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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Based on recent work demonstrating age-dependent ketogenic neuroprotection after traumatic brain injury (TBI), it was hypothesized that the neuroprotection among early post-weaned animals was related to induced cerebral transport of ketones after injury. Regional changes in monocarboxylate transporter 2 (MCT2) were acutely examined with immunohistochemistry after sham surgery or controlled cortical impact injury among postnatal day 35 and adult rats. ⋯ Using Western blotting, MCT2 expression was 80-88% greater in microvessels isolated from postnatal day 35 rats at all time points relative to adults. The increased MCT2 expression was temporally correlated with an age-related increase in cerebral uptake of ketones, when ketones were made available after injury.
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Review
Use of advanced neuroimaging techniques in the evaluation of pediatric traumatic brain injury.
Advanced neuroimaging techniques are now used to expand our knowledge of traumatic brain injury, and increasingly, they are being applied to children. This review will examine four of these methods as they apply to children who present acutely after injury. (1) Susceptibility weighted imaging is a 3-dimensional high-resolution magnetic resonance imaging technique that is more sensitive than conventional imaging in detecting hemorrhagic lesions that are often associated with diffuse axonal injury. (2) Magnetic resonance spectroscopy acquires metabolite information reflecting neuronal integrity and function from multiple brain regions and provides sensitive, noninvasive assessment of neurochemical alterations that offers early prognostic information regarding the outcome. (3) Diffusion weighted imaging is based on differences in diffusion of water molecules within the brain and has been shown to be very sensitive in the early detection of ischemic injury. ⋯ An important aspect of these advanced methods is that they demonstrate that 'normal-appearing' brain in many instances is not normal, i.e. there is evidence of significant undetected injury that may underlie a child's clinical status. Availability and integration of these advanced imaging methods will lead to better treatment and change the standard of care for use of neuroimaging to evaluate children with traumatic brain injury.
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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.