically, we will describe what is known about developmental differences in mitochondrial function in these areas, in both the normal, physiologic state and the pathologic state after pediatric TBI. The ability to identify and target aspects of mitochondrial dysfunction could lead to novel neuroprotective therapies for infants and children after severe TBI.
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Inflicted traumatic brain injury (iTBI) involves a combination of mechanical trauma and hypoxemia. Serum biomarker concentrations may provide objective information about their relative importance to the pathophysiology of iTBI. We compared the time course of neuron-specific enolase (NSE), S100B and myelin basic protein after pediatric hypoxic-ischemic brain injury, iTBI and noninflicted TBI (nTBI). ⋯ Initial NSE concentration was highest after nTBI. These results suggest that the biochemical response of the brain to iTBI is distinct from the response to nTBI and shares temporal similarities with hypoxic-ischemic brain injury. This may have important implications for the treatment and prognosis of children with iTBI.
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Randomized Controlled Trial Multicenter Study
Hypothermia pediatric head injury trial: the value of a pretrial clinical evaluation phase.
The utility of a pretrial clinical evaluation or run-in phase prior to conducting trials of complex interventions such as hypothermia therapy following severe traumatic brain injury in children and adolescents has not been established. ⋯ The pretrial clinical evaluation phase was useful to ensure compliance with complex hypothermia therapy and consensus-based clinical management guidelines of care successfully implemented across 17 of 18 centers. This study maneuver allowed us to complete a subsequent RCT in 225 children following severe traumatic brain injury.