Articles: traumatic-brain-injuries.
-
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.
-
Journal of biomechanics · Oct 2015
Collegiate women's soccer players suffer greater cumulative head impacts than their high school counterparts.
Soccer is the source of the highest concussion rates among female athletes and is associated with neurological deficits at many levels of play. Despite its importance to our understanding of head trauma in female athletes, little is known about the number and magnitude of head impacts experienced by female soccer players. ⋯ Given that the collegiate players took many more impacts throughout the season, their mean cumulative exposure to translational (cPTA) and angular accelerations (cPAA) were significantly higher than those of the high school players. Additional research is required to determine whether the differences in cumulative exposure are responsible for the elevated risk of concussion in collegiate soccer players or if there are additional risk factors.
-
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.
-
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.
-
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.