Articles: traumatic-brain-injuries.
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Traumatic brain injury (TBI) is the leading cause of death and disability among children in the United States. Affected children will often suffer from emotional, cognitive and neurological impairments throughout life. In the controlled cortical impact (CCI) animal model of pediatric TBI (postnatal day 16-17) it was demonstrated that injury results in abnormal neuronal hypoactivity in the non-injured primary somatosensory cortex (S1). ⋯ Notably, these rats showed less hyperactivity in behavioral tests. These results implicate TMS as a promising approach for reversing the adverse neuronal mechanisms activated post-TBI. Importantly, this intervention could readily be translated to human studies.
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To determine whether 6 weeks of exercise performed prior to traumatic brain injury (TBI) could improve post-TBI behavioral outcomes in mice, and if exercise increases neuroprotective molecules (vascular endothelial growth factor-A [VEGF-A], erythropoietin [EPO], and heme oxygenase-1 [HO-1]) in brain regions responsible for movement (sensorimotor cortex) and memory (hippocampus). ⋯ Improved TBI outcomes following exercise preconditioning are associated with increased expression of specific neuroprotective genes and proteins (VEGF-A and EPO, but not HO-1) in the brain.
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J Neurosurg Pediatr · Oct 2015
Observational StudyNoninvasive screening for intracranial hypertension in children with acute, severe traumatic brain injury.
The aim of this study was to determine the relationship between transcranial Doppler (TCD) derived pulsatility index (PI), end diastolic flow velocity (Vd), and intracranial pressure (ICP). The subjects in this study were 36 children admitted after severe traumatic brain injury (TBI) (postresuscitation Glasgow Coma Scale ≤ 8) undergoing invasive ICP monitoring. ⋯ Postinjury Day 0-1 MCA PI > 1.3 has good sensitivity and specificity at predicting an ICP ≥ 20 mm Hg. In those children with TBI who initially do not meet clear criteria for invasive ICP monitoring but who are at risk for development of intracranial hypertension, TCD may be used as a noninvasive tool to screen for the development of elevated ICP in the first 24 hours following injury.
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In an expanding elderly population, traumatic brain injury (TBI) remains a significant cause of death and disability. Guidelines for management of TBI, according to the Brain Trauma Foundation (BTF), include intracranial pressure (ICP) monitoring. Whether ICP monitoring contributes to outcomes in the elderly patients with TBI has not been explored. ⋯ Our findings suggest that the use of ICP monitoring according to BTF guidelines in elderly TBI patients does not provide outcomes superior to treatment without monitoring. The ideal group to benefit from ICP monitor placement remains to be elucidated.
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Chaperone-mediated autophagy (CMA) and the ubiquitin-proteasomal system (UPS) are two major protein degradation systems responsible for maintaining cellular homeostasis, but how these two systems are regulated after traumatic brain injury (TBI) remains unknown. TBI produces primary mechanical damage that must be repaired to maintain neuronal homeostasis. The level of lysosomal-associated membrane protein type 2A (LAMP2A) is the hallmark of CMA activity. ⋯ The increases in the levels of LAMP2A and 70 kDa heat-shock protein for CMA after TBI were seen mainly in the secondary lysosome-containing fractions. Confocal and electron microscopy further showed that increased LAMP2A or lysosomes were found mainly in neurons and proliferated microglia. Because CMA and the UPS are two major routes for elimination of different types of cellular aberrant proteins, the consecutive activation of these two pathways may serve as a protective mechanism for maintaining cellular homeostasis after TBI.