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[PMID]:28899007
[Au] Autor:Hong SJ; Bernhardt BC; Gill RS; Bernasconi N; Bernasconi A
[Ad] Endereço:Neuroimaging of Epilepsy Laboratory, Department of Neurology and McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada.
[Ti] Título:The spectrum of structural and functional network alterations in malformations of cortical development.
[So] Source:Brain;140(8):2133-2143, 2017 Aug 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neuroimaging studies of malformations of cortical development have mainly focused on the characterization of the primary lesional substrate, while whole-brain investigations remain scarce. Our purpose was to assess large-scale brain organization in prevalent cortical malformations. Based on experimental evidence suggesting that distributed effects of focal insults are modulated by stages of brain development, we postulated differential patterns of network anomalies across subtypes of malformations. We studied a cohort of patients with focal cortical dysplasia type II (n = 63), subcortical nodular heterotopia (n = 44), and polymicrogyria (n = 34), and compared them to 82 age- and sex-matched controls. Graph theoretical analysis of structural covariance networks indicated a consistent rearrangement towards a regularized architecture characterized by increased path length and clustering, as well as disrupted rich-club topology, overall suggestive of inefficient global and excessive local connectivity. Notably, we observed a gradual shift in network reconfigurations across subgroups, with only subtle changes in focal cortical dysplasia type II, moderate effects in heterotopia and maximal effects in polymicrogyria. Analysis of resting state functional connectivity also revealed gradual network changes, with most marked rearrangement in polymicrogyria; contrary to findings in the structural domain, however, functional architecture was characterized by decreases in both local and global parameters. Diverging results in the structural and functional domain were supported by formal structure-function coupling analysis. Our findings support the concept that time of insult during corticogenesis impacts the severity of topological network reconfiguration. Specifically, late-stage malformations, typified by polymicrogyria, may selectively disrupt the formation of large-scale cortico-cortical networks and thus lead to a more profound impact on whole-brain organization than early stage disturbances of predominantly radial migration patterns observed in cortical dysplasia type II, which likely affect a relatively confined cortical territory.
[Mh] Termos MeSH primário: Epilepsia/patologia
Epilepsia/fisiopatologia
Malformações do Desenvolvimento Cortical do Grupo I/patologia
Malformações do Desenvolvimento Cortical do Grupo I/fisiopatologia
Rede Nervosa/patologia
Rede Nervosa/fisiopatologia
Heterotopia Nodular Periventricular/patologia
Heterotopia Nodular Periventricular/fisiopatologia
Polimicrogiria/patologia
Polimicrogiria/fisiopatologia
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Córtex Cerebral/crescimento & desenvolvimento
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Neuroimagem
Tomografia por Emissão de Pósitrons
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx145


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[PMID]:28401614
[Au] Autor:Campana C; Zubler F; Gibbs S; de Carli F; Proserpio P; Rubino A; Cossu M; Tassi L; Schindler K; Nobili L
[Ad] Endereço:'C. Munari' Epilepsy Surgery Centre, Niguarda Hospital, Milan, Italy.
[Ti] Título:Suppression of interictal spikes during phasic rapid eye movement sleep: a quantitative stereo-electroencephalography study.
[So] Source:J Sleep Res;26(5):606-613, 2017 Oct.
[Is] ISSN:1365-2869
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tonic and phasic rapid eye movement (REM) sleep seem to represent two different brain states exerting different effects on epileptic activity. In particular, interictal spikes are suppressed strongly during phasic REM sleep. The reason for this effect is not understood completely. A different level of synchronization in phasic and tonic REM sleep has been postulated, yet never measured directly. Here we assessed the interictal spike rate across non-REM (NREM) sleep, phasic and tonic REM sleep in nine patients affected by drug resistant focal epilepsy: five with type II focal cortical dysplasia and four with hippocampal sclerosis. Moreover, we applied different quantitative measures to evaluate the level of synchronization at the local and global scale during phasic and tonic REM sleep. We found a lower spike rate in phasic REM sleep, both within and outside the seizure onset zone. This effect seems to be independent from the histopathological substrate and from the brain region, where epileptic activity is produced (temporal versus extra-temporal). A higher level of synchronization was observed during tonic REM sleep both on a large (global) and small (local) spatial scale. Phasic REM sleep appears to be an interesting model for understanding the mechanisms of suppression of epileptic activity.
[Mh] Termos MeSH primário: Eletroencefalografia
Epilepsias Parciais/fisiopatologia
Sono REM/fisiologia
[Mh] Termos MeSH secundário: Encéfalo/patologia
Encéfalo/fisiopatologia
Epilepsias Parciais/patologia
Epilepsia/patologia
Epilepsia/fisiopatologia
Feminino
Hipocampo/patologia
Hipocampo/fisiopatologia
Seres Humanos
Masculino
Malformações do Desenvolvimento Cortical do Grupo I/patologia
Malformações do Desenvolvimento Cortical do Grupo I/fisiopatologia
Convulsões/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE
[do] DOI:10.1111/jsr.12533


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[PMID]:28260047
[Au] Autor:Marinowic DR; Majolo F; Sebben AD; da Silva VD; Lopes TG; Paglioli E; Palmini A; Machado DC; da Costa JC
[Ad] Endereço:Brain Institute of Rio Grande do Sul (BraIns), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS 90610000, Brazil.
[Ti] Título:Induced pluripotent stem cells from patients with focal cortical dysplasia and refractory epilepsy.
[So] Source:Mol Med Rep;15(4):2049-2056, 2017 Apr.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Focal cortical dysplasia (FCD) is caused by numerous alterations, which can be divided into abnormalities of the cortical architecture and cytological variations; however, the exact etiology of FCD remains unknown. The generation of induced pluripotent stem cells (iPSCs) from the cells of patients with neurological diseases, and their subsequent tissue­specific differentiation, serves as an invaluable source for testing and studying the initial development and subsequent progression of diseases associated with the central nervous system. A total of 2 patients demonstrating seizures refractory to drug treatment, characterized as FCD Type IIb, were enrolled in the present study. Fibroblasts were isolated from residual skin fragments obtained from surgical treatment and from brain samples obtained during surgical resection. iPSCs were generated following exposure of fibroblasts to viral vectors containing POU class 5 homeobox 1 (OCT4), sex determining region Y­box 2 (SOX2), Kruppel­like factor 4 and c­MYC genes, and were characterized by immunohistochemical staining for the pluripotent markers homeobox protein NANOG, SOX2, OCT4, TRA1­60 and TRA1­81. The brain samples were tested with antibodies against protein kinase B (AKT), phosphorylated­AKT, mechanistic target of rapamycin (mTOR) and phosphorylated­mTOR. Analysis of the AKT/mTOR pathway revealed a statistically significant difference between the cerebral tissues of the two patients, which were of different ages (45 and 12 years old). Clones with the morphological features of embryonic cells were detected on the 13th day and were characterized following three subcultures. The positive staining characteristics of the embryonic cells confirmed the successful generation of iPSCs derived from the patients' fibroblasts. Therefore, the present study presents a method to obtain a useful cellular source that may help to understand embryonic brain development associated with FCD.
[Mh] Termos MeSH primário: Epilepsia/patologia
Células-Tronco Pluripotentes Induzidas/patologia
Malformações do Desenvolvimento Cortical do Grupo I/patologia
[Mh] Termos MeSH secundário: Células Cultivadas
Reprogramação Celular
Criança
Epilepsia/metabolismo
Feminino
Fibroblastos/metabolismo
Fibroblastos/patologia
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Masculino
Malformações do Desenvolvimento Cortical do Grupo I/metabolismo
Meia-Idade
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Serina-Treonina Quinases TOR/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6264


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[PMID]:28215400
[Au] Autor:Lim JS; Gopalappa R; Kim SH; Ramakrishna S; Lee M; Kim WI; Kim J; Park SM; Lee J; Oh JH; Kim HD; Park CH; Lee JS; Kim S; Kim DS; Han JM; Kang HC; Kim HH; Lee JH
[Ad] Endereço:Brain Korea 21 Plus Project, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science & Technology, Daejeon 34141, South Korea.
[Ti] Título:Somatic Mutations in TSC1 and TSC2 Cause Focal Cortical Dysplasia.
[So] Source:Am J Hum Genet;100(3):454-472, 2017 Mar 02.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Focal cortical dysplasia (FCD) is a major cause of the sporadic form of intractable focal epilepsies that require surgical treatment. It has recently been reported that brain somatic mutations in MTOR account for 15%-25% of FCD type II (FCDII), characterized by cortical dyslamination and dysmorphic neurons. However, the genetic etiologies of FCDII-affected individuals who lack the MTOR mutation remain unclear. Here, we performed deep hybrid capture and amplicon sequencing (read depth of 100×-20,012×) of five important mTOR pathway genes-PIK3CA, PIK3R2, AKT3, TSC1, and TSC2-by using paired brain and saliva samples from 40 FCDII individuals negative for MTOR mutations. We found that 5 of 40 individuals (12.5%) had brain somatic mutations in TSC1 (c.64C>T [p.Arg22Trp] and c.610C>T [p.Arg204Cys]) and TSC2 (c.4639G>A [p.Val1547Ile]), and these results were reproducible on two different sequencing platforms. All identified mutations induced hyperactivation of the mTOR pathway by disrupting the formation or function of the TSC1-TSC2 complex. Furthermore, in utero CRISPR-Cas9-mediated genome editing of Tsc1 or Tsc2 induced the development of spontaneous behavioral seizures, as well as cytomegalic neurons and cortical dyslamination. These results show that brain somatic mutations in TSC1 and TSC2 cause FCD and that in utero application of the CRISPR-Cas9 system is useful for generating neurodevelopmental disease models of somatic mutations in the brain.
[Mh] Termos MeSH primário: Epilepsia/genética
Malformações do Desenvolvimento Cortical do Grupo I/genética
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Adolescente
Animais
Encéfalo/metabolismo
Sistemas CRISPR-Cas
Linhagem Celular Tumoral
Criança
Classe I de Fosfatidilinositol 3-Quinases
Clonagem Molecular
Modelos Animais de Doenças
Feminino
Células HEK293
Seres Humanos
Masculino
Camundongos
Mutação
Neurônios
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
Saliva/química
Análise de Sequência de DNA
Sirolimo/farmacologia
Serina-Treonina Quinases TOR/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Proteins); 0 (tuberous sclerosis complex 1 protein); 4JG2LF96VF (tuberous sclerosis complex 2 protein); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.- (phosphoinositol-3 kinase regulatory subunit 2, human); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (PIK3CA protein, human); EC 2.7.11.1 (AKT3 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE


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[PMID]:28206669
[Au] Autor:Nakagawa JM; Donkels C; Fauser S; Schulze-Bonhage A; Prinz M; Zentner J; Haas CA
[Ad] Endereço:Experimental Epilepsy Research, Department of Neurosurgery, Medical Center-University of Freiburg, Freiburg, Germany.
[Ti] Título:Characterization of focal cortical dysplasia with balloon cells by layer-specific markers: Evidence for differential vulnerability of interneurons.
[So] Source:Epilepsia;58(4):635-645, 2017 Apr.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Focal cortical dysplasia (FCD) is a major cause of pharmacoresistant focal epilepsy. Little is known about the pathomechanisms underlying the characteristic cytoarchitectural abnormalities associated with FCD. In the present study, a broad panel of markers identifying layer-specific neuron subpopulations was applied to characterize dyslamination and structural alterations in FCD with balloon cells (FCD 2b). METHODS: Pan-neuronal neuronal nuclei (NeuN) and layer-specific protein expression (Reelin, Calbindin, Calretinin, SMI32 (nonphosphorylated neurofilament H), Parvalbumin, transducin-like enhancer protein 4 (TLE4), and Vimentin) was studied by immunohistochemistry on paraffin sections of FCD2b cases (n = 22) and was compared to two control groups with (n = 7) or without epilepsy (n = 4 postmortem cases). Total and layer-specific neuron densities were systematically quantified by cell counting considering age at surgery and brain region. RESULTS: We show that in FCD2b total neuron densities across all six cortical layers were not significantly different from controls. In addition, we present evidence that a basic laminar arrangement of layer-specific neuron subtypes was preserved despite the severe disturbance of cortical structure. SMI32-positive pyramidal neurons showed no significant difference in total numbers, but a reduction in layers III and V. The densities of supragranular Calbindin- and Calretinin-positive interneurons in layers II and III were not different from controls, whereas Parvalbumin-expressing interneurons, primarily located in layer IV, were significantly reduced in numbers when compared to control cases without epilepsy. In layer VI, the density of TLE4-positive projection neurons was significantly increased. Altogether, these data show that changes in cellular composition mainly affect deep cortical layers in FCD2b. SIGNIFICANCE: The application of a broad panel of markers defining layer-specific neuronal subpopulations revealed that in FCD2b neuronal diversity and a basic laminar arrangement are maintained despite the severe disturbance of cytoarchitecture. Moreover, it showed that Parvalbumin-positive, inhibitory interneurons are highly vulnerable in contrast to other interneuron subtypes, possibly related to the epileptic condition.
[Mh] Termos MeSH primário: Epilepsia/patologia
Interneurônios/classificação
Interneurônios/metabolismo
Malformações do Desenvolvimento Cortical do Grupo I/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Calbindina 2/metabolismo
Moléculas de Adesão Celular Neuronais/metabolismo
Contagem de Células
Criança
Pré-Escolar
Proteínas da Matriz Extracelular/metabolismo
Feminino
Seres Humanos
Lactente
Masculino
Meia-Idade
Proteínas do Tecido Nervoso/metabolismo
Proteínas de Neurofilamentos/metabolismo
Parvalbuminas/metabolismo
Fosfopiruvato Hidratase/metabolismo
Serina Endopeptidases/metabolismo
Estatísticas não Paramétricas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calbindin 2); 0 (Cell Adhesion Molecules, Neuronal); 0 (Extracellular Matrix Proteins); 0 (Nerve Tissue Proteins); 0 (Neurofilament Proteins); 0 (Parvalbumins); 108688-71-7 (neurofilament protein H); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.- (reelin protein); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13690


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[PMID]:28130467
[Au] Autor:Hong SJ; Bernhardt BC; Caldairou B; Hall JA; Guiot MC; Schrader D; Bernasconi N; Bernasconi A
[Ad] Endereço:From the Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital (S.-J.H., B.C.B., B.C., J.A.H., M.C.G., N.B., A.B.), Neuroimaging of Epilepsy Laboratory, McConnell Brain Imaging Centre (S.-J.H., B.C.B., B.C., D.S., N.B., A.B.), and Department of Pathology (M.C.G.), Mc
[Ti] Título:Multimodal MRI profiling of focal cortical dysplasia type II.
[So] Source:Neurology;88(8):734-742, 2017 Feb 21.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To characterize in vivo MRI signatures of focal cortical dysplasia (FCD) type IIA and type IIB through combined analysis of morphology, intensity, microstructure, and function. METHODS: We carried out a multimodal 3T MRI profiling of 33 histologically proven FCD type IIA (9) and IIB (24) lesions. A multisurface approach operating on manual consensus labels systematically sampled intracortical and subcortical lesional features. Geodesic distance mapping quantified the same features in the lesion perimeter. Logistic regression assessed the relationship between MRI and histology, while supervised pattern learning was used for individualized subtype prediction. RESULTS: FCD type IIB was characterized by abnormal morphology, intensity, diffusivity, and function across all surfaces, while type IIA lesions presented only with increased fluid-attenuated inversion recovery signal and reduced diffusion anisotropy close to the gray-white matter interface. Similar to lesional patterns, perilesional anomalies were more marked in type IIB extending up to 16 mm. Structural MRI markers correlated with categorical histologic characteristics. A profile-based classifier predicted FCD subtypes with equal sensitivity of 85%, while maintaining a high specificity of 94% against healthy and disease controls. CONCLUSIONS: Image processing applied to widely available MRI contrasts has the ability to dissociate FCD subtypes at a mesoscopic level. Integrating in vivo staging of pathologic traits with automated lesion detection is likely to provide an objective definition of lesional boundary and assist emerging approaches, such as minimally invasive thermal ablation, which do not supply tissue specimen.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Epilepsia/diagnóstico por imagem
Interpretação de Imagem Assistida por Computador
Imagem por Ressonância Magnética
Malformações do Desenvolvimento Cortical do Grupo I/diagnóstico por imagem
Imagem Multimodal
[Mh] Termos MeSH secundário: Adulto
Encéfalo/patologia
Encéfalo/fisiopatologia
Encéfalo/cirurgia
Diagnóstico Diferencial
Epilepsia Resistente a Medicamentos/diagnóstico por imagem
Epilepsia Resistente a Medicamentos/etiologia
Epilepsia Resistente a Medicamentos/patologia
Epilepsia Resistente a Medicamentos/fisiopatologia
Epilepsia/complicações
Epilepsia/patologia
Epilepsia/fisiopatologia
Feminino
Seguimentos
Substância Cinzenta/diagnóstico por imagem
Substância Cinzenta/patologia
Substância Cinzenta/fisiopatologia
Substância Cinzenta/cirurgia
Seres Humanos
Modelos Logísticos
Masculino
Malformações do Desenvolvimento Cortical do Grupo I/complicações
Malformações do Desenvolvimento Cortical do Grupo I/patologia
Malformações do Desenvolvimento Cortical do Grupo I/fisiopatologia
Reconhecimento Automatizado de Padrão
Sensibilidade e Especificidade
Substância Branca/diagnóstico por imagem
Substância Branca/patologia
Substância Branca/fisiopatologia
Substância Branca/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000003632


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[PMID]:28123950
[Au] Autor:Adler S; Wagstyl K; Gunny R; Ronan L; Carmichael D; Cross JH; Fletcher PC; Baldeweg T
[Ad] Endereço:Developmental Neurosciences, UCL Great Ormond Street Institute of Child Health, University College London, London, UK; Great Ormond Street Hospital for Children, London, UK.
[Ti] Título:Novel surface features for automated detection of focal cortical dysplasias in paediatric epilepsy.
[So] Source:Neuroimage Clin;14:18-27, 2017.
[Is] ISSN:2213-1582
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Focal cortical dysplasia is a congenital abnormality of cortical development and the leading cause of surgically remediable drug-resistant epilepsy in children. Post-surgical outcome is improved by presurgical lesion detection on structural MRI. Automated computational techniques have improved detection of focal cortical dysplasias in adults but have not yet been effective when applied to developing brains. There is therefore a need to develop reliable and sensitive methods to address the particular challenges of a paediatric cohort. We developed a classifier using surface-based features to identify focal abnormalities of cortical development in a paediatric cohort. In addition to established measures, such as cortical thickness, grey-white matter blurring, FLAIR signal intensity, sulcal depth and curvature, our novel features included complementary metrics of surface morphology such as local cortical deformation as well as post-processing methods such as the "doughnut" method - which quantifies local variability in cortical morphometry/MRI signal intensity, and per-vertex interhemispheric asymmetry. A neural network classifier was trained using data from 22 patients with focal epilepsy (mean age = 12.1 ± 3.9, 9 females), after intra- and inter-subject normalisation using a population of 28 healthy controls (mean age = 14.6 ± 3.1, 11 females). Leave-one-out cross-validation was used to quantify classifier sensitivity using established features and the combination of established and novel features. Focal cortical dysplasias in our paediatric cohort were correctly identified with a higher sensitivity (73%) when novel features, based on our approach for detecting local cortical changes, were included, when compared to the sensitivity using only established features (59%). These methods may be applicable to aiding identification of subtle lesions in medication-resistant paediatric epilepsy as well as to the structural analysis of both healthy and abnormal cortical development.
[Mh] Termos MeSH primário: Mapeamento Encefálico
Córtex Cerebral/diagnóstico por imagem
Epilepsia/complicações
Malformações do Desenvolvimento Cortical do Grupo I/diagnóstico por imagem
Malformações do Desenvolvimento Cortical do Grupo I/etiologia
[Mh] Termos MeSH secundário: Adolescente
Área Sob a Curva
Criança
Pré-Escolar
Epilepsia/diagnóstico por imagem
Epilepsia/etiologia
Feminino
Seres Humanos
Imagem Tridimensional
Aprendizado de Máquina
Imagem por Ressonância Magnética
Masculino
Oxigênio/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
S88TT14065 (Oxygen)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170127
[St] Status:MEDLINE
[do] DOI:10.1016/j.nicl.2016.12.030


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[PMID]:28054328
[Au] Autor:Falco-Walter J; Owen C; Sharma M; Reggi C; Yu M; Stoub TR; Stein MA
[Ad] Endereço:Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
[Ti] Título:Magnetoencephalography and New Imaging Modalities in Epilepsy.
[So] Source:Neurotherapeutics;14(1):4-10, 2017 Jan.
[Is] ISSN:1878-7479
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The success of epilepsy surgery is highly dependent on correctly identifying the entire epileptogenic region. Current state-of-the-art for localizing the extent of surgically amenable areas involves combining high resolution three-dimensional magnetic resonance imaging (MRI) with electroencephalography (EEG) and magnetoencephalography (MEG) source modeling of interictal epileptiform activity. Coupling these techniques with newer quantitative structural MRI techniques, such as cortical thickness measurements, however, may improve the extent to which the abnormal epileptogenic region can be visualized. In this review we assess the utility of EEG, MEG and quantitative structural MRI methods for the evaluation of patients with epilepsy and introduce a novel method for the co-localization of a structural MRI measurement to MEG and EEG source modeling. When combined, these techniques may better identify the extent of abnormal structural and functional areas in patients with medically intractable epilepsy.
[Mh] Termos MeSH primário: Córtex Cerebral/diagnóstico por imagem
Eletroencefalografia
Epilepsia/diagnóstico por imagem
Epilepsia/terapia
Imagem por Ressonância Magnética
Magnetoencefalografia
[Mh] Termos MeSH secundário: Córtex Cerebral/patologia
Córtex Cerebral/fisiopatologia
Seres Humanos
Interpretação de Imagem Assistida por Computador/métodos
Malformações do Desenvolvimento Cortical do Grupo I/diagnóstico por imagem
Malformações do Desenvolvimento Cortical do Grupo I/terapia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.1007/s13311-016-0506-7


  9 / 94 MEDLINE  
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[PMID]:27864929
[Au] Autor:Bartolini L; Whitehead MT; Ho CY; Sepeta LN; Oluigbo CO; Havens K; Freilich ER; Schreiber JM; Gaillard WD
[Ad] Endereço:Center for Neuroscience, Children's National Health System, George Washington University, Washington, District of Columbia, U.S.A.
[Ti] Título:Temporal lobe epilepsy and focal cortical dysplasia in children: A tip to find the abnormality.
[So] Source:Epilepsia;58(1):113-122, 2017 Jan.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To demonstrate an association between magnetic resonance imaging (MRI) findings and pathologic characteristics in children who had surgery for medically refractory epilepsy due to focal cortical dysplasia (FCD). METHODS: We retrospectively studied 110 children who had epilepsy surgery. Twenty-seven patients with FCD were included. Thirteen had temporal lobe epilepsy (TLE) and 14 had extra-temporal lobe epilepsy (ETLE). Three patients had associated mesial temporal sclerosis. Preoperative 3T MRIs interleaved with nine controls were blindly re-reviewed and categorized according to signal alteration. Pathologic specimens were classified according to the 2011 International League Against Epilepsy (ILAE) classification and compared to MRI studies. RESULTS: Rates of pathology subtypes differed between TLE and ETLE (χ (3) = 8.57, p = 0.04). FCD type I was more frequent in TLE, whereas FCD type II was more frequent in ETLE. In the TLE group, nine patients had temporal tip abnormalities. They all exhibited gray-white matter blurring with decreased myelination and white matter hyperintense signal. Blurring involved the whole temporal tip, not just the area of dysplasia. These patients were less likely to demonstrate cortical thickening compared to those without temporal tip findings (χ (1) = 9.55, p = 0.002). Three of them had FCD Ib, three had FCD IIa, two had FCD IIIa, and one had FCD IIb; MRI features could not entirely distinguish between FCD subtypes. TLE patients showed more pronounced findings than ETLE on MRI (χ (1) = 11.95, p = 0.003, odds ratio [OR] 18.00). In all cases of FCD, isolated blurring was more likely to be associated with FCD II, whereas blurring with decreased myelination was seen with FCD I (χ (6) = 13.07, p = 0.042). SIGNIFICANCE: Our study described associations between MRI characteristics and pathology in children with FCD and offered a detailed analysis of temporal lobe tip abnormalities and FCD subtypes in children with TLE. These findings may contribute to the presurgical evaluation of patients with refractory epilepsy.
[Mh] Termos MeSH primário: Encéfalo/patologia
Epilepsia do Lobo Temporal/diagnóstico por imagem
Epilepsia do Lobo Temporal/etiologia
Epilepsia/complicações
Malformações do Desenvolvimento Cortical do Grupo I/complicações
[Mh] Termos MeSH secundário: Adolescente
Encéfalo/diagnóstico por imagem
Encéfalo/metabolismo
Criança
Pré-Escolar
Eletroencefalografia
Epilepsia do Lobo Temporal/cirurgia
Feminino
Lateralidade Funcional
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Processamento de Imagem Assistida por Computador
Imagem Tridimensional
Lactente
Imagem por Ressonância Magnética
Masculino
Proteínas de Neurofilamentos/metabolismo
Fosfopiruvato Hidratase/metabolismo
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 0 (Neurofilament Proteins); 108688-71-7 (neurofilament protein H); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161120
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13615


  10 / 94 MEDLINE  
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[PMID]:27707870
[Au] Autor:Cloppenborg T; May TW; Blümcke I; Grewe P; Hopf LJ; Kalbhenn T; Pfäfflin M; Polster T; Schulz R; Woermann FG; Bien CG
[Ad] Endereço:Bethel Epilepsy Centre, Bielefeld, Germany.
[Ti] Título:Trends in epilepsy surgery: stable surgical numbers despite increasing presurgical volumes.
[So] Source:J Neurol Neurosurg Psychiatry;87(12):1322-1329, 2016 Dec.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Despite the success of epilepsy surgery, recent reports suggest a decline in surgical numbers. We tested these trends in our cohort to elucidate potential reasons. PATIENTS AND METHODS: Presurgical, surgical and postsurgical data of all patients undergoing presurgical evaluation in between 1990 and 2013 were retrospectively analysed. Patients were grouped according to the underlying pathology. RESULTS: A total of 3060 patients were presurgically studied, and resective surgery was performed in 66.8% (n=2044) of them: medial temporal sclerosis (MTS): n=675, 33.0%; benign tumour (BT): n=408, 20.0%; and focal cortical dysplasia (FCD): n=284, 13.9%. Of these, 1929 patients (94.4%) had a follow-up of 2 years, and 50.8% were completely seizure free (Engel IA). Seizure freedom rate slightly improved over time. Presurgical evaluations continuously increased, whereas surgical interventions did not. Numbers for MTS, BT and temporal lobe resections decreased since 2009. The number of non-lesional patients and the need for intracranial recordings increased. More evaluated patients did not undergo surgery (more than 50% in 2010-2013) because patients were not suitable (mainly due to missing hypothesis: 4.5% in 1990-1993 up to 21.1% in 2010-2013, total 13.4%) or declined from surgery (maximum 21.0% in 2010-2013, total 10.9%). One potential reason may be that increasingly detailed information on chances and risks were given over time. CONCLUSIONS: The increasing volume of the presurgical programme largely compensates for decreasing numbers of surgically remediable syndromes and a growing rate of informed choice against epilepsy surgery. Although comprehensive diagnostic evaluation is offered to a larger group of epilepsy patients, surgical numbers remain stable.
[Mh] Termos MeSH primário: Epilepsia/epidemiologia
Epilepsia/cirurgia
Procedimentos Neurocirúrgicos/tendências
Procedimentos Neurocirúrgicos/utilização
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Neoplasias Encefálicas/epidemiologia
Neoplasias Encefálicas/cirurgia
Criança
Pré-Escolar
Estudos de Coortes
Estudos Transversais
Epilepsia do Lobo Temporal/epidemiologia
Epilepsia do Lobo Temporal/cirurgia
Feminino
Seguimentos
Alemanha
Seres Humanos
Lactente
Recém-Nascido
Masculino
Malformações do Desenvolvimento Cortical do Grupo I/epidemiologia
Malformações do Desenvolvimento Cortical do Grupo I/cirurgia
Meia-Idade
Avaliação de Resultados (Cuidados de Saúde)
Resultado do Tratamento
Recusa do Paciente ao Tratamento/tendências
Revisão da Utilização de Recursos de Saúde/tendências
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161007
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2016-313831



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