RESUMEN
Electroencephalogram (EEG) is a neurophysiological test, which is widely used in human medicine for epilepsy diagnosis and other neurological disorders. For an adequate interpretation, it is necessary to know the electroencephalogram features for different stages of development. Despite the growing interest in its implementation in veterinary medicine, standardized descriptions of the EEG features of the different stages of brain development in dogs are restricted to studies with limited number of dogs and limited age groups. In this research, the electroencephalographic recording of 72 dogs of different breeds and ages was carried out under xylazine sedation to determine tracing characteristics by visual analysis and through statistical analysis of power spectrum. To establish the EEG features of recordings, 3 essential aspects were selected: (a) the presence or absence of slow waves of 4 to 6-7 Hz; (b) the comparison of the electrical activity recorded in the temporal and dorsal cortex channels; and (c) the visual increase of the alpha activity. Visual analysis on both reference and bipolar montage was performed by the authors and additionally blindly corroborated by two human neurophysiologists. The results allowed us to differentiate 5 age groups: 0-5, 6-11, 12-17, 18-23, and >24 months. Statistical analysis of the power spectrum was performed by analysis of variance (ANOVA) with a completely randomized design (CRD) under factorial arrangement by observing the effect of ages, channels and electroencephalographic rhythms on relative power. The results obtained matched those observed in the visual analysis. According to our results, the characteristics of the EEG corresponding to the adult animal begin to appear at 12 months of age but stabilize after 24 months of age. In this case, the evident differences in the processes of development and maturation of the neopallium and the rhinencephalon play a determining role. Our results differ from those obtained by other authors, probably due to the addition of a deep electrode that facilitates the recording of temporal cortical activity and its deeper rhinencephalic connections.
RESUMEN
Schizophrenia is considered a neurodevelopmental disorder; however, all the available treatment options are used when the disease becomes clinically significant in adolescence or early adulthood. Using a developmental rat model of schizophrenia, we examined whether neonatal treatment with memantine, an NMDA receptor modulator, can improve schizophrenic-like symptoms in adulthood. Early maternal deprivation in rats produces deficits in social interaction behaviors in adulthood. In contrast, memantine administrated in neonatal rats subjected to early maternal deprivation significantly reduces deficits in social interaction behaviors in adulthood. These results raise the possibility that pharmacological treatment with memantine at the early developmental stage helps people with a risk to develop schizophrenic-like symptoms.
RESUMEN
INTRODUÇÃO: A desnutrição e epilepsia são problemas prevalentes em países em desenvolvimento, principalmente na faixa etária pediátrica. OBJETIVOS: Tendo em vista o impacto que insultos como as crises convulsivas e a desnutrição geram no sistema nervoso central (SNC) de crianças, nosso estudo visa revisar a literatura atual sobre a relação entre desnutrição precoce e epilepsia em estudos clínicos e experimentais em ratos. METODOLOGIA: Revisão de literatura em revistas indexadas no Medline, no período de janeiro de 2000 até dezembro de 2008. RESULTADOS: Foram utilizados os unitermos epilepsy e malnutrition para a busca, sendo encontrados 1044 artigos, dos quais 56 foram selecionados para esta revisão. Procuramos resumir os principais achados referentes às alterações influenciadas pelas crises convulsivas e desnutrição no desenvolvimento do SNC. CONCLUSÕES: A análise desses artigos indicou que a desnutrição precoce acarreta déficit neuronal, com alterações cognitivas e modificações no desenvolvimento e crescimento em modelos experimentais, podendo haver maior suscetibilidade a crises convulsivas. Aparentemente, a desnutrição não é uma causa direta de epilepsia, mas pode diminuir o limiar para as crises epiléticas, havendo um efeito aditivo entre ambas.
INTRODUCTION: Malnutrition and epilepsy are main problems in developing countries, especially affecting children. PURPOSE: Considering the impact that insults like seizures and malnutrition have in the developing central nervous system (CNS), our study intends to review the current literature about the relation between epilepsy and early malnutrition in clinical and experimental studies in rats. METHODS: Literature review in Medline, during the period of January of 2000 to December 2008. RESULTS: Using the key words epilepsy and malnutrition, 1044 articles were found, from which we used 56 to this review. We intended to summarize the main findings that are refered to the alterations induced by seizures and malnutrition in the CNS development. CONCLUSION: The analysis of these articles indicated that early malnutrition lead to neuronal deficit, with cognitive alterations and growth and developmental disorders in experimental models, possibly causing more susceptibility to seizures. Apparently, malnutrition is not a direct cause of epilepsy, but it can decrease the threshold to seizures, suggesting an additive effect between these variables.
Asunto(s)
Niño , Desnutrición , Epilepsia , Cerebro/crecimiento & desarrolloRESUMEN
Gran parte de la morbilidad y mortalidad neonatal están determinadas por la lesión del cerebro en desarrollo. Un considerable número de los niños afectados presentarán secuelas neurológicas a largo plazo. A pesar de la importancia médica y social que presenta el problema, los avances alcanzados por la medicina neonatal no cuentan aún con una terapéutica eficaz para prevenir o aminorar las consecuencias de la lesión del cerebro en desarrollo. En la siguiente revisión nos proponemos actualizar las investigaciones más recientes en relación a los mecanismos de lesión y reparación del cerebro en desarrollo, basados en modelos animales que ilustran sobre los mecanismos plásticos de adaptación neuronal y funcional; el fin es un mejor conocimiento de los citados procesos que ayude al clínico en la práctica cotidiana de la neonatología.
Brain injury is a major contributor to neonatal morbidity and mortality, a considerable group of these children will develop long term neurological sequels. Despite the great clinical and social significance and the advances in neonatal medicine, no therapy yet does exist that prevent or decrease detrimental effects in cases of neonatal brain injury. Our objective was to review recent research in relation to the hypothesis for repair mechanism in the developing brain, based in animal models that show developmental compensatory mechanisms that promote neural and functional plasticity. A better understanding of these adaptive mechanisms will help clinicians to apply knowledge derived from animals to human clinical situations.