Articles: traumatic-brain-injuries.
-
Astaxanthin is a carotenoid pigment that possesses potent antioxidative, anti-inflammatory, antitumor, and immunomodulatory activities. Previous studies have demonstrated that astaxanthin displays potential neuroprotective properties for the treatment of central nervous system diseases, such as ischemic brain injury and subarachnoid hemorrhage. This study explored whether astaxanthin is neuroprotective and ameliorates neurological deficits following traumatic brain injury (TBI). ⋯ Our data suggest that astaxanthin reduces TBI-related injury in brain tissue by ameliorating AQP4/NKCC1-mediated cerebral edema and that NKCC1 contributes to the upregulation of AQP4 after TBI.
-
Journal of neurotrauma · Aug 2016
Randomized Controlled Trial Multicenter StudyExternal validation of the IMPACT prognostic models for traumatic brain injury on the SyNAPSe trial.
Prediction models for patients with traumatic brain injury (TBI) are important for multiple reasons, including case-mix adjustment, trial design, and benchmarking for quality-of-care evaluation. Models should be generalizable and therefore require regular external validation. We aimed to validate the International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT) prognostic models for moderate and severe TBI in a recent randomized controlled trial. ⋯ This pattern of miscalibration was consistent across all three models. In a contemporary trial setting, the IMPACT models have reasonable discrimination if enrollment restrictions apply. Observed changes in outcome distribution necessitate updating of previously developed prognostic models.
-
Journal of neurotrauma · Aug 2016
Multicenter StudyNeuroendocrine disturbances one to five or more years after traumatic brain injury and aneurysmal subarachnoid hemorrhage - data from the German Database on Hypopituitarism.
Neuroendocrine disturbances are common after traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH), but only a few data exist on long-term anterior pituitary deficiencies after brain injury. We present data from the Structured Data Assessment of Hypopituitarism after TBI and SAH, a multi-center study including 1242 patients. We studied a subgroup of 351 patients, who had sustained a TBI (245) or SAH (106) at least 1 year before endocrine assessment (range 1-55 years) in a separate analysis. ⋯ In patients observed ≥ 5 years after brain injury, the prevalence of somatotropic insufficiency increased over time to 24.1%, whereas corticotropic and thyrotrophic insufficiency became less frequent (2.5% and 0%, respectively). The prevalence differed regarding the diagnostic criteria (laboratory values vs. physician`s diagnosis vs. stimulation tests). Our data showed that neuroendocrine disturbances are frequent even years after TBI or SAH, in a cohort of patients who are still on medical treatment.
-
Journal of neurotrauma · Aug 2016
Resuscitation With Valproic Acid Alters Inflammatory Genes in a Porcine Model of Combined Traumatic Brain Injury and Hemorrhagic Shock.
Traumatic brain injury and hemorrhagic shock (TBI+HS) elicit a complex inflammatory response that contributes to secondary brain injury. There is currently no proven pharmacologic treatment for TBI+HS, but modulation of the epigenome has been shown to be a promising strategy. The aim of this study was to investigate whether valproic acid (VPA), a histone deacetylase inhibitor, modulates the expression of cerebral inflammatory gene profiles in a large animal model of TBI+HS. ⋯ DAVID analysis indicated that a cluster of inflammatory pathways held the highest rank and gene enrichment score. Real-time PCR data confirmed that VPA significantly down-expressed genes that ultimately regulate nuclear factor-kB (NF-kB)-mediated production of cytokines, such as TYROBP, TREM2, CCR1, and IL-1β. This high-throughput analysis of cerebral gene expression shows that addition of VPA to the resuscitation protocol significantly modulates the expression of inflammatory pathways in a clinically realistic model of TBI+HS.