Journal of neurotrauma
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Journal of neurotrauma · Jul 2020
Neuroinflammation Mediated by GMF Exacerbates Neuronal Injury in an in vitro Model of Traumatic Brain Injury.
Traumatic brain injury (TBI) is the primary cause of death and disability affecting over 10 million people in the industrialized world. TBI causes a wide spectrum of secondary molecular and cellular complications in the brain. However, the pathological events are still not yet fully understood. ⋯ In addition, injured WT cells showed increased levels of oxidation product 4-hydroxynonenal and 8-oxo-2'-deoxyguanosine compared with injured GMF-KO cells. Further, we found that injured WT cells showed a significantly increased expression of glial fibrillary acidic protein, ionized calcium binding adaptor molecule 1, and phosphorylated ezrin/radixin/moesin proteins, and reduced microtubule associated protein expression compared with injured GMF-KO cells after injury. Collectively, our results demonstrate that GMF exacerbates the oxidative stress-mediated neuroinflammation that could be brought about by TBI-induced astroglial activation.
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Journal of neurotrauma · Jul 2020
Pediatric traumatic brain injury causes long-term deficits in adult hippocampal neurogenesis and cognition.
Young children who have sustained severe traumatic brain injury (TBI) can suffer from debilitating neurocognitive deficits. Impairment of adult hippocampal neurogenesis is associated with cognitive deficits and depression. Very few studies have investigated the adult hippocampal neurogenesis after pediatric TBI. ⋯ We found that: 1) pediatric TBI caused significant deficits in hippocampal dependent cognitive functions; 2) the survival rates of adult-born neurons at both ipsilateral and contralateral hippocampus significantly decreased in the TBI group; 3) TBI induced ectopic migration of adult-born neurons at the dorsal dentate gyrus in both ipsilateral and contralateral hippocampus; 4) TBI increased astrogenesis in the hilus of the dentate gyrus; and 5) TBI results in abnormal microglial activation. In conclusion, pediatric TBI causes prolonged neuroinflammation and dysregulation of the adult hippocampal neurogenesis through young adulthood, which might be responsible for the cognitive deficits. Protection of adult hippocampal neurogenesis may potentially improve outcomes.
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Journal of neurotrauma · Jul 2020
Multicenter StudyEvaluation of the Fear Avoidance Behavior after Traumatic Brain Injury Questionnaire.
Fear avoidance behavior is related to symptom persistence and disability in various health conditions, such as chronic pain. Fear avoidance behavior also may impact recovery from mild traumatic brain injury (mTBI), but no measure of this construct has been psychometrically validated for the mTBI population. Adults who sustained an mTBI (n = 159) were recruited from three outpatient mTBI clinics. ⋯ Best fit to the unidimensional Rasch model was achieved after items were combined into three super items based on exploratory factor analysis and retaining the misfitting item χ2(6, n = 159) = 2.1, p = 0.06). The FAB-TBI appears to be a psychometrically sound measure of fear avoidance behavior after mTBI. Conversion tables are made available to convert scores into interval-level data for future research.
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Journal of neurotrauma · Jul 2020
The Cumulative Influence of Inflammatory Response Genetic Variation on Long-Term Neurobehavioral Outcomes following Pediatric Traumatic Brain Injury Relative to Orthopedic Injury: An Exploratory Polygenic Risk Score.
The addition of genetic factors to prognostic models of neurobehavioral recovery following pediatric traumatic brain injury (TBI) may account for unexplained heterogeneity in outcomes. The present study examined the cumulative influence of candidate genes involved in the inflammatory response on long-term neurobehavioral recovery in children with early childhood TBI relative to children with orthopedic injuries (OI). Participants were drawn from a prospective, longitudinal study evaluating outcomes of children who sustained TBI (n = 67) or OI (n = 68) between the ages of 3 and 7 years. ⋯ Higher inflammatory response PRS were associated with more executive dysfunction and behavior problems in children with TBI but not in children with OI. The cumulative influence of inflammatory response genes as measured by PRS explained additional variance in long-term neurobehavioral outcomes, over and above well-established predictors and single candidate SNPs tested individually. The results suggest that some of the unexplained heterogeneity in long-term neurobehavioral outcomes following pediatric TBI may be attributable to a child's genetic predisposition to a greater or lesser inflammatory response to TBI.
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Journal of neurotrauma · Jul 2020
Observational StudyUsing Variance to Explore the Diagnostic Utility of Baseline Concussion Testing.
The Graded Symptom Checklist (GSC), Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and King-Devick Test (KDT) are considered important components of concussion assessment. Whether baseline testing improves the diagnostic utility of these tests remains unclear. We performed an observational cohort study to investigate the within-subject and between-subjects variability of these tests over repeated assessments during two football seasons to examine whether baseline testing reduces variability in test performance. ⋯ A small, but significant, practice effect was observed for the BESS and KDT tests. When athletes are evaluated during a football season for concussion using the GSC, SAC, and BESS, comparing their scores to baseline performance is likely no more beneficial than comparing them to normative population data for identifying neurological changes associated with concussion. For the KDT, comparison to baseline testing is likely beneficial because of significantly higher between-subjects variability.