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Clin. biomed. res ; 41(3): 220-223, 20210000. tab
Article in English | LILACS | ID: biblio-1342397


Introduction: It is well established that cortical volume are decreased in patients with schizophrenia. One possible explanation is that the increased pro-inflammatory status in schizophrenia is related to volumetric decrease of gray matter. The aim of this study was to correlate interleukin 6 (IL-6) with cortical volume in patients with schizophrenia and controls. Methods: We selected 36 patients with schizophrenia and 35 controls. Interleukin 6 (IL-6) was correlated with cortical volume in patients with schizophrenia and controls. Results: IL-6 was negatively correlated with cortical volume (p = 0.027; rho = −0.370) in patients, but not in controls (p = 0.235). Discussion: Our results are in line with previous studies suggesting that chronic inflammatory activation in patients with schizophrenia could be one plausible mechanism that could contribute for the cortical volumetric decrease often seen in this population. However, this cross-sectional study with a small number of patients does not allow us to establish causal relations. (AU)

Humans , Male , Female , Adult , Middle Aged , Schizophrenia , Cerebral Cortex/physiopathology , Interleukin-6 , Cerebral Cortex , Inflammation
Braz. oral res. (Online) ; 35: e022, 2021. tab, graf
Article in English | LILACS, BBO | ID: biblio-1153612


Abstract This study aimed to determine the mean distances between apexes of the maxillary posterior teeth and the maxillary sinus, between apexes of the mandibular posterior teeth and the mandibular canal, and between the root apexes of all teeth and the adjacent cortical plates. A total of 800 cone-beam computed tomography (CBCT) scans (400 maxillary and 400 mandibular) were obtained from patients indicated for several treatments. The proximity between apexes and anatomical structures, and the relationship between apexes and adjacent cortical plates were assessed together with the risk of over-instrumentation. Paired-sample comparisons were performed by using the paired t-test. The means were compared by ANOVA, Kruskal-Wallis and Dwass-Steel-Critchlow-Fligner tests. a) Most of the apexes classified as A (high-risk proximity) were observed in maxillary first and second molars, in mandibular first and second molars, and in second premolars in relation to near anatomical structures. b) A predominance of class A (86.42%) was noticed in the first premolars, between apexes of maxillary teeth and adjacent cortical plates. c) The distance between apexes of mandibular teeth and buccal cortical plates showed a predominance of medium-risk proximity (B) in all the groups, except the first premolars, with the highest risk (82.22%), and the second molars, with low-risk proximity (C) to distal and mesiobuccal apexes (91.77% and 89.62%). CBCT images are important for endodontic diagnosis and treatment, since many teeth have high risk proximity to near anatomical structures and adjacent cortical plates.

Humans , Maxillary Sinus , Tooth Root/diagnostic imaging , Cerebral Cortex , Cone-Beam Computed Tomography , Molar/diagnostic imaging
Pesqui. vet. bras ; 40(12): 1077-1087, Dec. 2020. tab, graf, ilus
Article in English | ID: biblio-1155034


The central nervous system is vulnerable to complications caused by diabetes. These complications lead to increased oxidative stress in the brain, resulting in damage to the cerebral cortex, among other regions. Insulin and hypoglycemic agents are still the most widely used treatments. However, current research with an experimental model of diabetes suggests the use of antioxidants, such as melatonin. Thus, we tested the hypothesis that exogenous melatonin may decrease or prevent the effects of diabetes in the frontal cortex of the rat brain. Fifty albino rats were allocated into five groups: GC = rats without diabetes induction, GD = diabetic rats induced by streptozotocin, GDM = streptozotocin-induced and melatonin-treated diabetic rats, GDI = diabetic rats induced by streptozotocin and treated with insulin, GDMI = diabetic rats induced by streptozotocin and treated with melatonin and insulin simultaneously. Diabetes was induced by intraperitoneal administration of streptozotocin (60mg/kg). Insulin (5U/day) was administered subcutaneously and melatonin (10mg/kg) by drinking water; both treatments last days after. We analyzed animals' weight, the cytokines IL-6 and TNF-α, apoptosis, glycogen, and did morphometry and histopathology of the frontal cortex were analyzed. The results showed that the cerebral cortex of the diabetic animals presented axonal degeneration, reduced number of neurons in the cortex, reduced glycogen, increased IL-6 and TNF-α expression, high apoptotic index, and reduced animal weight and the brain. Treatment with melatonin associated or not with insulin prevented such effects. Thus, we conclude that melatonin associated with insulin may be an alternative for avoiding the impact of diabetes in the brain's frontal cortex.(AU)

O sistema nervoso central é vulnerável a complicações originadas pelo diabetes estresse oxidativo no cérebro e resultando em lesões no córtex cerebral, dentre outras regiões. A insulina e hipoglicemiantes ainda são os tratamentos mais utilizados, entretanto, pesquisas atuais com modelo experimental do diabetes sugerem a utilização de antioxidantes como, por exemplo, a melatonina. Assim, testamos a hipótese de que a melatonina exógena pode diminuir ou prevenir os efeitos do diabetes no córtex frontal do cérebro de ratos. Foram utilizados 50 ratos albinos, divididos em 5 grupos: GC = ratos sem indução ao diabetes, GD = ratos induzidos ao diabetes pela estreptozotocina, GDM = ratos induzidos ao diabetes pela estreptozotocina e tratados com melatonina, GDI = ratos induzidos ao diabetes pela estreptozotocina e tratados com insulina, GDMI = ratos induzidos ao diabetes pela estreptozotocina e tratados com melatonina e insulina simultaneamente. O diabetes foi induzido pela administração intraperitoneal de estreptozotocina (60mg/kg). A insulina (5U/dia) foi administrada por via subcutânea e a melatonina (10mg/kg) pela água de beber. Ambos tratamentos foram realizados durante 30 dias após a indução. Foram analisados o peso dos animais, do cerebro, as citocinas IL-6 e TNF-α, apoptose, glicogênio, além da morfometria e histopatologia do córtex frontal. Os resultados mostraram que o córtex cerebral dos animais diabéticos apresentou degeneração axonal, redução do número de neurônios no córtex, redução do glicogênio, aumento da expressão do IL-6 e TNF-α, elevação do índice apoptótico, além da redução do peso dos animais e do cérebro. O tratamento com melatonina associada ou não a insulina preveniu tais efeitos. Assim, concluímos que a melatonina associada ou não a insulina pode ser uma alternativa na prevenção dos efeitos do diabetes no córtex frontal do cérebro.(AU)

Animals , Rats , Immunohistochemistry , Cerebral Cortex , Melatonin , Rats/abnormalities , Apoptosis , Oxidative Stress
Int. j. morphol ; 38(5): 1217-1222, oct. 2020. graf
Article in English | LILACS | ID: biblio-1134428


SUMMARY: Repeated stress is a risk factor for memory impairment and neurological abnormalities in both humans and animals. We sought to investigate the extent of (i) brain tissue injury; (ii) nitrosative and oxidative stress in brain tissue homogenates; (iii) apoptotic and survival biomarkers in brain tissue homogenates; and (iv) immobility and climbing abilities, induced over a period of three weeks by chronic unpredictable stress (CUS). Wistar rats were either left untreated (Control group) or exposed to a variety of unpredictable stressors daily before being sacrificed after 3 weeks (model group). Assessment of depression-like behavior was performed and animals were then culled and harvested brain tissues were stained with basic histological staining and examined under light microscopy. In addition, brain tissue homogenates were prepared and assayed for these parameters; inducible nitric oxide synthase (iNOS), malondialdehyde (MDA), superoxide dismutase (SOD), caspase-3, and B-cell lymphoma 2 (Bcl-2). Histology images showed CUS induced profound damage to the cerebral cortex as demonstrated by severe neuronal damage with shrunken cells, disrupted atrophic nuclei, perineuronal vacuolation and swollen glial cells. CUS also significantly (p<0.05) induced iNOS, MDA, and caspase-3, whereas SOD and Bcl-2 brain tissue levels were inhibited by CUS. In addition, data from the depression-like behavior, forced swimming test showed significant (p<0.05) increase in animal immobility and decrease in climbing ability in the model group of rats. Thus, here we demonstrated a reliable rat model of chronic stress-induced brain injury, which can further be used to investigate beneficial drugs or agents used for a period of three weeks to protect against CUS-induced brain damage.

RESUMEN: El estrés crónico es un factor de riesgo para el deterioro de la memoria y las anomalías neurológicas tanto en humanos como en animales. Intentamos investigar el alcance de lesión del tejido cerebral; (ii) estrés nitrosativo y oxidativo en homogeneizados de tejido cerebral; (iii) biomarcadores apoptóticos y de supervivencia en homogeneizados de tejido cerebral; y (iv) inmovilidad y habilidades de escalada, inducidas durante un período de tres semanas por estrés crónico impredecible (ECI). Se dejaron sin tratamiento (grupo control) ratas Wistar, o se expusieron a una variedad de factores estresantes impredecibles diariamente antes de ser sacrificadas después de 3 semanas (grupo modelo). Se realizó una evaluación del comportamiento similar a la depresión y luego se sacrificaron los animales y se tiñeron los tejidos cerebrales con tinción histológica básica y se examinaron con microscopía óptica. Además, se prepararon homogeneizados de tejido cerebral y se analizaron los siguientes parámetros; óxido nítrico sintasa inducible (iNOS), malondialdehído (MDA), superóxido dismutasa (SOD), caspasa- 3 y linfoma de células B 2 (Bcl-2). Las imágenes histológicas mostraron que el CUS indujo un daño profundo en la corteza cerebral como lo demuestra el daño neuronal severo con células encogidas, núcleos atróficos alterados, vacuolación perineuronal y células gliales inflamadas. ECI también indujo significativamente (p <0,05) iNOS, MDA y caspase-3, mientras que los niveles de tejido cerebral SOD y Bcl-2 fueron inhibidos por ECI. Además, los datos del comportamiento similar a la de- presión, la prueba de natación forzada mostró un aumento significativo (p <0,05) en la inmovilidad animal y una disminución en la capacidad de escalada en el grupo modelo de ratas. Por lo tanto, aquí demostramos un modelo confiable de daño cerebral crónico en rata inducido por el estrés, que se puede utilizar para investigar medicamentos o agentes beneficiosos usados durante un período de tres semanas para proteger el daño cerebral inducido por ECI.

Animals , Male , Rats , Stress, Psychological/complications , Brain Damage, Chronic/pathology , Superoxide Dismutase/analysis , Behavior, Animal , Brain Injuries/metabolism , Biomarkers , Cerebral Cortex , Chronic Disease , Analysis of Variance , Rats, Wistar , Apoptosis , Oxidative Stress , Nitric Oxide Synthase/analysis , Proto-Oncogene Proteins c-bcl-2 , Depression , Disease Models, Animal , Caspase 3/analysis , Nitrosative Stress , Malondialdehyde/analysis
Rev. bras. neurol ; 56(2): 46-52, abr.-jun. 2020. ilus, tab
Article in English | LILACS | ID: biblio-1103037


The nature of memory and the search for its localization have been a subject of interest since Antiquity. After millennia of hypothetical concepts the core memory-related structures finally began to be identified through modern scientifically-based methods at the diencephalic, hippocampal, and neocortical levels. However, there was a clear temporal delay between the finding of these anatomic structures ignoring their function, and their identification related to memory function. Thus, the core structures begun to be identified with a pure anatomical view in the late Middle Ages on, while the memory function related to them was discovered much later, in the late Modern Period.

A natureza da memória e a busca de sua localização tem sido objeto de interesse desde a Antiguidade. Após milênios de conceitos hipotéticos as estruturas centrais relacionadas com a memória finalmente começaram a ser identificadas através de métodos modernos com base científica, nos níveis diencefálico, hipocampal e neocortical. Entretanto, houve um claro retardo temporal entre o achado dessas estruturas anatômicas ignorando sua função e sua identificação relacionada à função da memória. Assim, as estruturas centrais começaram a ser identificadas com uma visão puramente anatômica da Idade Média tardia em diante, enquanto a função da memória relacionada com as mesmas foi descoberta muito mais tarde, no Período Moderno tardio.

Humans , History, 19th Century , History, 20th Century , Cerebral Cortex/anatomy & histology , Cerebrum/anatomy & histology , Memory/physiology , Neocortex , Diencephalon , Hippocampus
Braz. J. Psychiatry (São Paulo, 1999, Impr.) ; 42(1): 6-13, Jan.-Feb. 2020. tab, graf
Article in English | LILACS | ID: biblio-1055355


Objective: To test the feasibility and to present preliminary results of a neuroimaging protocol to evaluate adolescent depression in a middle-income setting. Methods: We assessed psychotropic medication-free adolescents (age range 14-16 years) with a diagnosis of major depressive disorder (MDD). Participants underwent a comprehensive clinical evaluation and both structural and functional magnetic resonance imaging (fMRI). In this pilot study, a preliminary single-group analysis of resting-state fMRI (rs-fMRI) data was performed, with a focus on the default mode network (DMN), cognitive control network (CCN), and salience network (SN). Results: The sample included 29 adolescents with MDD (mean age 16.01, SD 0.78) who completed the protocol. Only two participants were excluded due to MRI quality issues (head movement), and were not included in the analyses. The scans showed significant connectivity between the medial prefrontal cortex and posterior cingulate cortex (DMN), the ACC and anterior insula (SN), and the lateral prefrontal cortex and dorsal parietal cortex (CCN). Conclusion: We demonstrated the feasibility of implementing a complex neuroimaging protocol in a middle-income country. Further, our preliminary rs-fMRI data revealed patterns of resting-state connectivity consistent with prior research performed in adolescents from high-income countries.

Humans , Male , Adolescent , Magnetic Resonance Imaging/methods , Depressive Disorder, Major/diagnostic imaging , Neuroimaging/methods , Quality Control , Socioeconomic Factors , Brazil , Cerebral Cortex/diagnostic imaging , Feasibility Studies , Surveys and Questionnaires , Reproducibility of Results , Depressive Disorder, Major/physiopathology , Neural Pathways , Neuropsychological Tests
Article in English | WPRIM | ID: wpr-785551


Repetitive transcranial magnetic stimulation (rTMS) has been known to improve the motor function through modulation of excitability in the cerebral cortex. However, most studies with rTMS were limited to post-stroke patients with mild to moderate motor impairments. The effect of rTMS on severe upper-limb motor impairment remains unclear. Therefore, this study investigated the effects of rTMS on the upper extremity function in post-stroke patients with severe upper-limb motor impairment. Subjects were divided into 3 groups, low-, high-frequency rTMS and control group were received stimulation 10 times for 2 weeks. The motor scale of Fugl-Meyer Assessment (FMA) and cortical excitability on the unaffected hemisphere were measured before and after performing 10 rTMS sessions. The motor scale of upper extremity FMA (UE-FMA) and shoulder component of the UE-FMA were significantly improved in both low- and high-frequency rTMS groups. However, no significant improvement was observed in the wrist and hand components. No significant differences were noted in low- and high-frequency rTMS groups. The amplitude of motor evoked potential on the unaffected hemisphere showed a significant decrease in the low- and high-frequency stimulation groups. rTMS may be helpful in improving upper extremity motor function even in post-stroke patients with severe upper-limb motor impairment.

Cerebral Cortex , Evoked Potentials, Motor , Hand , Humans , Recovery of Function , Shoulder , Transcranial Magnetic Stimulation , Upper Extremity , Wrist
Int. j. morphol ; 37(4): 1437-1443, Dec. 2019. graf
Article in English | LILACS | ID: biblio-1040150


While various neurodegenerative diseases affect cortical mass differently, finding an optimal and accurate method for measuring the thickness and surface area of cerebral cortex remains a challenging problem due to highly convoluted surface of the cortex. We therefore investigated cortical thickness in a sample of cadaveric specimens at the Discipline of Clinical Anatomy, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa to provide some clue as to possible variations in the parameters. Following ethical approval, 60 brain samples were uniformly sectioned (5 mm thickness) and eight slices taken from each brain across regions of interest (ROI) prepared and stained by Mulligan's technique. Thickness was measured at selected angles (0º, 45º, 90º, 135º and 180º) for both right and left cerebral hemispheres. Mulligan's stain produced good cortical differentiation and clear images that enabled manual delineation of structures. Cortical thickness ranged from 3 to 5 millimeters across the ROI. Interestingly, there was rightward hemispheric asymmetry of cortical thickness of selective slices at suggested angles which is related to structurally and functionally important brain regions. Moreover, there was no significant correlation between the surface area of superficial cortex and the deep nuclei at the same level. The superficial cortex and deep nuclei are manifested independently in normal aging, neuropsychiatric or developmental disorders. Providing accurate morphometric evaluation of cortical thickness and area based on gross staining of the brain slices could provide qualitative data that may support the study of human cerebral cortex even in disease conditions.

Si bien varias enfermedades neurodegenerativas afectan a la masa cortical de manera diferente, encontrar un método óptimo y preciso para medir el grosor y el área de la superficie de la corteza cerebral sigue siendo un problema difícil debido a la superficie altamente enrevesada de la corteza. Por lo tanto, investigamos el grosor cortical en una muestra de cadáveres del Departamento de Anatomía Clínica de la Facultad de Medicina Nelson R. Mandela de la Universidad de KwaZulu-Natal, Sudáfrica, para proporcionar alguna pista sobre posibles variaciones en dichos parámetros. Después de la aprobación ética, 60 muestras de cerebro se seccionaron uniformemente (5 mm de grosor) y se tomaron ocho cortes de cada cerebro en regiones de interés (ROI) preparadas y teñidas con la técnica de Mulligan. El espesor se midió en los ángulos seleccionados (0º, 45º, 90º, 135º y 180º) para los hemisferios cerebrales derecho e izquierdo. La tinción de Mulligan produjo una buena diferenciación cortical e imágenes claras que permitieron la delineación manual de las estructuras. El grosor cortical osciló entre 3 y 5 milímetros a través del ROI. Curiosamente, hubo una asimetría hemisférica hacia la derecha del grosor cortical de los cortes en ángulos sugeridos que se relacionan con regiones cerebrales estructural y funcionalmente importantes. Además, no hubo una correlación significativa entre el área de la superficial de la corteza superficial y los núcleos profundos en el mismo nivel. La corteza superficial y los núcleos profundos se manifiestan de manera independiente en el envejecimiento normal, en los trastornos neuropsiquiátricos o del desarrollo. Realizar una evaluación morfométrica precisa del grosorcortical y el área basada en la tinción macroscópica de los cortes del cerebro, podría proporcionar datos cualitativos que puedan respaldar el estudio de la corteza cerebral humana incluso en condiciones de enfermedad.

Humans , Male , Female , Middle Aged , Aged , Aged, 80 and over , Staining and Labeling/methods , Brain/anatomy & histology , Cadaver , Cerebral Cortex/anatomy & histology , Gray Matter/anatomy & histology
Pensam. psicol ; 17(1): 19-32, ene.-jun. 2019. tab, graf
Article in Spanish | LILACS | ID: biblio-1020099


Resumen Objetivo. El ejercicio físico (EF) se relaciona con estructuras cerebrales y funcionamiento cognitivo; sin embargo, se desconocen indicadores de frecuencia, duración e intensidad del EF asociados a procesos neuropsicológicos. Estudiar la relación y las posibles diferencias entre las funciones ejecutivas (FE) y los indicadores del EF (frecuencia, duración y tiempo que lleva practicando EF). Método. Se seleccionó una muestra intencional de treinta sujetos físicamente activos, pareados por sexo ( Medad = 22.9, DE = 8.5). Se aplicó la totalidad de la Batería de Funciones Ejecutivas y Lóbulos Frontales (Banfe). Resultados. El desempeño neuropsicológico se relacionó con la frecuencia del EF en tareas que evalúan capacidades de control inhibitorio, seguimiento de límites y normas, memoria de trabajo visoespacial y anticipación de acciones de orden progresivo y regresivo. La duración y el tiempo de entrenamiento presentaron relación con la planeación, respeto por los límites y la inhibición. Aquellos participantes que se ejercitan más de seis veces por semana presentaron mejor desempeño en los aciertos y menor número de errores en el control inhibitorio. No se diferencia el desempeño neuropsicológico en función a indicadores y tipo de EF. Conclusión. Se confirma la hipótesis acerca de que el EF se asocia con procesos neuropsicológicos. Se abren posibles implicaciones científicas, educativas y clínicas.

Abstract Objective. Physical Exercise (PE) is related to cerebral structures and cognitive functioning. Nevertheless, PE indicators of frequency, duration, intensity and neuropsychological processes are unknown. The goal was to study the relationship and the possible differences between executive functions (EF) and PE indicators (frequency, duration and time PE is being practiced). Method. We selected an intentional sample of thirty physically active subjects, paired by sex (Age mean = 22.9, SD = 8.5). We used the whole assessment of Executive Functions and Frontal Lobes Battery (BANFE). Results. Neuropsychological performance was related to the PE frequency in tasks that assess inhibitory control, monitoring of limits and rules, visual-spatial working memory and predicting in reversal and progressive order actions. The duration and time of training showed relationship with planning and inhibition control. The participants who exercise more than six times a week showed a better performance and less number of inhibition control mistakes. Neuropsychological performance dependent on indicators and type of PE are not distinguished. Conclusion. The hypothesis is confirmed. There is a relationship between PE and neuropsychological processes with possible scientific, educational and clinical implications.

Resumo Escopo. O Exercício Físico (EF) está relacionado com estruturas cerebrais e funcionamento cognitivo. Porém são desconhecidos indicadores de frequência, duração e intensidade de EF associados aos processos neuropsicológicos. Estudar a relação e as possíveis diferenças entre as Funções Executivas (FE) e indicadores do EF (Frequência, Duração e Tempo que leva praticando EF). Metodologia. Foi selecionada uma amostra intencional de trinta sujeitos ativamente físicos, pareados por sexo ( Midade= 22.9, DE= 8.5). Foi aplicada a totalidade da Bateria de Funções Executivas e Lóbulos Frontais (BANFE). Resultados. O desempenho neuropsicológico esteve relacionado com a Frequência do EF em tarefas que avaliam capacidades de controle inibitório, seguimento de limites e normas, memória de trabalho vioespacial, e antecipação de ações de ordem progressiva e regressiva. A duração e o tempo de treinamento apresentaram relação com o planejamento, respeito pelos limites e a inibição. Aqueles participantes que se exercitaram mais de seis vezes por semana apresentaram melhor desempenho nos sucessos e menor número de erros no controle inibitório. Não houve diferença no desempenho neuropsicológico em função a indicadores e tipo de EF. Conclusão. Foi confirmada a hipótese de que o EF está associado com processos neuropsicológicos. Foram abertas possíveis implicações científicas, educativas e clínicas.

Humans , Young Adult , Exercise , Neuropsychology , Cerebral Cortex , Cognition
Rev. bras. psiquiatr ; 41(2): 101-111, Mar.-Apr. 2019. tab, graf
Article in English | LILACS | ID: biblio-990827


Objective: To compare results of positron emission tomography (PET) with carbon-11-labeled Pittsburgh compound B (11C-PIB) obtained with cerebellar or global brain uptake for voxel intensity normalization, describe the cortical sites with highest tracer uptake in subjects with mild Alzheimer's disease (AD), and explore possible group differences in 11C-PIB binding to white matter. Methods: 11C-PIB PET scans were acquired from subjects with AD (n=17) and healthy elderly controls (n=19). Voxel-based analysis was performed with statistical parametric mapping (SPM). Results: Cerebellar normalization showed higher 11C-PIB uptake in the AD group relative to controls throughout the cerebral cortex, involving the lateral temporal, orbitofrontal, and superior parietal cortices. With global uptake normalization, greatest cortical binding was detected in the orbitofrontal cortex; decreased 11C-PIB uptake in white matter was found in the posterior hippocampal region, corpus callosum, pons, and internal capsule. Conclusion: The present case-control voxelwise 11C-PIB PET comparison highlighted the regional distribution of amyloid deposition in the cerebral cortex of mildly demented AD patients. Tracer uptake was highest in the orbitofrontal cortex. Decreased 11C-PIB uptake in white-matter regions in this patient population may be a marker of white-matter damage in AD.

Humans , Male , Female , Aged , Aged, 80 and over , Carbon Radioisotopes , Cerebral Cortex/diagnostic imaging , Positron-Emission Tomography/methods , Alzheimer Disease/diagnostic imaging , White Matter/diagnostic imaging , Severity of Illness Index , Case-Control Studies
Arq. neuropsiquiatr ; 77(4): 260-267, Apr. 2019.
Article in English | LILACS | ID: biblio-1001357


ABSTRACT The use of methods to evaluate cortical activity in neonates has great importance in modern medicine, as it allows the observation and evaluation of several clinical aspects, which guarantees that the health team has knowledge about possible intervention measures that may be necessary in the treatment of newborns. Objective: This systematic review aimed to compare the main technologies available for the evaluation of brain functions in neonates, among them: the conventional electroencephalogram (EEG), the amplitude-integrated electroencephalogram (aEEG) and the geodesic sensor net EEG. Methods: A search was conducted forarticles from national and international periodicals included in the Web of Science, LILACS, SciELO and Medline electronic databases. Results: The search found 39 among 155 articles of interest and the analyses indicated that, in the clinical environment, the use of both conventional EEG and aEEG is highly recommended, as the combination of their functions allows, for example, a greater number of subclinical seizures to be detected. Conversely, the use of a geodesic sensor net EEG could be of great value, as it allows a large amount of data to be analyzed. Conclusion: This analysis may be useful in studies and research related to diseases and symptoms, such as seizures, a current challenge for neonatal neuromonitoring, as well as aspects of neurological development and functional studies. However, despite many advances in technology, electroencephalography in preterm neonates remains a challenge worldwide and still requires more robust research and efforts towards the best clinical assistance in this extremely early stage of life.

RESUMO Métodos para avaliar a atividade cortical em neonatos têm grande importância na Medicina moderna, pois permitem a observação e avaliação de diversos aspectos clínicos, garantindo que a equipe de saúde tenha conhecimento sobre possíveis medidas de intervenção que possam ser necessárias no tratamento de recém-nascidos. Objetivo: Esta revisão sistemática tem como objetivo comparar as principais tecnologias disponíveis para a avaliação das funções cerebrais em neonatos: eletroencefalograma convencional (EEG), eletroencefalograma de amplitude integrada (aEEG) e eletroencefalograma da rede do sensor geodésico. Métodos: Os artigos foram selecionados em periódicos nacionais e internacionais, incluídos nas bases de dados eletrônicas Web of Science, LILACS, SciELO e Medline. Resultados: Foram encontrados 39 artigos de interesse entre 155 artigos. As análises indicaram que, em relação ao ambiente clínico, o uso associativo de EEG convencional e aEEG é altamente recomendado, pois permite a combinação de funções, facilitando, por exemplo, que um maior número de convulsões sub-clínicas seja detectado. Por outro lado, o uso do eletroencefalograma da rede do sensor geodésico seria de grande valor, uma vez que permite que uma grande quantidade de dados seja analisada. Conclusão: Essa análise pode ser útil em estudos e pesquisas relacionados a doenças e sintomas, como convulsões, um desafio atual para a neuromonitorização neonatal, bem como aspectos de desenvolvimento neurológico e estudos funcionais. No entanto, apesar de muitos avanços tecnológicos, a eletroencefalografia em recém-nascidos prematuros ainda é um desafio em todo o mundo e requer pesquisas e esforços mais robustos para a melhor assistência clínica neste estágio extremamente precoce da vida.

Humans , Infant, Newborn , Infant, Premature , Cerebral Cortex/diagnostic imaging , Electroencephalography/methods , Seizures/diagnostic imaging , Intensive Care Units, Neonatal
Article in Chinese | WPRIM | ID: wpr-774082


OBJECTIVE@#To study the methylation level and dynamic change of 5-hydroxymethylcytosine (5hmC) in mitochondrial DNA (mtDNA) in the cerebral cortex of neonatal rats with hypoxic-ischemic brain damage.@*METHODS@#A total of 24 male Sprague-Dawley rats aged 7 days were randomly divided into control group, 24-hour model group and 48-hour model group (n=8 each). Common carotid artery ligation combined with hypoxic treatment was performed to establish an animal model of hypoxic-ischemic brain damage. The rats in the control group were not given ligation or hypoxic treatment. Oxidative bisulfite sequencing was used to measure the level of 5hmC in the cerebral cortex. Western blot was used to measure the expression of 5hmC-related enzymes TET1, TET2 and DNMT1.@*RESULTS@#The 24- and 48-hour model groups had a significantly higher level of 5hmC than the control group (P<0.05). Western blot showed a significant increase in the expression of DNMT1 in the 24- and 48-hour model groups (P<0.05). Compared with the control group, the 24- and 48-hour model groups had significant differences in the 5hmC level at multiple mitochondrial genetic loci (P<0.05).@*CONCLUSIONS@#The level of DNMT1, a key enzyme for 5hmC modification in mtDNA, in the cerebral cortex increases in neonatal rats with hypoxic-ischemic brain damage, suggesting that there is an abnormal methylation level of 5hmC after hypoxic-ischemic brain damage, which might be associated with the regulation of hypoxic-ischemic brain damage.

Animals , Animals, Newborn , Cerebral Cortex , DNA, Mitochondrial , Hypoxia-Ischemia, Brain , Male , Rats , Rats, Sprague-Dawley
Article in Chinese | WPRIM | ID: wpr-774072


OBJECTIVE@#To summarize and analyze the etiology, clinical manifestations and imaging features of children with cerebral infarction.@*METHODS@#A retrospective analysis was performed for the clinical data of 54 children with cerebral infarction, including etiology, clinical manifestations, distribution of infarcts, type of infarcts and clinical outcome.@*RESULTS@#Of the 54 children, 93% had a clear cause, among whom 46% had the coexistence of multiple factors, and the top three causes were infection (54%), vascular disease (40%) and trauma (26%). Major clinical manifestations included limb paralysis (85%), pyrexia (20%), disturbance of consciousness (19%) and convulsion (17%). As for the location of infarcts, 80% of the infarcts were located in the cerebral cortex and 52% in the basal ganglia. Major types of infarcts were small-area infarcts (74%) and multifocal infarcts (56%). Viral encephalitis was the most common cause of cerebral infarction caused by infection, with the cerebral cortex as the most common location of infarcts (21/23, 91%) and multiple infarcts as the most common type of infarcts (13/23, 57%). Among the 12 children with cerebral infarction caused by nonspecific endarteritis, 10 (83%) had infarcts located in the basal ganglia and only one child had multiple infarcts. Among the five children with cerebral infarction caused by moyamoya disease, four children (80%) had infarcts located in the cerebral cortex, and large-area infarction (4/5, 80%) and multifocal infarction (4/5, 80%) were the major types of infarcts. Among the children with traumatic cerebral infarcts, 92% had infarcts located in the basal ganglia, and small-area infarcts (92%) and single infarcts (85%) were the major types of infarcts. Among the 46 children with limb paralysis, 34 (74%) had infarcts located in the basal ganglia; 50% of the children with disturbance of consciousness had infarcts located in the basal ganglia. Subcortical infarcts were observed in all six children with epilepsy. Seventy-five percent of the infarcts located in the cerebral cortex and 87% of the infarcts located in the basal ganglia had a good prognosis. Among the two children with cerebral infarcts located in the brainstem, one had the sequela of hemiplegia and the other had the sequela of cognitive impairment. Eighty-eight percent of the children with cerebral infarction caused by infection and 82% of the children with traumatic cerebral infarction tended to have a good prognosis, and 83% of the children with cerebral infarction caused by nonspecific endarteritis had good prognosis. Recurrence was observed in all three children with cerebral infarction caused by vascular malformations. Of the five children with cerebral infarction caused by moyamoya disease, one child died and four children survived with the sequela of localized brain atrophy, among whom one child also had the sequela of epilepsy.@*CONCLUSIONS@#Infection, vascular disease and trauma are the most common causes of cerebral infarction in children, and limb paralysis is the most common clinical manifestation. Cerebral cortex is the most common infarct site, and small-area infarcts and multifocal infarcts are the most common types of infarcts, which tend to have a better prognosis.

Basal Ganglia , Cerebral Cortex , Cerebral Infarction , Child , Humans , Magnetic Resonance Imaging , Recurrence , Retrospective Studies
Acta Physiologica Sinica ; (6): 581-587, 2019.
Article in Chinese | WPRIM | ID: wpr-777153


The purpose of this study was to establish a method to record the dynamic process of vascular regeneration and remodeling in rat cerebral ischemic regions. An animal brain window model was established to continuously observe the changes of rat cortical vascular ischemia in vivo, and the model of cerebral ischemia was established by photochemical embolization. Optical coherence tomography (OCT) was performed to record the formation of vascular blockage and the injury and regeneration of small vessels during cerebral ischemia recovery. The results showed that 30 min of laser irradiation could completely block the cortical vessels in rats. Within 24-48 h after ischemia, the degree of brain injury was the greatest, and the number of blood vessels in the ischemic region reached the minimum. Then the blocked blood vessels began to be dredged, and the small blood vessels around the ischemic area began to regenerate. Small blood vessels in the superficial/deep layers of the cortex disappeared significantly after laser irradiation. During 10 d after ischemia, the blocked blood vessels were gradually dredged and recovered. On the 10th day after laser irradiation, a large number of neovascularization appeared in the superficial layer of cortex, but the deep vessels did not recover. These results indicate that the method established in this study can observe the changes of blood vessel in cerebral ischemic region continuously, which lays a foundation for further quantitative study on the dynamics of embolized blood vessels and peripheral capillaries during the recovery of cerebral ischemia.

Animals , Brain , Brain Ischemia , Cerebral Cortex , Rats , Regeneration
Article in Chinese | WPRIM | ID: wpr-776501


OBJECTIVE@#To understand and analyze the rules of endurance exercise on the cerebral cortex adaptive mechanism in aged rats.@*METHODS@#In this study, 3-month-old (n=20), 13-month-old (n=24) and 23-month-old (n=24) specific-pathogen free (SPF) male Sprague-Dawley Rat (SD) rats were divided into young (Y-SED), middle-aged (M-SED) and old-aged (O-SED) sedentary control group, and the corresponding Y-EX, M-EX and O-EX in the endurance exercise runner group. The 10-weeks of regular moderate-intensity aerobic exercise intervention were carried out in the endurance exercise runner group. The exercise mode is treadmill exercise (slope 0), and the exercise intensity gradually increases from 60%~65% of the maximum oxygen consumption (V·O) to 70%~75%, and the exercise time is 10 weeks. Hematoxylin and eosin (HE) staining was used to detect age-related morphological changes. The expressions of superoxide dismutase(SOD) and brain-derived neurotrophic factor (BDNF) and the expressions of synapsin 1 (SYN1) and Ca/calmodulin- dependent protein kinases IIα (CaMK IIα) / AMP-activated protein kinase α1(AMPKα1) / mammalian target of rapamycin (mTOR) pathway -related genes were detected.@*RESULTS@#The cerebral cortex structure of the rats in each group showed age-related aging changes, the expression of SOD in the cortex showed a gradual decline, the expression of BDNF showed an age-increasing trend, and the expression levels of SYN1 and CaMK IIα were increased with age. The changes in AMPKα1 and SirT2 and IP3R, AKT1 and mTOR mRNA levels were increased slightly in middle-aged rats and decreased in aged rats. Compared with the rats in each sedentary control group, the nucleus of the cerebral cortex was tightly arranged and the number of nuclei observed under the microscope was increased significantly in each exercise group. Exercise promoted the expressions of SOD, BDNF and synaptophysin SYN1 in the cortex of rats, and the expression levels of SOD and BDNF in aged rats were up-regulated significantly (P< 0.01). The expression level of SYN1 in rats was up-regulated significantly (P<0.05) in the young and aged rats. The expression of CaMK IIα in the cortex of middle-aged and aged rats was up-regulated (P<0.01), while the expression level of CaMK IIα in young rats was down-regulated (P<0.01). Exercise could up-regulate the expression level of AMPKα1 in the cortex of young rats (P< 0.05), but not in middle-aged and old-age rats. Exercise could up-regulate the expression of SirT2 in the cortex of rats in all age groups (P<0.05). Exercise up-regulated the expression of phosphoinositide 3-kinase (IP3R)/ protein kinase B 1(AKT1) /mTOR in the cortex of rats, among which young IP3R was significantly up-regulated (P<0.01) in the young group, mTOR was significantly up-regulated in young and middle-aged group (P<0.01), and mTOR was also significantly up-regulated in the aged group (P<0.05).@*CONCLUSION@#Endurance exercise up-regulates BDNF expression, regulates CaMKIIα signaling, activates AMPK signaling pathway and IP3R / AKT1 / mTOR signaling pathway, and improves synaptic plasticity in the cortex.

Age Factors , Animals , Cerebral Cortex , Physiology , Male , Neuronal Plasticity , Physical Conditioning, Animal , Physical Endurance , Rats , Rats, Sprague-Dawley , Signal Transduction
Laboratory Animal Research ; : 172-179, 2019.
Article in English | WPRIM | ID: wpr-786406


Glutamate leads to neuronal cell damage by generating neurotoxicity during brain development. The objective of this study is to identify proteins that differently expressed by glutamate treatment in neonatal cerebral cortex. Sprague-Dawley rat pups (post-natal day 7) were intraperitoneally injected with vehicle or glutamate (10 mg/kg). Brain tissues were isolated 4 h after drug treatment and fixed for morphological study. Moreover, cerebral cortices were collected for protein study. Two-dimensional gel electrophoresis and mass spectrometry were carried out to identify specific proteins. We observed severe histopathological changes in glutamate-exposed cerebral cortex. We identified various proteins that differentially expressed by glutamate exposure. Identified proteins were thioredoxin, peroxiredoxin 5, ubiquitin carboxy-terminal hydrolase L1, proteasome subunit alpha proteins, isocitrate dehydrogenase, and heat shock protein 60. Heat shock protein 60 was increased in glutamate exposed condition. However, other proteins were decreased in glutamate-treated animals. These proteins are related to anti-oxidant, protein degradation, metabolism, signal transduction, and anti-apoptotic function. Thus, our findings can suggest that glutamate leads to neonatal cerebral cortex damage by regulation of specific proteins that mediated with various functions.

Animals , Brain , Cerebral Cortex , Chaperonin 60 , Electrophoresis, Gel, Two-Dimensional , Glutamic Acid , Humans , Infant, Newborn , Isocitrate Dehydrogenase , Mass Spectrometry , Metabolism , Neurons , Peroxiredoxins , Proteasome Endopeptidase Complex , Proteolysis , Proteomics , Rats , Rats, Sprague-Dawley , Signal Transduction , Thioredoxins , Ubiquitin Thiolesterase
Laboratory Animal Research ; : 124-131, 2019.
Article in English | WPRIM | ID: wpr-786395


Cerebral ischemia is a major cause of neurodegenerative disease. It induces neuronal vulnerability and susceptibility, and leads to neuronal cell death. Resveratrol is a polyphenolic compound that acts as an anti-oxidant. It exerts a neuroprotective effect against focal cerebral ischemic injury. Akt signaling pathway is accepted as a representative cell survival pathway, including proliferation, growth, and glycogen synthesis. This study investigated whether resveratrol regulates Akt/glycogen synthase kinase-3β (GSK-3β) pathway in a middle cerebral artery occlusion (MCAO)-induced ischemic brain injury. Adult male rats were intraperitoneally injected with vehicle or resveratrol (30 mg/kg) and cerebral cortices were isolated 24 h after MCAO. Neurological behavior test, corner test, brain edema measurment, and 2,3,5-triphenyltetrazolium chloride staining were performed to elucidate the neuroprotective effects of resveratrol. Phospho-Akt and phospho-GSK-3β expression levels were measured using Western blot analysis. MCAO injury led to severe neurobehavioral deficit, infraction, and histopathological changes in cerebral cortex. However, resveratrol treatment alleviated these changes caused by MCAO injury. Moreover, MCAO injury induced decreases in phospho-Akt and phospho-GSK-3β protein levels, whereas resveratrol attenuated these decreases. Phosphorylations of Akt and GSK-3β act as a critical role for the suppression of apoptotic cell death. Thus, our finding suggests that resveratrol attenuates neuronal cell death in MCAO-induced cerebral ischemia and Akt/GSK-3β signaling pathway contributes to the neuroprotective effect of resveratrol.

Adult , Animals , Behavior Rating Scale , Blotting, Western , Brain Edema , Brain Injuries , Brain Ischemia , Cell Death , Cell Survival , Cerebral Cortex , Glycogen , Humans , Infarction, Middle Cerebral Artery , Male , Middle Cerebral Artery , Neurodegenerative Diseases , Neurons , Neuroprotective Agents , Phosphorylation , Rats
Laboratory Animal Research ; : 132-139, 2019.
Article in English | WPRIM | ID: wpr-786394


Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 µg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.

Adult , Animals , Astrocytes , Body Weight , Cerebral Cortex , Cytokines , Glial Fibrillary Acidic Protein , Humans , Injections, Intraperitoneal , Male , Mice , Microglia , Necrosis , Neuroglia , NF-kappa B , Oxidative Stress , Reactive Oxygen Species
Article in Chinese | WPRIM | ID: wpr-781256


OBJECTIVE@#To study the role of Nrf2/ARE signaling pathway in cypermethrin-induced oxidative stress and apoptosis of cerebral cortex neurons in C57BL/6 mice.@*METHODS@#The cortical neurons of C57BL/6 mice were cultured and identified, and a cypermethrin-induced cell injury model was established by treating the cells with 0, 25, 50 and 100 μmol/L of cypermethrin for 48 h. CCK-8 assay was used to analyze the effects of cypermethrin on the cell viability, and the fluorescence probe DCFH-DA was used for detecting intracellular reactive oxygen species (ROS); flow cytometry was performed for determining the apoptosis rate of the cells. The mRNA and protein expression levels of Nrf2 and its downstream genes HO-1 and NQO1 were detected using qPCR and Western blotting.@*RESULTS@#Exposure to cypermethrin at different doses inhibited the viability of the cultured cortical neurons. With the increase of cypermethrin dose, the viability of the neurons decreased progressively, the intracellular ROS and the cell apoptosis rate increased, and the neuronal injury worsened. At the dose of 50 and 100 μmol/L, cypermethrin significantly down-regulated the expressions of HO-1, NQO1 and Nrf2 at both the mRNA and protein levels in the cells ( < 0.01).@*CONCLUSIONS@#Cypermethrin exposure shows a dose-dependent neurotoxicity by inhibiting Nrf2/ARE signaling pathway, down-regulating the expression of Nrf2 and its downstream genes HO-1, NQO1 mRNA and protein, and inducing oxidative damage and apoptosis in primary mouse cortical neurons, .

Animals , Carboxylic Ester Hydrolases , Cerebral Cortex , Mice , Mice, Inbred C57BL , NF-E2-Related Factor 2 , Neurons , Pyrethrins , Signal Transduction