Articles: traumatic-brain-injuries.
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Journal of neurotrauma · May 2016
Juvenile Traumatic Brain Injury Increases Alcohol Consumption and Reward in Female Mice.
Traumatic brain injury (TBI) is closely and bi-directionally linked with alcohol use, as by some estimates intoxication is the direct or indirect cause of one-third to one-half of all TBI cases. Alcohol use following injury can reduce the efficacy of rehabilitation and increase the chances for additional injury. Finally, TBI itself may be a risk factor for the development of alcohol use disorders. ⋯ Environmental enrichment administered after injury reduced axonal degeneration and prevented the increase in drinking behavior. Additionally, brain-derived neurotrophic factor gene expression, which was reduced by TBI, was normalized by environmental enrichment. Together, these results suggest a novel model of alterations in reward circuitry following trauma during development.
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The central nervous system has limited capacity for regeneration after traumatic injury. Transplantation of neural stem/progenitor cells (NPCs) has been proposed as a potential therapeutic approach while insulin-like growth factor I (IGF-I) has neuroprotective properties following various experimental insults to the nervous system. We have previously shown that NPCs transduced with a lentiviral vector for IGF-I overexpression have an enhanced ability to give rise to neurons in vitro but also in vivo, upon transplantation in a mouse model of temporal lobe epilepsy. ⋯ Transplanted cells differentiated toward the oligodendroglial, but not the neuronal or astrocytic lineages, expressing the early and late oligodendrocyte markers NG2, Olig2, and CNPase. The newly generated oligodendrocytes reached maturity and formed myelin internodes. Our current and previous observations illustrate the high plasticity of transplanted NPCs which can acquire injury-dependent phenotypes within the host CNS, supporting the fact that reciprocal interactions between transplanted cells and the host tissue are an important factor to be considered when designing prospective cell-based therapies for CNS degenerative conditions.
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Journal of neurotrauma · May 2016
Multicenter StudyTensor-Based Morphometry Reveals Volumetric Deficits in Moderate/Severe Pediatric Traumatic Brain Injury.
Traumatic brain injury (TBI) can cause widespread and prolonged brain degeneration. TBI can affect cognitive function and brain integrity for many years after injury, often with lasting effects in children, whose brains are still immature. Although TBI varies in how it affects different individuals, image analysis methods such as tensor-based morphometry (TBM) can reveal common areas of brain atrophy on magnetic resonance imaging (MRI), secondary effects of the initial injury, which will differ between subjects. ⋯ We found a number of smaller clusters of volume reduction in the cingulate gyrus, thalamus, and fusiform gyrus, and throughout the frontal, temporal, and parietal cortices. Additionally, we found extensive associations between our cognitive performance measure and regional brain volume. Our results indicate a pattern of atrophy still detectable 1-year post-injury, which may partially underlie the cognitive deficits frequently found in TBI.
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In elderly patients with severe traumatic brain injury, the use of aggressive versus conservative management remains controversial. The aim of this study was to assess the outcome of surgical alternatives for treatment of severe traumatic intracranial hematoma in patients ≥65 years old and identify factors that may contribute to the outcome. ⋯ This study showed that Glasgow Coma Scale score (≤5) was a major determinant of outcome in elderly patients with severe traumatic brain injury. However, surgical treatment reduced mortality and improved outcome in the elderly patients in this study.
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Recently, several randomized controlled trials (RCT) investigating the effectiveness of decompressive craniectomy in the context of neurocritical illnesses have been completed. Thus, a meta-analysis to update the current evidence regarding the effects of decompressive craniectomy is necessary. We searched PUBMED, EMBASE and the Cochrane Central Register of Controlled Trials. ⋯ Decompressive craniectomy significantly reduced the risk of death for patients suffering malignant MCAI (risk ratio [RR] 0.46, 95% confidence interval [CI]: 0.36-0.59, P<0.00001) in comparison with no reduction in the risk of death for patients with severe TBI (RR: 0.83, 95% CI: 0.48-1.42, P=0.49). However, there was no significant difference in the composite risk of death or dependence at the final follow-up between the decompressive craniectomy group and the conservative treatment group for either malignant MCAI or severe TBI. The present meta-analysis indicates that decompressive craniectomy can significantly reduce the risk of death for patients with malignant MCAI, although no evidence demonstrates that decompressive craniectomy is associated with a reduced risk of death or dependence for TBI patients.