Autopsy of a child with Spinal muscular atrophy Type I (Werdnig-Hoffmann disease)

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.

Multicystic encephalomalacia: An autopsy report of 4 cases

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.

Propentofylline decreases hypothalamic astrogliosis induced by hypercaloric diet in the rat / A propentofilina diminui a astrogliose hipotalâmica induzida pela dieta hipercalórica no rato

ABSTRACT Obesity is associated with a chronic and low-grade inflammatory response in the hypothalamus, where astrogliosis occurs with the upregulation of the astrocyte structural protein GFAP. As propentofylline (PPF) has inhibitory effects on astrocyte and microglial activation during inflammation, this study aimed to investigate if this xanthine derivative could decrease the astrocyte reaction induced by a hypercaloric diet (HD). Male Wistar rats were divided into four groups: NDS - rats receiving a normocaloric diet (ND) and daily saline solution; NDP - rats receiving ND and daily PPF (12.5 mg/kg/day, intraperitoneal route); HDS - rats receiving HD and saline solution, HDP - rats receiving HD and PPF. On the 21st day, rats were anesthetized, and perfused, and brains were collected for GFAP immunohistochemical study in the hypothalamus. Results showed that HD induced increased weight gain and hypothalamic astrogliosis. Propentofylline decreased the expression of GFAP in the HDP group, although it did not affect the weight gain induced by this diet.

RESUMO A obesidade está associada com uma resposta inflamatória crônica e de baixo grau no hipotálamo, onde ocorre astrogliose com a superexpressão da proteína astrocitária GFAP. Como a propentofilina (PPF) possui efeitos inibitórios sobre a ativação astrocitária e microglial durante a inflamação, este estudo visou a investigar se esta xantina podia diminuir a reação astrocitária induzida pela dieta hipercalórica (HD). Ratos Wistar machos foram divididos em 4 grupos: NDS- ratos recebendo dieta normocalórica (ND) e solução salina diária; NDP- ratos recebendo ND e PPF diária (12.5 mg/kg/dia, via intraperitoneal); HDS- ratos recebendo HD e solução salina, HDP- ratos recebendo HD e PPF. No 21° dia, os ratos foram perfundidos e os encéfalos, coletados para estudo imuno-histoquímico para a GFAP no hipotálamo. Os resultados mostram que a HD induziu aumento do ganho de peso e astrogliose no hipotálamo. A PPF diminuiu a expressão de GFAP no grupo HD, embora não tenha afetado o ganho de peso induzido por esta dieta.

Glial scar-modulation as therapeutic tool in spinal cord injury in animal models

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.

Partial epilepsy: A pictorial review of 3 TESLA magnetic resonance imaging features

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.

Cirugía de epilepsia con electrocorticografía intraoperatoria / Epilepsy surgery with intraoperative electrocorticography

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

Mecanismos de neurodegeneración en la epilepsia del lóbulo temporal / Mechanisms of neurodegeneration in temporal lobe epilepsy

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...

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

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.

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?

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.

Reduced occurrence of programmed cell death and gliosis in the retinas of juvenile rabbits after shortterm treatment with intravitreous bevacizumab

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.

Early destructive lesions in the developing brain: clinical and electrographic correlates

OBJECTIVE: Early brain insults can cause cavitary lesions including porencephaly (POR) and multicystic encephalopathy (MCE). The objective of this study was to investigate clinical and electrographic correlates associated to these types of destructive brain lesions. METHOD: Patients with POR and MCE were selected and submitted to clinical and Video-EEG monitoring. The following variables were analyzed: demographic data, type of lesion, presence of gliosis, perinatal complications, epilepsy, brain atrophy, and presence and frequency of epileptiform discharges. RESULTS: Twenty patients were included, 65 percent males, 35 percent females, ages ranging from 1 to 40 years, 14 with MCE and 6 with POR. Eighteen patients had hemiparesis, 19 had epilepsy (current or in the past), seven of them had refractory seizures, and 16 had epileptiform discharges. All patients with MCE had gliosis while only 2 with POR had it. CONCLUSIONS: No correlation was observed between type of lesion and clinical and electrographical outcome. However, a positive correlation was observed between frequency of discharges and presence of brain atrophy, and between MCE and gliosis.

OBJETIVO: Insultos cerebrais precoces podem causar lesões cavitárias incluindo porencefalias (POR) e encefalomalacias multicisticas (EMC). O objetivo deste estudo foi investigar correlatos clínicos e eletrográficos associados a estes dois tipos de lesões destrutivas. MÉTODO: Pacientes com POR e EMC foram selecionados e submetidos à avaliação neurológica e monitorização vídeo-eletrencefalográfica, analisando-se as seguintes variáveis: dados demográficos, tipo de lesão, presença de gliose, complicações perinatais, epilepsia, atrofia cerebral, presença e freqüência de descargas epilépticas. RESULTADO: Vinte pacientes foram incluídos, sendo 65 por cento do sexo masculino, 35 por cento do feminino, idades entre 1 e 40 anos, sendo 14 com EMC e 6 com POR. Dezoito pacientes tinham hemiparesia, 19 tinham ou tiveram epilepsia (7 deles refratários ao tratamento medicamentoso) e 16 deles tinham paroxismos epileptiformes. Todos com MCE tinham gliose associada, contra apenas 2 dos pacientes com POR. CONCLUSÃO: Não houve correlação entre tipo de lesão e evolução clínica e eletrográfica. Houve, entretando, correlação positiva entre freqüência de descargas epilépticas e presença de atrofia cerebral, e entre lesão do tipo EMC e presença de gliose.

Plasticidade neuronal associada à epilepsia do lobo temporal mesial: insights a partir de estudos em humanos e em modelos animais / Neuronal plasticity associated with mesial temporal lobe epilepsy: insights form human and animal model studies

A epilepsia do lobo temporal (ELT), a forma mais frequente das epilepsias resistentes ao tratamento farmacológico entre a população adualta, se caracteriza por perda neuronal hipocampal e comprometimento cognitivo progressivos. Estudos em pacientes com ELT e em modelos animais têm demonstrado a ocorrência de fenômenos de plasticidade neuronal exuberantes e dinâmicos na formação hipocampal. O estudo desses fenômenos é fundamental para a definição dos mecanismos responsáveis pela gênese e progressão da ELT, e a partir destes, para o desenvolvimento de melhores estratégias terapêuticas. Esta revisão de estudos em humanos e modelos animais trata sobre alterações plásticas que ocorrem como a perda neuronal, neurogênese, mudanças em dendritos, axônios, sinapses e glia, tentando estabelecer o provável papel destas na ELT

Frontoparietal cortical atrophy with gliosis in the gray matter of cerebral cortex: case report

The case of a patient who suffered from progressive amnesia, depressive humor, language and visuospatial disturbances, and hallucination episodies with interference at the daily living activities is reported. She had moderate neuropsichological diffuse deficits at the first examination, especially at the executive and visuo-constructive functions. Her cerebrospinal fluid test presented high total protein. Magnetic resonance image showed slight white matter increase in periventricular, semi-oval center bilateral and left external capsule regions, besides light frontal and parietal lobe atrophy, bilaterally. Brain single photon emission computerized tomography revealed both a bilateral moderate frontal and a severe parietal lobe hypoperfusion, especially on the left side. Macroscopic examination showed cortical atrophy, severe on the frontal, moderate on the parietal and mild on the posterior third temporal lobes, bilaterally. There was a slight atrophy on the neostriatum in the basal ganglia. The histopathological findings of the autopsy showed severe neuronal loss with intensive gemioscytic gliosis and variable degrees of status spongiosus in cortical layer. Hematoxylin-eosin and Bielschowsky staining did not show neuronal swelling (balooned cell), argyrophilic inclusion (Pick's bodies), neurofibrillary tangles nor senile plaques. Immunohistochemical staining for anti-ubiquitin, anti-tau, anti-beta-amyloide, and anti-prion protein were tested negative

Un caso de Creutzfeldt-Jakob en el noreste de México y revisión de conceptos actuales sobre enfermedad por priones / A case of creuzfeldt-Jakob disease in northeastern Mexico and a review of current concepts in prion-related diseases

Se presenta el caso de un hombre de 50 años originario y residente de Saltillo, Coahuila, México, con síndrome demencial y mioclonías de 15 meses de evolución, que había sido incorrectamente diagnosticado en diferentes instituciones. El electroencefalograma mostró descargas lateralizadas al hemisferio derecho con formación de espigas, poliespigas y ondas agudas con patrón periódico. La biopsia cerebral evidenció encefalopatía espon-giforme, con despoblación neuronal y astrocitosis reactiva. Se revisan los conceptos actuales sobre enfermedad por priones.

Sporadic creutzfeldt-Jakob disease. A clinical-neuropathological analysis of nine definite cases

The authors have analyzed clinico-neuropathologically nine cases of the definite sporadic form of Creutzfeldt-Jakob disease (CJD). All cases were female, with mean age of 62.7 years. Eighty-nine percent of the patients exhibited prodromal and initial psychiatric symptoms; definite signs of dementia, and myoclonus were present in 100 per cent of cases. The EEG was abnormal in all cases and pseudoperiodic paroxysms were present in 56 per cent of the patients. Their evolution time ranged from 3 to 19 months. Neuropathologically, brain and cerebellar atrophy, spongiosis, astrocytosis and neuronal loss were present in 100 per cent of the patients. In 5 (56 per cent) of these 9 cases, prion protein (PrP) amyloid plaques were detected in the cerebellum, by optical- and electronmicroscopy. There was a positive correlation between the number of plaques and the evolution time. The authors outline the similarities of their cases in the elderly with the new variant of CJD described in young people.

Gliosis masiva retiniana: consideraciones clinicopatológicas

La gliosis masiva retiniana es una proliferación reactiva benigna de la astrología retiniana que asume patrón pseudotumoral. Se puede localizar sectorialmente en la retina, especialmente en la periferia u ocupar toda la cavidad ocular. Esta proliferación glial se asocia a cambios reactivos, reparativos, inflamatorios o proliferativos de otras estructuras oculares que complican el cuadro y dificultan el diagnóstico como son la hiperplasia adenomatoide del epitelio pigmentado y no pigmentado del cuerpo ciliar, la metaplasia ósea y mieloide, etc. El diagnóstico de la histogénesis se alcanza por medio de la histoinmunoquímica y la microscopía electrónica de transmisión

Desarrollo dendrítico de las células piramidales de la neocorteza en víctimas del síndrome de muerte súbita infantil / Neocortical pyramidal cell dendritic development in victims of the sudden infant death syndrome

En pacientes fallecidos por síndrome de muerte súbita infantil se han descrito alteraciones de la maduración neuronal en el tronco cerebral y gliosis. Propósito: determinar si existen alteraciones en niños fallecidos por síndrome de muerte súbita infantil. Sujetos y método: mediciones de densidad, longitud y volumen del cilindro dendrítico de las células piramidales en preparaciones de la corteza motora de cuatro lactantes fallecidos por síndrome de muerte súbita infantil y cuatro controles muertos por neumonía. Las preparaciones fueron teñidas con la técnica de Golgi-Cox y evaluados con métodos morfométricos. Resultados: no se encontraron diferencias significativas en la densidad, número de ramas dendríticas a diferentes distancias del soma neuronal y volumen del cilindro dendrítico basal entre los lactantes fallecidos por neumonía y los considerados como casos de muerte súbita infantil, pero en estos últimos se registró, a diferencia de los controles, marcado proliferación de la glia. Conclusión: en lactantes fallecidos por síndrome de muerte súbita la maduración neuronal podría no ser afectada por aquellos factores que, en cambio, inducirían un retardo de la maduración histológica de núcleos del tronco encefálico y gliosis difusa del tejido nervioso. La gliosis sugiere exposición crónica a situaciones de hipoxia

Linfoma primario del sistema nervioso central / Primary lymphoma of the central nervous system

El linfoma primario del sistema nervioso central (LPSNS) era considerado un tumor primario infrecuente del SNC pero actualmente se asiste a un aumento de casos, especialmente en pacientes inmunocompetentes, por causas no bien determinadas. Esto ha coincidido con la ocurrencia de pacientes consecutivos no inmunodeprimidos en el Departamento de Neurología-Neurocirugía del Hospital Clínico de la Universidad de Chile, que fueron operados con criterio oncológico y luego sometidos a quimioterapia y radioterapia, con buenos resultados, según esquema De Angelis, que ha probado ser el de mayor sobrevida. Se revisa bibliografía y se discuten casos reportados (3), planteándose el valor de la resección-descompresión en la forma tumoral focal con hipertensión endocraneana, para que una vez descompensado el paciente se someta a quimioterapia (MTX) y radioterapia en casos seleccionados, ya que se discute su beneficio frente a sus complicaciones

Vitrectomia no tratamento do pucker macular / Vitrectomy for macular pucker

Vitrectomia com "peeling" de membrana foi realizada para o tratamento de 34 casos consecutivos de pucker macular com acuidade visual pior ou igual 20/80. O pucker macular era idiopático (11 olhos); ou estava associado a descolamento de retina ou ruptura de retina tratados (15 olhos), uveíte (5 olhos), trauma penetrante (2 olhos) e retinopatia por células falciformes (1 olho). A acuidade visual melhorou em 28 olhos (82,4 por cento), permaneceu a mesma em 5 olhos (14,7 por cento) e piorou em um olho (2,9 por cento). Näo houve diferença estatisticamente significativa no resultado da cirurgia com relaçäo à etiologia da membrana. Dois olhos (5,9 por cento) apresentaram descolamento de retina no pós-operatório imediato e foram tratados com sucesso. De 20 olhos fácicos, 6 (30 por cento) apresentaram opacificaçäo cristaliniana após 1 ano de cirurgia. Dois olhos (5,9 por cento) apresentaram recidiva da membrana epirretiniana

Gliose pré-macular idiopática: Análise das repercussöes angiográficas secundárias ou associadas / Idiopathic premacular gliosis: Angiographic study of secondary findings

Analisaram-se retrospectivamente 28 casos com diagnóstico clínico e angiográfico de fibrose pré-macular a fim de detectar os eventos retinianos associados ou intercorrentes. Em 67,8 por cento dos casos, estas situaçöes foram notadas, e em 17,8 por cento teve-se evidência indiscutível de vazamento.