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Pesquisa : C23.550.369 [Categoria DeCS]
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Id: biblio-1131855
Autor: Madakshira, Manoj Gopal; Gupta, Kirti; Uthamalingam, Preithy; Kapatia, Gargi; Saini, Shiv Sajan.
Título: Multicystic encephalomalacia: An autopsy report of 4 cases
Fonte: Autops. Case Rep;10(4):e2020208, 2020. graf.
Idioma: en.
Resumo: Multicystic encephalomalacia is varying sized cystic lesions in the brain encountered in developing fetuses or infants. These cysts start at the periventricular area and may extend onto the cortex. The cause of the formation of these cystic lesions is secondary to an ischemic or hypoxic insult, which leads to liquefactive necrosis and subsequent formation of gliotic cyst walls having an admixture of microglia. We discuss four autopsy cases that had multicystic encephalomalacia to highlight the scenarios in which these lesions are encountered.
Descritores: Encefalomalacia/complicações
-Autopsia
Microglia
Gliose
Hipóxia
Limites: Humanos
Masculino
Recém-Nascido
Tipo de Publ: Relatos de Casos
Responsável: BR26.7 - Serviço de Biblioteca e Documentação Científica


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Id: biblio-1131809
Autor: Madakshira, Manoj Gopal; Singla, Sonal; Gupta, Kirti; Zahan, Sayeeda; Paria, Pradip; Sahu, Jitendra Kumar.
Título: Autopsy of a child with Spinal muscular atrophy Type I (Werdnig-Hoffmann disease)
Fonte: Autops. Case Rep;10(2):e2020157, Apr.-June 2020. graf.
Idioma: en.
Resumo: Spinal muscular atrophy (SMA) is a heritable neuromuscular disorder which encompasses a large group of genetic disorders characterized by slowly progressive degeneration of lower motor neurons. The mutation is seen in the SMN1 gene mapped on chromosome 5. Depending on the age of the onset and the degree of severity, SMA has three subtypes. We discuss the autopsy findings in a case of Type 1 SMA also known by the name Werdnig-Hoffmann disease, to highlight the primary changes in the spinal cord, and skeletal muscle with association changes in the liver and terminal respiratory complications.
Descritores: Atrofias Musculares Espinais da Infância/patologia
-Autopsia
Evolução Fatal
Gliose
Doenças Genéticas Inatas
Fígado
Limites: Humanos
Masculino
Lactente
Tipo de Publ: Relatos de Casos
Conferência Clínica
Responsável: BR26.7 - Serviço de Biblioteca e Documentação Científica


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Id: lil-107269
Autor: Andrade, Gerardo; Avendaño Valdez, José.
Título: Gliosis masiva de la retina / Massive retinal gliosis
Fonte: Rev. Inst. Nac. Oftalmol;10(1/2):21-3, ene.-dic. 1989. ilus.
Idioma: es.
Resumo: En un período de cuatro años se revisan 80 casos de leucocoria, encontrándose dos casos anatomopatológicos de gliosis masiva de retina. Se efectúa estudios de microscopía electrónica y estudio inmunohistoquímico. Los hallazgos demostraron que la masa pseudotumoral se debía a proliferación de células fusiformes de citoplasma eosinofílico fibrilar y que el método de la peroxidasa antiperoxidasa confirmó como tejido glial. La microscopía electrónica demostró un patrón similar al presentado por las células de Muller
Descritores: Retina/patologia
Oftalmopatias
Gliose/etiologia
Gliose/patologia
-Microftalmia/etiologia
Astrócitos/patologia
Neoplasias Oculares/complicações
Tipo de Publ: Relatos de Casos
Responsável: PE1.1 - Oficina Universitária de Biblioteca


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AMBROSIO, Carlos Eduardo
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Id: biblio-837676
Autor: Orlandin, Jéssica Rodrigues; Ambrósio, Carlos Eduardo; Lara, Valéria Maria.
Título: Glial scar-modulation as therapeutic tool in spinal cord injury in animal models
Fonte: Acta cir. bras;32(2):168-174, Feb. 2017. tab.
Idioma: en.
Resumo: Abstract Purpose: Spinal Cord injury represents, in veterinary medicine, most of the neurological attendances and may result in permanent disability, death or euthanasia. Due to inflammation resulting from trauma, it originates the glial scar, which is a cell interaction complex system. Its function is to preserve the healthy circuits, however, it creates a physical and molecular barrier that prevents cell migration and restricts the neuroregeneration ability. Methods: This review aims to present innovations in the scene of treatment of spinal cord injury, approaching cell therapy, administration of enzyme, anti-inflammatory, and other active principles capable of modulating the inflammatory response, resulting in glial scar reduction and subsequent functional improvement of animals. Results: Some innovative therapies as cell therapy, administration of enzymes, immunosuppressant or other drugs cause the modulation of inflammatory response proved to be a promising tool for the reduction of gliosis. Conclusion: Those tools promise to reduce gliosis and promote locomotor recovery in animals with spinal cord injury.
Descritores: Traumatismos da Medula Espinal/terapia
Cicatriz/veterinária
Gliose/veterinária
-Células-Tronco
Medicina Veterinária
Cicatriz/patologia
Recuperação de Função Fisiológica
Modelos Animais de Doenças
Gliose/etiologia
Gliose/patologia
Limites: Animais
Ratos
Responsável: BR1.1 - BIREME


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Id: lil-658971
Autor: Peixoto-Santos, José Eduardo; Galvis-Alonso, Orfa Yineth; Velasco, Tonicarlo R; Kandratavicius, Ludmyla; Assirati Jr, João Alberto; Carlotti, Carlos Gilberto; Scandiuzzi, Renata Caldo; Serafini, Luciano Neder; Leite, João Pereira.
Título: Different levels of MT-I/II between patients with MTLE with or without seizure generalization: does hippocampal MT-I/II affects seizure spread, or does seizure spread promotes differential expression of MT-I/II? / Níveis diferentes de MT-I/II entre pacientes com MTLE com ou sem crise generalizada: os níveis hipocampais de MT-I/II afetam o alastramento das crises, ou o alastramento das crises promove expressão diferencial de MT-I/II?
Fonte: J. epilepsy clin. neurophysiol;18(1):16-20, jan.-mar. 2012. tab.
Idioma: en.
Projeto: FAPESP; . CNPq; . CAPES.
Resumo: In the central nervous system, zinc is released along with glutamate during neurotransmission and, in excess, can promote neuronal death. Experimental studies have shown that metallothioneins I/II (MT-I/II), which chelate free zinc, can affect seizures and reduce neuronal death after status epilepticus. Our aim was to evaluate the expression of MT-I/II in the hippocampus of patients with temporal lobe epilepsy (TLE). Hippocampi from patients with pharmacoresistant mesial temporal lobe epilepsy (MTLE) were evaluated for expression of MT-I/II and for neuronal, astroglial, and microglial populations. Compared to control cases, MTLE group displayed widespread increase in MT-I/II expression, astrogliosis and reduced neuronal population. MT-I/II levels did not correlate with any clinical variables, but patients with secondary generalized seizures (SGS) had less MT-I/II than patients without SGS. In conclusion, MT-I/II expression was increased in hippocampi from MTLE patients and our data suggest that it may be associated with different seizure spread patterns.

No sistema nervoso central, o zinco é liberado juntamente com o glutamato durante a neurotransmissão e, quando liberado em excesso, pode promover morte neuronal. Estudos indicam que as metalotioneínas I/II (MT-I/II), proteínas quelantes de zinco livre, podem afetar parâmetros relacionados às crises e reduzir a morte neuronal subsequente a um status epilepticus. Nosso objetivo foi avaliar a expressão de MT-I/II no hipocampo de pacientes com epilepsia do lobo temporal (ELT). Hipocampos de pacientes com ELT mesial (ELTM) resistente ao tratamento farmacológico foram avaliados para a expressão de MT-I/II e para as populações neuronal e astroglial. Quando comparadas com o grupo controle, pacientes com ELTM apresentaram aumento na expressão de MT-I/II, astrogliose e redução na densidade neuronal. Não foram observadas correlações entre os níveis de MT-I/II e as características clínicas dos pacientes, mas pacientes com crises secundariamente generalizadas apresentaram um aumento menor nos níveis de MT-I/II que os pacientes sem estas crises. Em resumo, um aumento na expressão de MT-I/II é observado em pacientes com ELTM e nossos dados sugerem que o aumento pode estar associado a diferentes padrões de crises epilépticas.
Descritores: Zinco
Epilepsia
Gliose
Homeostase
Limites: Humanos
Responsável: BR16.1 - Biblioteca de Ciências da Saúde


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Id: biblio-998544
Autor: Palacios, Claudio; Suárez, Julio César; Nieto, Flavia; Herrera, Enrique José; Pueyrredón, Francisco José; Surur, Alberto; Theaux, Ricardo; Ryan, Juan Manuel; Viano, Juan Carlos.
Título: Cirugía de epilepsia con electrocorticografía intraoperatoria / Epilepsy surgery with intraoperative electrocorticography
Fonte: Rev. argent. neurocir;28(2):63-67, mayo 2014. ilus.
Idioma: es.
Resumo: OBJETIVO: presentar nuestra experiencia en cirugía de epilepsia con electrocorticografía intraoperatoria, en 19 pacientes. MATERIAL Y MÉTODO: estudio retrospectivo basado en historias clínicas de pacientes con epilepsia lesional operados en el Sanatorio Allende, de Córdoba, entre el 1 de diciembre de 1997 y el 30 de noviembre de 2013. En esta serie hubo 14 enfermos menores de 20 años y sólo 5 mayores de esa edad. Las lesiones fueron: en 10 (52,6%) displasias corticales, en 6 (31,5%) tumores, en 2 gliosis cicatrizal y en 1 cavernoma frontal. La localización fue temporal en 4 (21%) y extratemporal en 15 (79%). Tenían epilepsia refractaria 13 (67,3%) enfermos. RESULTADOS: el tratamiento fue satisfactorio si analizamos el control de las crisis. Actualmente 14 (73,6%) están libres de crisis, sólo 4 de ellos tienen un EEG anormal, por lo cual continúan medicados. De los 5 (26,4%) enfermos que continúan con crisis, 3 tienen episodios esporádicos y tienen una sola medicación; los otros 2 tienen crisis frecuentes por lo cual reciben 3 fármacos antiepilépticos. CONCLUSIÓN: la electrocorticografía intraoperatoria nos ha permitido identificar con precisión el foco epileptógeno, que en muchos casos esta adyacente o distante de la lesión

INTRODUCTION: to present our experience in epilepsy surgery with intraoperative electrocorticography in 19 patients. MATERIAL AND METHOD: retrospective study based on clinical records of patients with epilepsy operated on between December 1997 and November 2013 in Sanatorio Allende of Córdoba. In this series there were 14 patients younger than 20 years. Included: 10 (52,6) cortical displeases, 6 (31,5%) tumours, 2 cicatricial gliosis, and 1 cavernoma. The localization was temporal in 4 (21%), and extratemporal in 15 (79%). Thirteen (67,3%) patients had medically intractable epilepsies. RESULTS: in terms of epilepsy, surgical treatment with intraoperative electrocorticography was satisfactory. At the present: 14(73%) are free of seizures; only 4 had abnormal EEG and go on with anticonvulsive medication. Five patients to remain with epilepsy, only 2 of them had frequent crisis and required three anticonvulsive drugs. CONCLUSION: the intraoperative electrocorticography permitted to identify the epileptogenic area with accuracy. This area may be situated adjacent or distant to the primary lesion
Descritores: Epilepsia
Epilepsia Resistente a Medicamentos
Eletrocorticografia
Gliose
Neoplasias
Limites: Humanos
Responsável: AR423.1 - Biblioteca


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Id: lil-759295
Autor: Abud, Lucas Giansante; Thivard, Lionel; Abud, Thiago Giansante; Nakiri, Guilherme Seizem; Santos, Antonio Carlos dos; Dormont, Didier.
Título: Partial epilepsy: A pictorial review of 3 TESLA magnetic resonance imaging features
Fonte: Clinics;70(9):654-661, Sept. 2015. ilus.
Idioma: en.
Resumo: Epilepsy is a disease with serious consequences for patients and society. In many cases seizures are sufficiently disabling to justify surgical evaluation. In this context, Magnetic Resonance Imaging (MRI) is one of the most valuable tools for the preoperative localization of epileptogenic foci. Because these lesions show a large variety of presentations (including subtle imaging characteristics), their analysis requires careful and systematic interpretation of MRI data. Several studies have shown that 3 Tesla (T) MRI provides a better image quality than 1.5 T MRI regarding the detection and characterization of structural lesions, indicating that high-field-strength imaging should be considered for patients with intractable epilepsy who might benefit from surgery. Likewise, advanced MRI postprocessing and quantitative analysis techniques such as thickness and volume measurements of cortical gray matter have emerged and in the near future, these techniques will routinely enable more precise evaluations of such patients. Finally, the familiarity with radiologic findings of the potential epileptogenic substrates in association with combined use of higher field strengths (3 T, 7 T, and greater) and new quantitative analytical post-processing techniques will lead to improvements regarding the clinical imaging of these patients. We present a pictorial review of the major pathologies related to partial epilepsy, highlighting the key findings of 3 T MRI.
Descritores: Epilepsias Parciais/diagnóstico
Imagem por Ressonância Magnética/métodos
-Neoplasias Encefálicas/diagnóstico
Neoplasias Encefálicas/patologia
Malformações Vasculares do Sistema Nervoso Central/diagnóstico
Malformações Vasculares do Sistema Nervoso Central/patologia
Epilepsias Parciais/patologia
Gliose/diagnóstico
Gliose/patologia
Malformações do Desenvolvimento Cortical/diagnóstico
Malformações do Desenvolvimento Cortical/patologia
Esclerose
Esclerose Tuberosa/diagnóstico
Esclerose Tuberosa/patologia
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: lil-691792
Autor: Chala, Catalina Lapuente; Valbuena, Carlos Augusto Rengifo; Rodriguez, Marco Fidel Ávila; Rubio, Angel Céspedes.
Título: Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine modelof cerebral infarction by arterial embolization / Efecto regulatorio del dimetilsulfóxido (DMSO) sobre la reactividad astrocitaria en un modelo murino de infarto cerebral por embolización arterial
Fonte: Colomb. med;44(1):31-36, Jan.-Mar. 2013. ilus, graf.
Idioma: en.
Resumo: Introduction:The pathophysiology of cerebral ischemia is essen-tial for early diagnosis, neurologic recovery, the early onset of drugtreatment and the prognosis of ischemic events. Experimental modelsof cerebral ischemia can be used to evaluate the cellular response phe-nomena and possible neurological protection by drugs.Objective:To characterize the cellular changes in the neuronal po-pulation and astrocytic response by the effect of Dimethyl Sulfoxide(DMSO) on a model of ischemia caused by cerebral embolism.Methods:Twenty Wistar rats were divided into four groups (n = 5).The infarct was induced with α-bovine thrombin (40 NIH/Unit.). Thetreated group received 90 mg (100 μl) of DMSO in saline (1:1 v/v) in-traperitoneally for 5 days; ischemic controls received only NaCl (pla-cebo) and two non-ischemic groups (simulated) received NaCl andDMSO respectively. We evaluated the neuronal (anti-NeuN) and as-trocytic immune-reactivity (anti-GFAP). The results were analyzed bydensitometry (NIH Image J-Fiji 1.45 software) and analysis of variance(ANOVA) with the Graph pad software (Prism 5).Results:Cerebral embolism induced reproducible and reliable lesionsin the cortex and hippocampus (CA1)., similar to those of focal mo-dels. DMSO did not reverse the loss of post-ischemia neuronal im-mune-reactivity, but prevented the morphological damage of neurons,and significantly reduced astrocytic hyperactivity in the somato-sen-sory cortex and CA1 (P <0.001).Conclusions:The regulatory effect of DMSO on astrocyte hyperreac-tivity and neuronal-astroglial cytoarchitecture , gives it potential neu-roprotective properties for the treatment of thromboembolic cerebralischemia in the acute phase.
Descritores: Isquemia Encefálica
Embolia
Neuroglia
-Astrócitos
Gliose
Imuno-Histoquímica
Limites: Ratos
Responsável: CO49.1 - Biblioteca San Fernando


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Id: lil-682332
Autor: Feria-Romero, Iris A; Alonso-Vanegas, Mario; Rocha-Arrieta, Luisa; Villeda-Hernández, Juana; Escalante-Santiago, David; Lorigados-Pedré, Lourdes; Morales-Chacón, Lilia; Grijalva-Otero, Israel; Orozco-Suárez, Sandra.
Título: Mecanismos de neurodegeneración en la epilepsia del lóbulo temporal / Mechanisms of neurodegeneration in temporal lobe epilepsy
Fonte: Rev. chil. neuro-psiquiatr;51(2):137-148, abr. 2013. ilus.
Idioma: es.
Projeto: Instituto de Ciencia y Tecnología del GDF (México); . Fondo de Investigación en Salud.
Resumo: Epilepsy affects 1 and 2 percent of the worldwide population, while temporal lobe epilepsy (TLE) covers 40 percent of all epilepsy cases. Controversy in defining epilepsy as a neurodegenerative disease exists because, no there is enough evidence to show seizures and status epilepticus (SE) as cause for irreversible neuronal damage. Epileptogenic insult at the beginning of the disease produces an acute and delayed neuronal death, resulting in gliosis, but also triggers compensatory processes such as angiogenesis, cell proliferation and reorganization of extracellular matrix as receptors, channels and drug transporter proteins. In neurogenesis and axonal regrowth, the age of onset is crucial for the formation of abnormal neurons and aberrant circuits as a result of seizures; approximately 30 percent begin in the temporal lobe. These disturbances continue in parallel or sequentially during the course of epilepsy, which implies a great challenge in the search of new treatments...

La epilepsia es una enfermedad que afecta entre el 1 al 2 por ciento de la población mundial, siendo la epilepsia del lóbulo temporal (ELT) la que abarca el 40 por ciento de todos los casos de epilepsia. La controversia en definir a la epilepsia como una enfermedad neurodegenerativa, se debe a que no hay pruebas suficientes que demuestren como las convulsiones y el estado de mal epiléptico (SE) provocan un daño neuronal irreversible. El insulto epileptógenico presente al inicio de la enfermedad genera la muerte neuronal aguda y tardía, para dar lugar a la gliosis; pero también se desencadenan procesos compensatorios como la angiogénesis, la proliferación celular y una reorganización tanto de la matriz extracelular como de los receptores, canales y proteínas transportadoras de fármacos. En el caso de la neurogénesis y recrecimiento axonal, la edad de inicio es determinante para la formación de neuronas anormales y circuitos aberrantes como consecuencia de las convulsiones, dónde aproximadamente un 30 por ciento comienzan en el lóbulo temporal. Estas alteraciones se continúan en paralelo o de forma secuencia! durante la evolución de la epilepsia, lo que implica un gran desafío en la búsqueda de nuevos tratamientos...
Descritores: Epilepsia do Lobo Temporal/complicações
Epilepsia do Lobo Temporal/fisiopatologia
-Degeneração Neural/etiologia
Degeneração Neural/fisiopatologia
Gliose
Inflamação
Neovascularização Patológica
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Allodi, Silvana
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Id: lil-610625
Autor: Fusco, Maria Alice; Portes, André Luís Freire; Allodi, Silvana; Moraes Junior, Haroldo Vieira de; Monteiro, Mário Luiz Ribeiro; Miguel, Nádia Campos de Oliveira.
Título: Reduced occurrence of programmed cell death and gliosis in the retinas of juvenile rabbits after shortterm treatment with intravitreous bevacizumab
Fonte: Clinics;67(1):61-67, 2012. ilus.
Idioma: en.
Resumo: OBJECTIVE: Bevacizumab has been widely used as a vascular endothelial growth factor antagonist in the treatment of retinal vasoproliferative disorders in adults and, more recently, in infants with retinopathy of prematurity. Recently, it has been proposed that vascular endothelial growth factor acts as a protective factor for neurons and glial cells, particularly in developing nervous tissue. The purpose of this study was to investigate the effects of bevacizumab on the developing retinas of juvenile rabbits. METHODS: Juvenile rabbits received bevacizumab intravitreously in one eye; the other eye acted as an untreated control. Slit-lamp and fundoscopic examinations were performed both prior to and seven days after treatment. At the same time, retina samples were analyzed using immunohistochemistry to detect autophagy and apoptosis as well as proliferation and glial reactivity. Morphometric analyses were performed, and the data were analyzed using the Mann-Whitney U test. RESULTS: No clinical abnormalities were observed in either treated or untreated eyes. However, immunohistochemical analyses revealed a reduction in the occurrence of programmed cell death and increases in both proliferation and reactivity in the bevacizumab-treated group compared with the untreated group. CONCLUSIONS: Bevacizumab appears to alter programmed cell death patterns and promote gliosis in the developing retinas of rabbits; therefore, it should be used with caution in developing eyes.
Descritores: Inibidores da Angiogênese/efeitos adversos
Anticorpos Monoclonais Humanizados/efeitos adversos
Gliose/patologia
Retina/efeitos dos fármacos
Células Ganglionares da Retina/efeitos dos fármacos
-Morte Celular/efeitos dos fármacos
Gliose/induzido quimicamente
Injeções Intravítreas
Modelos Animais
Distribuição Aleatória
Retina/crescimento & desenvolvimento
Células Ganglionares da Retina/patologia
Estatísticas não Paramétricas
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
Limites: Animais
Masculino
Coelhos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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