Edaravone improves the post-traumatic brain injury dysfunction in learning and memory by modulating Nrf2/are signal pathway

OBJECTIVES: To investigate the molecular mechanism of edaravone (EDA) in improving the post-traumatic brain injury (TBI) dysfunction in learning and memory. METHODS: In vitro and in vivo TBI models were established using hydrogen peroxide (H2O2) treatment for hippocampal nerve stem cells (NSCs) and surgery for rats, followed by EDA treatment. WST 1 measurement, methylthiazol tetrazolium assay, and flow cytometry were performed to determine the activity, proliferation, and apoptosis of NSCs, and malondialdehyde (MDA), lactic dehydrogenase (LDH), and reactive oxygen species (ROS) detection kits were used to analyze the oxides in NSCs. RESULTS: Following EDA pretreatment, NSCs presented with promising resistance to H2O2-induced oxidative stress, whereas NSCs manifested significant increases in activity and proliferation and a decrease in apoptosis. Meanwhile, for NSCs, EDA pretreatment reduced the levels of MDA, LDH, and ROS, with a significant upregulation of Nrf2/antioxidant response element (ARE) signaling pathway, whereas for EDA-treated TBI rats, a significant reduction was observed in the trauma area and injury to the hippocampus, with improvement in memory and learning performance and upregulation of Nrf2/ARE signaling pathway. CONCLUSIONS: EDA, by regulating the activity of Nrf2/ARE signal pathway, can improve the TBI-induced injury to NSCs and learning and memory dysfunction in rats.

Traumatismo encefalocraneano en pediatría / Traumatic brain injury in pediatrics

Traumatic Brain Injury (TBI) is an important Public Health issue in Chile and the world. It represents a frequent cause of consultation, constituting a significant cause of morbidity and mortality in the population under 45 years of age. Accidents are the main reason for TBI among the pediatric population, but child abuse is an important cause in children below 2 y.o. A proper evaluation is essential to develop timely and efficient treatment that avoids or decreases brain damage and eventual complications. For this purpose, it is essential that brain physiology and physiopathological changes triggered by TBI are clear and well known. Current concepts are presented in this paper, emphasizing brain hemodynamics, metabolism, and brain self-regulation.

El traumatismo encefalocraneano (TEC) es un importante problema de salud pública tanto en Chile como en el mundo. Representa un motivo de consulta frecuente constituyendo una de las mayores causas de morbi-mortalidad en la población menor de 45 años. Los accidentes son la principal causa de TEC en la población pediátrica, pero el maltrato infantil es una causa etiológica importante a considerar en los menores de 2 años. Realizar una correcta evaluación al paciente con TEC es fundamental para instaurar un tratamiento oportuno y eficiente con el fin de evitar y/o disminuir el daño cerebral y así prevenir eventuales complicaciones. Para ello es imprescindible el conocimiento de la fisiología cerebral y los cambios fisiopatológicos que se desencadenan posterior al TEC, conceptos que son revisados en este artículo con énfasis en la hemodinamia cerebral, metabolismo y autorregulación cerebral.

Monitorización de presión tisular de oxígeno cerebral en pacientes pediátricos con traumatismo encéfalo craneal grave: reporte de dos casos / Cerebral oxygen tissue pressure monitoring in children with severe traumatic brain injury: 2 case-reports

Traumatic brain injury (TBI) is one of the most frequent causes of mortality in childhood. The treatment of patients with severe TBI is directed to prevention, early detection and treatment of secondary injuries due to extra and/or intracranial etiologies. Brain ischemia is a central cause of brain damage and its prevention has become a primary goal for intensivists. New techniques have developed to detect brain ischemia directly bedside the patient, through the monitoring of oxygen tissue pressure (PtiO2). Our objective is to report 2 pediatric patients with severe TBI and PtiO2 monitoring, in order to ilustrate the possibility that offers this technique in early detection of brain ischemia and review the current literature. We analyzed the clinical records of the patients with coma Glasgow score below 8. The intracranial pressure and PtiO2 monitoring was made through a catheter implanted in the encephalic matter. The device allowed early detection of secondary injuries and an optimal therapeutic approach in the patients, both with good outcome at discharge. The PtiO2 monitoring showed high safety and reliability.

Introducción: El traumatismo encéfalo craneal (TEC) grave es una de las principales causas de morbilidad y mortalidad en la infancia. La misión primaria del intensivista está dirigida a prevenir, detectar y tratar precozmente injurias secundarias debido a causas extra y/o intracraneales, siendo una de las más relevantes la isquemia cerebral. Nuevas técnicas han sido desarrolladas para diagnosticar directamente y junto a la cama del paciente la presencia de ella, siendo una de las más promisorias la monitorización de la presión de oxigenación tisular cerebral (PtiO2). Objetivo: Reportar 2 casos pediátricos de TEC grave en quienes monitorizamos la PtiO2, e ilustrar las posibilidades que ofrece esta técnica en la detección de isquemia cerebral, la conducta derivada de la información obtenida y explorar el estado actual de la literatura. Caso y Método: Revisión de fichas clínicas de dos pacientes, en quienes se instaló un dispositivo para monitorizar presión intracraneana (PIC) y PtiO2. La información obtenida del monitoreo permitió pesquisar precozmente segundas noxas, derivando en cambios de conducta terapéutica con resultado funcional satisfactorio al alta. Conclusión: La información obtenida permitió guiar una terapia óptima al comprender mejor la fisiopatología de lo que estaba ocurriendo con la PIC y PtiO2. El método demostró ser seguro y confiable.