Relevant bibliographies by topics / Generalized Epilepsy

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Academic literature on the topic 'Generalized Epilepsy'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Generalized Epilepsy"

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Sullivan, Joseph E., and Dennis J. Dlugos. "Idiopathic generalized epilepsy." Current Treatment Options in Neurology 6, no. 3 (June 2004): 231–42. http://dx.doi.org/10.1007/s11940-004-0015-6.

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Agashe, Shruti, Gregory Worrell, Jeffrey Britton, Katherine Noe, Anthony Ritaccio, Elaine C. Wirrell, Katherine C. Nickels, Gregory D. Cascino, and David Burkholder. "Cenobamate in Generalized Epilepsy and Combined Generalized and Focal Epilepsy." Neurology: Clinical Practice 13, no. 2 (February 15, 2023): e200133. http://dx.doi.org/10.1212/cpj.0000000000200133.

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Background and ObjectivesCenobamate (CNB) is a United States Food and Drug Administration–approved antiseizure medication (ASM) for focal-onset seizures; however, its potential clinical effectiveness as a broad-spectrum ASM is not established. CNB has a proposed dual mechanism of action with preferential blockade of persistent sodium currents and positive allosteric modulation of the γ-aminobutyric acid-A (GABA-A) receptor. We evaluated the efficacy of CNB in drug refractory patients with genetic generalized epilepsies (GGE) or combined generalized and focal epilepsies (CGFE), including developmental and epileptic encephalopathies.MethodsWe performed a retrospective review and identified the following: cohort 1 (n = 4) with GGE, of which 2 patients had idiopathic generalized epilepsy, and cohort 2 with CGFE (n = 9), of which 4 patients had Lennox-Gastaut syndrome and 1 had Dravet syndrome.ResultsIn cohort 1, all 3 patients with frequent generalized tonic-clonic seizures (GTCs) had a greater than 50% reduction in GTCs. In cohort 2, reduction in both generalized and focal-onset seizures was noted. In these groups together, the mean reduction of all seizure types was 58%, and ≥50% responder rate was 70% (SD = ±34.16, median = 50%). No worsening of generalized-onset seizures occurred in either cohort. Seventy-seven percent of patients experienced side effects, warranting a modification of treatment managed by slower titration, dose reduction of CNB, or discontinuing other ASMs.DiscussionIn our retrospective case series, CNB seems to be an effective ASM for patients with drug-resistant GGE and CGFE. The ongoing CNB trial assessing effectiveness for primary GTCs will provide more data on generalized-onset seizures.Classification of EvidenceThis study provides Class IV evidence that CNB in generalized epilepsy and combined generalized and focal epilepsy reduces seizure frequency.
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Jayaram, Shoba, Modhi Alkhaldi, and Asim Shahid. "The Role and Controversies of Electroencephalogram in Focal versus Generalized Epilepsy." Journal of Pediatric Epilepsy 10, no. 02 (February 19, 2021): 058–64. http://dx.doi.org/10.1055/s-0041-1722869.

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AbstractAs early in 1935, Gibbs et al described electroencephalogram (EEG) features of large slow waves seen in “petit mal” seizures and change in background rhythm to a higher frequency, greater amplitude pattern in “grand mal” seizures. Studies have shown many typical EEG features in focal onset as well as generalized epilepsies.2 3 It is usually easy to delineate focal epilepsy cases when EEG onset of seizures is clear as seen in Benign focal epileptiform discharges of childhood.4 However, it is not uncommon to see cases where epileptiform discharges are not very clear. For example, there can be secondary bilateral synchrony or generalized onset of epileptiform discharges in some cases of focal epilepsy5 and nongeneralized EEG features is cases of generalized epilepsy like absence seizures.6 The awareness of occurrence of focal clinical and EEG features in generalized epilepsy is particularly important to help to select appropriate AEDs and also to avoid inappropriate consideration for epilepsy surgery.7 Lüders et al8 have shown that multiple factors like electroclinical seizure evolution, neuroimaging (both functional and anatomical) have to be analyzed in depth before defining an epileptic syndrome. Here, we are providing few examples of different situations where it is still mysterious to figure out focal onset seizures with secondary generalization versus primary generalized epilepsy.
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Ibrahim Abdullah Mahmood, Ahmed Tahseen Muslim, and Hussein Ghani Kaddoori. "The utility of hematological indices in differentiation between general and focal onset epilepsy." Biomedicine 42, no. 1 (March 5, 2022): 64–71. http://dx.doi.org/10.51248/.v42i1.890.

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Introduction and Aim: Epilepsy is one of the most common neurological disorders with mainly focal and generalized onset types. Discrimination between these types is of paramount importance because the prescription of antiepileptic drugs (AEDs) depends on such decimation. Currently this made mainly upon the medical history of the patient. The aim of the study is to evaluate the role of hematological indices in discrimination between focal and generalize onset epilepsy. Patients and Methods: This cross-sectional study included a total of 100 patients with epilepsy (mean age 21.44±10.5, range 6-52, 67 males and 33 females). Blood samples were collected for the participant and complete blood count (CBC) was performed. Furthermore, serum concentration of K+ and Na+ was determined. Results: There were 38 patients with generalized and 62 patients with focal onset epilepsy. In multivariate initial analysis, each of mean platelet volume (MPV) (odds ratio (OR)= 2.56, 95%CI=1.09-13.22, p= 0.046) and serum Na+ (OR= 3.85, 95%CI=1.13-13.19, p= 0.032) were significantly associated with generalized onset epilepsy. Furthermore, two AEDs: carbamazepine and valproic acid were also independently associated with generalized and local onset epilepsy, respectively. Conclusion: These data indicate the possible utility of MPV in the discrimination between generalized and focal onset epilepsy. However, further studies are required for more reliable conclusions.
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Koepp, M. J. "Juvenile myoclonic epilepsy - a generalized epilepsy syndrome?" Acta Neurologica Scandinavica 112, s181 (December 2005): 57–62. http://dx.doi.org/10.1111/j.1600-0404.2005.00511.x.

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Millichap, J. Gordon. "Idiopathic Generalized Epilepsy Syndromes." Pediatric Neurology Briefs 9, no. 9 (September 1, 1995): 68. http://dx.doi.org/10.15844/pedneurbriefs-9-9-7.

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Pedersen, Mangor, Magdalena Kowalczyk, Amir Omidvarnia, Piero Perucca, Samuel Gooley, Steven Petrou, Ingrid E. Scheffer, Samuel F. Berkovic, and Graeme D. Jackson. "Human GABRG2 generalized epilepsy." Neurology Genetics 5, no. 4 (June 7, 2019): e340. http://dx.doi.org/10.1212/nxg.0000000000000340.

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ObjectiveTo map functional MRI (fMRI) connectivity within and between the somatosensory cortex, putamen, and ventral thalamus in individuals from a family with a GABAergic deficit segregating with febrile seizures and genetic generalized epilepsy.MethodsWe studied 5 adults from a family with early-onset absence epilepsy and/or febrile seizures and a GABAA receptor subunit gamma2 pathogenic variant (GABRG2[R43Q]) vs 5 age-matched controls. We infer differences between participants with the GABRG2 pathogenic variant and controls in resting-state fMRI connectivity within and between the somatosensory cortex, putamen, and ventral thalamus.ResultsWe observed increased fMRI connectivity within the somatosensory cortex and between the putamen and ventral thalamus in all individuals with the GABRG2 pathogenic variant compared with controls. Post hoc analysis showed less pronounced changes in fMRI connectivity within and between the primary visual cortex and precuneus.ConclusionsAlthough our sample size was small, this preliminary study suggests that individuals with a GABRG2 pathogenic variant, raising risk of febrile seizures and generalized epilepsy, display underlying increased functional connectivity both within the somatosensory cortex and in striatothalamic networks. This human network model aligns with rodent research and should be further validated in larger cohorts, including other individuals with generalized epilepsy with and without known GABA pathogenic variants.
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Fujikawa, D. G. "Generalized Epilepsy: Neurobiological Approaches." Neurology 42, no. 6 (June 1, 1992): 1261. http://dx.doi.org/10.1212/wnl.42.6.1261-b.

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Dugan, P., C. Carlson, J. Bluvstein, D. J. Chong, D. Friedman, and H. E. Kirsch. "Auras in generalized epilepsy." Neurology 83, no. 16 (September 17, 2014): 1444–49. http://dx.doi.org/10.1212/wnl.0000000000000877.

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Avoli, M. "Feline generalized penicillin epilepsy." Italian Journal of Neurological Sciences 16, no. 1-2 (March 1995): 79–82. http://dx.doi.org/10.1007/bf02229078.

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Dissertations / Theses on the topic "Generalized Epilepsy"

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Oliveira, Elton Pallone de. "Estudo crítico dos modelos experimentais em epilepsia espontânea do tipo ausência." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-24052011-135103/.

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A epilepsia é uma das afecções neurológica mais comum na população mundial. Trata-se de uma condição crônica altamente incapacitante que acomete indivíduos de ambos os sexos e de todas as faixas etárias, com um discreto predomínio em homens e, maior freqüência em crianças abaixo de dois anos e idosos acima de 65 anos. As conseqüências de morbidade e mortalidade desta patologia repercutem negativamente na sociedade e, conseqüentemente na economia global. Estima-se que de 60 a 100 milhões de pessoas ao redor do mundo apresentaram alguma condição epiléptica durante suas vidas. Segundo alguns autores a incidência da epilepsia varia de 11 a 131/100 mil habitantes por ano e a prevalência de 1,5 a 30/1000 habitantes por ano, sendo que os maiores valores encontram-se nos países em desenvolvimento, particularmente na America Latina e na África. As epilepsias generalizadas idiopáticas (EGI) constituem-se cerca de um terço de todas as formas de epilepsias e são 15 a 20% mais freqüentes em relação aos demais tipos de epilepsia. As EGI do tipo ausência, as quais são estritamente relacionadas à faixa etária infantil e adolescente podem muitas vezes (2,8 5,7% dos casos) afetar pacientes com idade superior a 15 anos. A fisiopatologia, assim como, as causas reais da ocorrência e/ou recorrência das crises de ausência na idade adulta não estão completamente esclarecidos e se representam um importante desafio para os epileptologistas. As epilepsias generalizadas idiopáticas (EGIs), (etiologia genética) são classificadas em: a) crises de ausência típicas, b) crises de ausência atípicas, c) crises de ausência com fatores especiais, d) crises mioclônicas, e) crises mioclônicas atônicas, f) crises mioclônicas tônicas, g) crises clônicas, h) crises tônicas e, i) crises atônicas. O tratamento e comumente farmacológico e as crises são controladas na maioria dos casos, no entanto, cerca de um terço dos pacientes são refratários às drogas anticonvulsivantes. Tendo como principal finalidade a elucidação de mecanismos básicos e, auxílio no desenvolvimento de abordagens terapêuticas eficazes para esses pacientes, pesquisadores do mundo inteiro dedicam muitos esforços para o desenvolvimento de modelos experimentais capazes de mimetizar o fenômeno que se pretende reproduzir. Dentre os principais modelos experimentais em EGIs, pode-se citar: (1) o modelo de epilepsia generalizada induzida por penicilina em gatos; (2) modelos de investigação da bicuculina; (3) indução por estimulação elétrica; (4) ratos geneticamente epilépticos de Strasbourg (GAERS); (5) cepa WAG/Rij; (6) modelo do gama-hidroxibutirato (GHB) e (7) os camundongos mutantes. Tais modelos experimentais têm provido meios para que os pesquisadores possam avaliar e quantificar adequadamente as alterações neuronais que ocorrem durante os processos epileptógenos tanto in vitro ou in vivo, possibilitando importantes avanços no desenvolvimento de novas abordagens terapêuticas e, melhora na qualidade de vida de portadores de epilepsia
Epilepsy is a very commom neurological disorders in world population. It is a chronicle condition highly disabling that affects both genera male and female independent of your age with a soft predominance in men and is more frequent in child under 2 years old and adult above 65 years old. The morbidity and mortality consequences of this disorder have many negative repercussions at society and global economy consequently. It is estimated about 60 to 100 millions of people around the world present any epileptic condition during their lives. According some researchers the epilepsy incidence varies about 11 to 131/100 thousand habitants for year and the prevalence between 1.5 to 30/1000 habitants for year, about this statics the higher values are found in developing countries, Latin America and Africa particularly. The Idiopathic Generalized Epilepsy (IGE) are about a third of all others kinds of epilepsies and are 15 to 20% more frequent tha n others types of epilepsies. The absences IGEs are strictly related with childhood and adolescence age group and sometimes can affect patients (2.8 5.7 of cases) with age higher than 15 years old. The physiopathology as the real causes of to occur and to reoccur of absences crises in adult age are not completely enlightened and represent a important challenge to epileptlogists. The IGEs (genetic etiology) are classified in: a) typical absence seizures, b) atypical absence seizures, c) absence seizures with special factors, d) mioclonics seizures, f) tonic mioclonic seizures, g) clone seizures, h) tonic seizures and i) atonic seizures. The treatment commonly is pharmacologic and seizures are controlled in major parts of cases although about a third of patients are refratory to anticonvulsants drugs. Having as principal finality the elucidation of basic mechanisms and help of development of effectiv e therapeutical approaches to these patients, researchers around the world spend many efforts to develop experimental models able to reproduce the phenomena that want to reproduce. Among the principal experimental models of IGEs, it is possible to cite: (1) the general epilepsy model induced by penicillin in cats; (2) the models of investigation of bicuculin; (3) induction by electrical stimulation; (4) Genetic Absence Epilepsy Rats of Strasbourg (GAERS); (5) cepa WAG/Rij; (6) the model of gamma-hydroxybutyric (GHB) and (7) mutant rats. These experimental models have promoted ways to researchers can to evaluate and quantify adequately the neuronal alterations that occur during epileptigenes process both in vitro or in vivo, making possible important advances in development of new therapeutical approaches and improvement in quality of life of epilepsy carriers
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Kay, Benjamin P. "Resting-State Functional Connectivity in Treatment-Resistant Idiopathic Generalized Epilepsy." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1380612937.

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Lin, Katia [UNIFESP]. "Estudo anátomo-funcional por ressonância magnética em pacientes com epilepsia mioclônica juvenil." Universidade Federal de São Paulo (UNIFESP), 2009. http://repositorio.unifesp.br/handle/11600/9493.

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Objetivo: As bases neuroanatômicas e as anormalidades bioquímicas subjacentes à epilepsia mioclônica juvenil (EMJ) não são totalmente conhecidas. Apesar de o tálamo atuar na sincronização de diversas regiões do córtex cerebral durante uma crise, há evidências sugerindo que nem todos os neurônios corticais são afetados de forma homogênea. Compreender a participação destas redes neuronais específicas na EMJ pode esclarecer alguns de seus mecanismos fisiopatológicos. O objetivo deste estudo foi investigar as diferenças metabólicas e estruturais cerebrais entre pacientes com EMJ e controles normais. Métodos: Todos os pacientes possuíam o diagnóstico de EMJ baseado em história e semiologia das crises, eletrencefalografia (EEG), vídeo-EEG e neuroimagem por ressonância magnética (RM) convencional normal, conforme os critérios da Comissão de Classificação e Terminologia da International League Against Epilepsy, 1989. Sessenta pacientes com EMJ foram submetidos a protocolos de espectroscopia de prótons e morfometria baseada em voxels (VBM) por RM de 1,5 T. O grupo controle foi constituído por 30 voluntários saudáveis, pareados por sexo, idade e dominância manual. Este estudo foi realizado após aprovação do comitê de ética da instituição e obtenção de consentimento informado, por escrito, de todos os participantes. Resultados: Demonstrou-se redução da razão de N-acetilaspartato/Creatina (NAA/Cr) dos pacientes com EMJ em relação ao grupo controle nos córtices frontal, pré-frontal e no tálamo. Observou-se diferença na razão do complexo glutamato-glutamina (GLX)/Cr nos córtices frontal, pré-frontal, ínsula, corpo estriado e cíngulo posterior entre os dois grupos. Análise por regressão múltipla nos pacientes com EMJ demonstrou maior correlação funcional entre o tálamo e o córtex pré-frontal. Também foi encontrada correlação negativa entre NAA/Cr e a duração da epilepsia. Análise estrutural quantitativa por VBM demonstrou redução do volume da substância cinzenta no tálamo, ínsula e cerebelo bilateralmente e aumento do volume do córtex frontal nos pacientes. Conclusões: O comprometimento de algumas regiões cerebrais nestes pacientes sugere envolvimento de um circuito tálamo-cortical específico na fisiopatologia desta síndrome, considerada “generalizada”. Reduções em NAA podem representar perda ou lesão de neurônios ou axônios bem como disfunções metabólicas, enquanto o GLX é considerado um neurotransmissor excitatório, envolvido na patogênese das crises epilépticas. As anormalidades estruturais encontradas reforçam a existência de uma rede ictogênica anátomo-funcional específica na EMJ e o conceito de ‘system epilepsies’.
Purpose: The neuroanatomical basis and the neurochemical abnormalities that underlie juvenile myoclonic epilepsy (JME) are not fully understood. While the thalamus plays a central role in synchronization of widespread regions of the cerebral cortex during a seizure, emerging evidence suggests that all cortical neurons may not be homogeneously involved. The purpose of this study was to investigate the cerebral metabolic and structural differences between JME patients and normal controls. Methods: All patients had a JME diagnosis based on seizure history and semiology, EEG recording, normal magnetic resonance neuroimaging (MRI) and video-EEG according to the Commission on Classification and Terminology of the International League Against Epilepsy, 1989. Sixty JME patients (JME-P) were submitted to 1.5 T MRI multi-voxel proton spectroscopy and voxel-based morphometry (VBM). The control group consisted of 30 age and sex-matched healthy volunteers. The Institutional Ethics Committee approved the study, and informed consent was obtained from all participants. Results: Group analysis demonstrated lower N-acetyl-aspartate/Creatine (NAA/Cr) ratio among patients compared to controls on prefrontal, frontal cortices and thalamus. Patients had a statistically significant difference in glutamate-glutamine complex (GLX)/Cr on prefrontal and frontal cortices, insula, striatum and posterior cingulate gyrus. When evaluating the relationship among the various components of this epileptic network among JME-P, the strongest correlation occurred between thalamus and prefrontal cortex and a significant negative correlation between NAA/Cr and duration of epilepsy was found. Also, VBM demonstrated significantly reduced gray matter volume (GMV) in thalami, insula cortices and cerebellar hemispheres bilaterally; while significantly increased GMV was observed in right superior frontal, orbitofrontal and medial frontal gyri among JME-P when compared to controls. Conclusions: The identification of a specific network of neurochemical dysfunction and slight structural abnormalities in patients with JME, with diverse involvement of particular structures within the thalamocortical circuitry, suggests that cortical hyperexcitability in JME is not necessarily diffuse, supporting the knowledge that the focal/generalized distinction of epileptogenesis should be reconsidered and reinforcing the concept of ‘system epilepsies’.
TEDE
BV UNIFESP: Teses e dissertações
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Porter, Joanne. "An investigation into the implicaitons of emotional intelligence for psychosocial problems in temporal lobe epilepsy and idiopathic generalized epilepsy." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500146.

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Betting, Luiz Eduardo Gomes Garcia. "Epilepsia generalizada idiopatica : aspectos etnicos, eletroencefalograficos e de neuroimagem l." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309309.

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Orientadores: Fernando Cendes, Li Li Min
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: Epilepsias generalizadas idiopáticas (EGI) constituem de 20-40% das epilepsias e de forma oposta às epilepsias parciais, anormalidades estruturais não são esperadas. De acordo com a idade de início e o tipo principal de crise, as EGI são divididas principalmente em epilepsia ausência infantil e juvenil (EA), epilepsia mioclônica juvenil (EMJ) e epilepsia com crises tônico-clônicas generalizadas (CTCG). Os limites entre estas subsíndromes são imprecisos e a classificação muitas vezes é difícil. Devido às características semelhantes, alguns autores consideram a EGI como uma única patologia com múltiplos fenótipos (continuum biológico). O eletroencefalograma (EEG) auxilia no diagnóstico das EGI especialmente quando evidencia descargas do tipo espícula onda-lenta generalizadas com atividade de base normal. Entretanto, o EEG pode ser normal e até mesmo mostrar focalidades dificultando o diagnóstico. A ressonância magnética (RM) não é realizada de forma rotineira em pacientes com EGI. Contudo, novas técnicas de aquisição e processamento de imagens vêm detectando anormalidades sutis nestes indivíduos. O objetivo deste estudo foi investigar a fisiopatologia das EGI através da análise de características clínicas, eletroencefalográficas e de neuroimagem. Inicialmente, as características dos EEGs de 180 pacientes com diagnóstico clínico de EGI foram avaliadas. 493 exames foram analisados. Em 33% dos pacientes o EEG inicial foi característico e em 22% o exame evidenciou focalidades. Após a identificação de focalidades utilizamos a neuroimagem convencional (análise visual) na avaliação de 134 pacientes com EGI. Observamos anormalidades na RM de 27 (20%) pacientes. A maioria das anormalidades não apresentou relação direta com as crises. Utilizamos a técnica da morfometria baseada em voxel (MBV) para investigar lesões discretas eventualmente não identificadas na neuroimagem de rotina. Esta técnica permite a comparação entre grupos de imagens aumentando a chance de detecção de anormalidades. Observamos aumento na concentração de substância cinzenta (CSC) localizada no córtex frontal de pacientes com EMJ (n=44) e EA (n=24). Observamos também uma maior CSC na região anterior do tálamo nos pacientes com crises de ausência (n=47). Avaliando as focalidades clínicas e de EEG de 22 pacientes com EGI utilizando a MBV, observamos áreas de aumento da CSC em 8 dos 9 (89%) pacientes com EMJ, 5 dos 6 (83%) pacientes com EA e 5 dos 7 (71%) pacientes com CTCG ao despertar. A volumetria do tálamo foi realizada para investigar o aumento de CSC sugerido pela MBV. A comparação entre 147 pacientes e um grupo controle evidenciou um maior volume da região anterior do tálamo nos pacientes com crises de ausência. Nossos resultados revelam que a fisiopatologia das EGI envolve o tálamo e o córtex cerebral. As diversas alterações na neuroimagem quantitativa apresentadas por cada subsíndrome sugerem um diferente mecanismo para as EGI. Este achado fortalece o conceito de diferentes doenças com fenótipos semelhantes. Mais do que isso, nossos achados indicam, uma alteração estrutural no cérebro destes indivíduos. Os diversos fenótipos estão relacionados a diferentes mecanismos fisiopatológicos. As focalidades observadas no EEG e na RM refletem a patogênese das crises em pacientes com EGI
Abstract: Idiopathic generalized epilepsies (IGE) represent 20-40% of all epilepsies and opposed to partial epilepsies, structural abnormalities are not expected. According to the age of onset and the main seizure type, IGE are divided mainly in childhood and juvenile absence epilepsy (AE), juvenile myoclonic epilepsy (JME) and generalized tonic-clonic seizures (GTCS). The limits between these subsyndromes are unclear and sometimes classification is difficult. Because of the similar characteristics, some authors consider IGE as a single pathology with multiple phenotypes (biological continuum). Electroencephalogram (EEG) helps the IGE diagnosis specially when it shows the generalized spike and wave discharges with normal background. However, the EEG may be normal or even disclose focalities difficulting the diagnosis. Magnetic resonance imaging (MRI) is not routinely performed in patients with IGE. In spite of this, new techniques of acquisition and processing of the images are detecting subtle abnormalities in these individuals. The objective of this study was to investigate the pathophysiology of the IGE using the clinical, EEG and neuroimaging features. Initially, the characteristics of the EEGs of 180 patients with clinical diagnosis of IGE were evaluated. 493 exams were analyzed. In 33% of the patients the initial EEG was characteristic and in 22% the exam revealed focalities. After the identification of the focalities, we used conventional neuroimaging (visual analysis) on the evaluation of 134 patients with IGE. We observed abnormalities in the MRI of 27 (20%) patients. Most of the abnormalities were not directly related to the seizures. We used the voxel base morphometry (VBM) technique to evaluate the images. This technique allows comparisons between groups of images increasing the chances of detecting abnormalities. We observed increased gray matter concentration (GMC) localized in the frontal cortex of patients with JME (n=44) and AE (n=24). We also observed increased GMC in the anterior thalamic region of patients with absence seizures (n=47). Evaluating the clinical and EEG focalities of 22 patients with IGE using VBM, we observed areas of increased GMC in 8 of 9 (89%) patients with JME, 5 of 6 (83%) patients with AE and 5 of 7 (71%) patients with GTCS on awakening. The volumetry of the thalamus was performed to investigate the increased GMC suggested by the VBM. The comparison between 147 patients with a control group showed increased volume of the anterior thalamic region in patients with absence seizures. Our results revealed that the pathophysiology of the IGE involves the thalamus and the cerebral cortex. The several abnormalities on the neuroimage presented by each subsyndrome suggest a different mechanism for the IGE. This finding strengths the concept of multiple diseases with similar phenotypes. Furthermore, our findings indicate a structural abnormality in the brain of these individuals. The several phenotypes are related with different pathophysiological mechanisms. The focalities present on the EEG and in the MRI reflect the pathogenesis of the seizures in patients with IGE
Doutorado
Neurociencias
Doutor em Fisiopatologia Medica
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Eroglu, Ezgi. "Association Between Gamma Aminobutyric Acid (gaba) Type B Receptors Gene Polymorphisms And Idiopathic Generalized Epilepsy." Master's thesis, METU, 2012. http://etd.lib.metu.edu.tr/upload/12614056/index.pdf.

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Epilepsy is neurological disorder affecting 0.5 to 1% of the population all around the world. It is characterized by the seizures, which are the sudden alterations of behavior due to a temporary change in electrical functioning of the brain. Idiopathic generalized epilepsy (IGE) accounts for one-fifth of all the other epilepsy types, and several gene mutations were identified as the causes of IGE. In general, voltage-gated and ligand-gated ion channel mutations are linked with seizure formation. Gamma amino butyric acid (GABA), the most important inhibitory neurotransmitter of the central nervous system, and its receptors are commonly mentioned in the pathophysiology of epilepsies. Decrease in the inhibitory effect of GABA in neurons causes epileptic discharges resulting in seizure development. The study population consisted of a total of 176 idiopathic generalized epilepsy (IGE) patients, 83 subjects having psychogenic non-epileptic seizures (PNES), 86 non-epileptic control subjects from Turkey. Total blood samples were obtained from Gü
lhane Military Medical Academy Hospital Neurology Department, Ankara. There was no statistically difference between the patient and control groups in terms of age. Genomic DNA isolations were performed and genotyping of G1465A and C59T polymorphisms of GABAB1 gene
rs1999501, rs967932, rs3780428 and rs944688 polymorphisms of GABAB2 gene were determined by PCR-RFLP technique. In this study, GABAB1 G1465A polymorphic allele was not observed in Turkish population. For GABAB1 C59T polymorphism, polymorphic allele frequencies were found as 0.097 in IGE patients
0.072 in PNES subjects and 0.105 in non-epileptic control subjects. No significant difference is identified for C59T polymorphism in all three groups. Four SNPs of GABAB2 were studied
rs967932 was found to increase the risk of IGE 3.6-fold (P=0.031) compared to PNES subjects, polymorphic allele frequencies were found as 0.060 in IGE patients
0.018 in PNES subjects and 0.035 in non-epileptic control subjects. For rs1999501 polymorphism, polymorphic allele frequencies were found as 0.077 in IGE patients
0.048 in PNES subjects and 0.093 in non-epileptic control subjects. For rs3780428 polymorphism, polymorphic allele frequencies were found as 0.267 in IGE patients
0.235 in PNES subjects and 0.256 in non-epileptic control subjects. For rs944688 polymorphism, polymorphic allele frequencies were found as 0.196 in IGE patients
0.260 in PNES subjects and 0.227 in non-epileptic control subjects. No significant difference was identified for rs1999501, rs3780428 and rs944688 polymorphisms among IGE patients, PNES subjects and non-epileptic control groups. IGE risk was 6.54-fold higher for subjects having combined GA genotype for rs967932 and GG genotype for rs3780428 when compared with PNES subjects (P=0.042). The combination of CC genotype for rs1999501, GG genotype for rs967932 and TT genotype for rs944688 had around 9-fold protective effect against IGE when both compared with PNES subjects (P=0.038) and non-epileptic control subjects (P=0.041).
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Eriksson, Ann-Sofie. "A pharmacokinetic and pharmacodynamic study of an antiepileptic drug (lamotrigine) in young patients with drug-resistant generalized epilepsy /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4205-6/.

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Tian, Nan. "SLEEP-RELATED GENERALIZED TONIC SEIZURE AND HIGH FREQUENCY OSCILLATION (HFOs) IN A MESIAL TEMPORAL LOBE EPILEPSY MOUSE MODEL." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1277440218.

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Coco, S. "SCREENING DEI GENI ¿PACEMAKER¿ IN PAZIENTI CON EPILESSIA IDIOPATICA GENERALIZZATA: IDENTIFICAZIONE DI UNA MUTAZIONE RECESSIVA NEL CANALE HHCN2." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/169153.

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It is well established that several forms of inheritable idiopathic epilepsy sindrome are ion channelopathies, that is pathologies associated with dysfunctional ion channels, even if the functional link between channel dysfunction and clinical phenotype is often unresolved. Hyperpolarization-activated, Cyclic-Nucleotide gated (HCN) channels are a class of voltage- and cAMP-dependent channels. They mediate the hyperpolarization-activated Ih current, which control synaptic integration and intrinsic excitability in various brain areas. Ih is pathologically altered after experimentally-induced seizures and has been proposed to have a role in different forms of epileptogenesis. Hcn1 and Hcn2 genes variants have been identified in patients with febrile seizure or GEFS+. While existing data therefore clearly show a link between HCN channel dysfunction and epileptogenesis, no specific mutation-induced HCN channel modification has so far been correlated functionally with increased neuronal excitability. To investigate this we used a candidate gene approach and screened a panel of idiopathic generalized epilepsy patients and related families for mutations in the Hcn1 and Hcn2 genes. We found a form of sporadic IGE associated with a recessive point mutation in the gene coding for the HCN2 channel. The protein mutation E515K is located in the C-linker region (exon 5 of the Hcn2 gene). Functional analysis revealed that homomeric mutant, but not heteromeric wild-type/E515K channels, have a negative shift in the activation kinetics. Furthermore, the time-constant curve for homomeric E515K channels was also shifted to the negative direction. Moreover, omomeric mutant, but not heteromeric wild type/mutant channels, showed a lowering of the threshold of action potential firing and a strongly increased cell excitability and firing frequency when compared to wild-type channels. In conclusion, our results show that the homozygous E515K mutation in human HCN2 channels is a loss-of-function mutation causing a large negative shift of the activation curve and slowing of activation, and a consequent strong reduction of Ih availability near resting voltages. These changes cause a substantial increase of neuronal excitability, a condition predisposing to epileptogenesis, and are associated with a recessive type of inheritance compatible with the idiopathic generalized epilepsy of the proband in the family pedigree.
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Braga, Aline Marques da Silva [UNESP]. "Análise quantitativa das descargas epileptiformes generalizadas e da neuroimagem de pacientes com epilepsia generalizada idiopática." Universidade Estadual Paulista (UNESP), 2016. http://hdl.handle.net/11449/138325.

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Fundação de Amparo à Pesquisa do Estado de Mato Grosso (FAPEMAT)
Fundamento: Evidências experimentais de modelos animais de crises de ausência sugerem focalidades no início das descargas generalizadas. Estudos clínicos indicam que pacientes com o diagnóstico de epilepsia generalizada idiopática (EGI) exibem anormalidades focais que envolvem o circuito tálamo-cortical no eletroencefalograma (EEG) e na neuroimagem. Objetivos: Investigar a presença de características focais nas descargas generalizadas interictais usando análise quantitativa do EEG (EEGq) e avaliar o córtex do giro do cíngulo usando múltiplas abordagens quantitativas de neuroimagem. Métodos: 75 EEGs de 64 pacientes foram analisados. A primeira espícula generalizada inequívoca foi marcada para cada descarga. Três métodos de análise de fonte geradora da atividade observada foram aplicados: transformação do dipolo em imagem (dipole source imaging-DSI), abordagem LORETA aplicada iterativamente (CLARA), e análise de dipolo equivalente de componentes independentes com análise de agrupamentos. Após processamento do EEG, 32 pacientes (18 mulheres, 32 ± 11) fizeram ressonância magnética. Foram utilizados três métodos para comparar o giro do cíngulo de pacientes e controles: morfometria baseada em voxel (VBM), análise cortical e análise de formato. Resultados: 753 descargas generalizadas foram analisadas. Usando as três técnicas, o lobo frontal foi a principal fonte das descargas (70%), seguido pelos lobos parietal e occipital (14%) e, por fim, os núcleos da base (12%). As principais fontes anatômicas das descargas generalizadas foram o córtex da porção anterior do giro do cíngulo (36%) e giro frontal medial (23%). A VBM mostrou atrofia de substância cinzenta na porção anterior do giro do cíngulo (972 mm3) e no istmo (168 mm3). Análises individuais do córtex do giro do cíngulo mostraram resultados semelhantes. Comparações de superfície mostraram anormalidades principalmente na porção posterior do giro do cíngulo (718.12 mm2). A análise de formato demonstrou uma predominância de anormalidades nas porções anterior e posterior do giro do cíngulo. Discussão: A análise de fonte não mostrou uma fonte única comum a todas as descargas generalizadas mas indicou predominância do giro do cíngulo e lobo frontal. Além disso, o estudo sugere a existência de anormalidades estruturais sutis no giro do cíngulo, principalmente nas porções anterior e posterior.
Background: Experimental evidence from animal models of absence seizures suggests a focal source for the initiation of generalized spike-and-wave (GSW) discharges. Clinical studies indicate that patients diagnosed with idiopathic generalized epilepsy (IGE) exhibit focal electroencephalographic and subtle structural abnormalities, which involve the thalamo-cortical circuitry. Aims: The objectives of the current investigation were to investigate whether interictal generalized discharges exhibit focal characteristics using qEEG analysis and to perform a comprehensive analysis of the cingulate cortex using multiple quantitative structural neuroimaging techniques. Methods: 75 EEG recordings from 64 patients were analyzed. The first unequivocally confirmed generalized spike was marked for each discharge. Three methods of source imaging analysis were applied: dipole source imaging (DSI), classical LORETA analysis recursively applied (CLARA), and equivalent dipole of independent components with cluster analysis. After EEG analysis, 32 patients (18 women, 30± 10 years) and 36 controls (18 women, 32 ±11 years) were imaged by 3 Tesla magnetic resonance (MRI). We used three models to compare cingulate gyrus of patients and the control group: voxel-based morphometry (VBM), cortical analyses and shape analyses. Results: A total of 753 GSW discharges were spatiotemporally analyzed. Source analysis using all three techniques revealed that the frontal lobe was the principal source of GSW discharges (70%), followed by the parietal and occipital lobes (14%), and the basal ganglia (12%). The main anatomical sources of the generalized discharges were the anterior cingulate cortex (36%) and the medial frontal gyrus (23%). VBM analyses of cingulate gyrus showed areas of gray matter atrophy, mainly in the anterior cingulate gyrus (972 mm3) and the isthmus (168 mm3). Individual analyses of the cingulate cortex were similar between patients with IGE and controls. Surface- based comparisons revealed abnormalities located mainly in the posterior cingulate cortex (718.12 mm2). Shape analyses demonstrated a predominance of abnormalities in the anterior and posterior portions of cingulate gyrus abnormalities. Discussion: Source analysis did not reveal a common focal source of generalized discharges. However, there was a predominance of GSW discharges originating from the cingulate gyrus and the frontal lobe. Furthermore, this study suggests that patients with IGE have structural abnormalities in the cingulate gyrus mainly localized at the anterior and posterior portions. This finding is subtle and variable among patients.
FAPEMAT: 11/16452-2
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Books on the topic "Generalized Epilepsy"

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Avoli, Massimo, Pierre Gloor, George Kostopoulos, and Robert Naquet, eds. Generalized Epilepsy. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3.

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Massimo, Avoli, ed. Generalized epilepsy: Neurobiological approaches. Boston: Birkhäuser, 1990.

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1951-, Marescaux C., Vergnes M. 1935-, and Bernasconi R. 1929-, eds. Generalized non convulsive epilepsy: Focus on GABA-B receptors. Wien: Springer-Verlag, 1992.

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R, Degen, and Dreifuss Fritz E, eds. Benign localized and generalized epilepsies of early childhood. Amsterdam: Elsevier, 1992.

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Alain, Malafosse, ed. Idiopathic generalized epilepsies: Clinical, experimental and genetic aspects. London: John Libbey, 1994.

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Marescaux, C., M. Vergnes, and R. Bernasconi, eds. Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors. Vienna: Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-9206-1.

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S, Duncan J., and Panayotopoulos C. P, eds. Eyelid myoclonia with absences. London: John Libbey, 1996.

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Moeller, Friederike, Ronit M. Pressler, and J. Helen Cross. Genetic generalized epilepsy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0027.

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This chapter provides an overview of generalized epilepsies (GGE), which comprises a group of epilepsy syndromes of presumed genetic origin. They are classified into several syndromes according to their age, depending on clinical manifestation and associated electroencephalogram (EEG) features. The chapter introduces the concept of GGE before addressing different GGE syndromes, describing their clinical presentation, EEG features, treatment, prognosis, and underlying genetics. The following GGE syndromes are discussed in order of their age of onset—myoclonic astatic epilepsy, childhood absence epilepsy, epilepsy with myoclonic absences, eyelid myoclonia with absences, juvenile absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with generalized tonic seizures on awakening. This is followed by an overview on pathophysiological mechanisms underlying GGE.
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Avoli. Generalized Epilepsy: Neurobiological Approaches. Springer, 2012.

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AVOLI. Generalized Epilepsy: Neurobiological Approaches. Birkhauser Verlag, 2012.

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Book chapters on the topic "Generalized Epilepsy"

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Jasper, H. H. "Historical Introduction." In Generalized Epilepsy, 1–15. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_1.

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Brailowsky, S., C. Silva-Barrat, Ch Ménini, D. Riche, and R. Naquet. "Anticonvulsant Effects of Intracortical Chronic Infusion of GABA in Generalized Epilepsy." In Generalized Epilepsy, 126–36. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_10.

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Kostopoulos, G., and C. Psarropoulou. "In Vitro Electrophysiology of a Genetic Model of Generalized Epilepsy." In Generalized Epilepsy, 137–57. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_11.

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Steriade, M. "Spindling, Incremental Thalamocortical Responses, and Spike-Wave Epilepsy." In Generalized Epilepsy, 161–80. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_12.

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Huguenard, J. R., D. A. Coulter, and D. A. Prince. "Physiology of Thalamic Relay Neurons: Properties of Calcium Currents Involved in Burst-Firing." In Generalized Epilepsy, 181–89. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_13.

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Gloor, P., M. Avoli, and G. Kostopoulos. "Thalamocortical Relationships in Generalized Epilepsy with Bilaterally Synchronous Spike-and-Wave Discharge." In Generalized Epilepsy, 190–212. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_14.

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Avoli, M., P. Gloor, and G. Kostopoulos. "Focal and Generalized Epileptiform Activity in the Cortex: In Search of Differences in Synaptic Mechanisms, Ionic Movements, and Long-Lasting Changes in Neuronal Excitability." In Generalized Epilepsy, 213–31. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_15.

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Fariello, R. G. "Pharmacology of the Inhibitory Systems in Primary Generalized Epilepsy of “Petit Mal” Type." In Generalized Epilepsy, 232–37. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_16.

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Vergnes, M., Ch Marescaux, A. Depaulis, G. Micheletti, and J. M. Warter. "Spontaneous Spike-and-Wave Discharges in Wistar Rats: A Model of Genetic Generalized Nonconvulsive Epilepsy." In Generalized Epilepsy, 238–53. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_17.

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Mirsky, A. F., and C. C. Duncan. "Behavioral and Electrophysiological Studies of Absence Epilepsy." In Generalized Epilepsy, 254–69. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3_18.

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Conference papers on the topic "Generalized Epilepsy"

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Santos, Maria do Carmo Vasconcelos, Mariana Moreira Soares de Sa, Emanuelle Ferreira Barreto, Aline Cursio Moraes, Roberta Kelly Netto Vinte Guimarães, and Antonio Pereira Gomes Neto. "Progressive myoclonic epilepsy: case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.688.

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Context: Progressive myoclonic epilepsy (PMS) begins in childhood or during adolescence, being a heterogeneous group of symptomatic progressive progressive generalized epilepsy. Composed of cortical myoclonus, multiple epileptic seizures, delayed or regressed neuropsychomotor development and cerebellar manifestations. Genetics is heterogeneous with a similar clinical presentation, which makes etiological definition difficult. Report a clinical case of generalized epilepsy, myoclonus, cerebellar condition and severe mental impairment. Analysis of medical records of a patient at Santa Casa de Belo Horizonte. Case report: MVPP, 17 years old, previously healthy, adopted son, normal neuropsychomotor development, first generalized tonic-clonic seizure at 8 years old, recurrence at 12 years old, being initiated by Valproato and Clobazam. In 2018 there was a worsening of the crises, perceived myoclonus, added Lamotrigine and Oxcarbazepine. EEG with continuous diffuse epileptic activity of subclinical epilepticus status and unchanged skull MRI. In 2019 he started with gait ataxia, balance changes, dysarthria, dysmetria, cognitive decline, loss of functionality and refractoriness to treatment. Valproate reduced and oxcarbazepine suspended. Video- EEG with ictal pattern of generalized wave polyspicle. Deteriorated cerebellar condition with extensive propaedeutic without alterations. There was no feasibility of genetic testing at the time. Methylprednisolone pulse therapy with partial improvement. Unsuccessful attempt to levetiracetam due to psychotic symptom. He presented lowering of the sensorium, bronchoaspiration and orotracheal intubation. He evolved with myoclonic status, adjusted for anti-crisis drugs, midazolam, thiopental, tracheostomy and gastrostomy. He maintained super- refractory status, being opted for callosotomy. He died within weeks of the procedure. Conclusion: The early diagnosis of PMS is a challenge, and its evolution is usually debilitating, with a poor prognosis and scarce specific treatment. Whenever possible, a genetic study is needed to define an etiological diagnosis.
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Kaibara, Felipe, Iscia Cendes, and Rodrigo Secolin. "Analysis of candidate SNPs in patients with genetic generalized epilepsy." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720191863.

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Luo, Cheng, De-zhong Yao, Dong Zhou, and Qi-yong Gong. "Altered intrinsic functional organization of the brain in idiopathic generalized epilepsy." In ICBEM). IEEE, 2011. http://dx.doi.org/10.1109/nfsi.2011.5936820.

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Soares, Mariana, Ana Clara Mota Gonçalo, Kaline dos Santos Kishishita Castro, and Victoria de Menezes Sá Lazera. "Use of cannabidiol as a therapeutic method in epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.388.

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Introduction: Cannabis sativa has several therapeutic properties and has been used for millennials for healing purposes. Among its benefits are analgesic, antiemetic and tranquilizing effects, acting strongly on the nervous system. Objective: This study aims to emphasize the importance of Cannabidiol as a therapeutic purpose for epilepsy, especially in Brazil, where its use is still controlled. Method: A systematic literature review, using bibliographic searches carried out in the electronic databases LILACS, PubMed and SciELO with the descriptors “cannabidiol” and “epilepsy”. Of 1645 searches found, 06 were used in the study. Results: Epileptic seizures can be generalized or partial and are determined by the affected area. The treatment for epilepsy are drugs that decrease the arousal capacity of neural tissue and a significant percentage of individuals cannot control them with traditional drugs alone. Endocannabinoids work in response to epileptiform activity, to activate CB1 receptors for excitatory neurons, to contain excess neuronal activity, which occurs during seizures. It is proven that patients who use it do not have toxic adverse effects. Conclusions: In Brazil, Cannabis is a controlled drug and the fact that it is imported, interfere in the treatment, who is interrupted while patient waits the new dosage. The importance of cannabidiol as a target for research and studies is verified, as it has ample potential in the treatment of epilepsy and reduces brain damage caused by it. In order that patients with epilepsy, have improvements in their quality of life.
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Ke, Ming, Xiaoxin Duan, Fan Zhang, and Xiaoping Yang. "The research of the generalized tonic-clonic seizure epilepsy by resting state Fmri." In First International Conference on Information Sciences, Machinery, Materials and Energy. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/icismme-15.2015.346.

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Krug, Dieter, Anton Chernihovskyi, Hannes Osterhage, Christian Elger, and Klaus Lehnertz. "Estimating Generalized Synchronization in Brain Electrical Activity from Epilepsy Patients with Cellular Nonlinear Networks." In 2006 10th International Workshop on Cellular Neural Networks and Their Applications. IEEE, 2006. http://dx.doi.org/10.1109/cnna.2006.341606.

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Prabhakar, Sunil Kumar, and Harikumar Rajaguru. "Cascaded feed forward neural networks and generalized regression for epilepsy risk level classification — A study." In 2016 3rd MEC International Conference on Big Data and Smart City (ICBDSC). IEEE, 2016. http://dx.doi.org/10.1109/icbdsc.2016.7460358.

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Shunan, Li, Li Donghui, Deng Bin, Wei Xile, Wang Jiang, and Wai-Loc Chan. "A novel feature extraction method for epilepsy EEG signals based on robust generalized synchrony analysis." In 2013 25th Chinese Control and Decision Conference (CCDC). IEEE, 2013. http://dx.doi.org/10.1109/ccdc.2013.6561869.

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Milleret-Pignot, C., E. Panagiotakaki, J. De Bellescize, J. Toulouse, I. Sabatier, M. Carneiro, C. Ruello, M. Nicolino, and A. Arzimanoglou. "Epilepsy and EEG Patterns in Children Diagnosed with Hyperinsulinism. Report of Two Cases Presented as Atypical Generalized Epilepsy and Review of EEGS of 15 Supplementary Cases." In Abstracts of the 47th Annual Meeting of the SENP (Société Européenne De Neurologie Pédiatrique). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685427.

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Sconzo Polydoro, Marina, CLARISSA LIN YASUDA, DANIELLE S. GARCIA, MARINA ALVIM, and FERNANDO CENDES. "Multimodal evaluation of grey and white matter in patients with generalized epilepsy according to seizure control." In XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-51024.

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Reports on the topic "Generalized Epilepsy"

1

Xin, Wu, and Xue Tao. The efficacy and safety of neuromodulation in refractory epilepsy: a systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0042.

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Review question / Objective: To assess the efficacy and safety of different neuromodulation applied to the refractory epilepsy and provide a better choice for clinical practice. Condition being studied: Epilepsy is a frequent neurologic illness defined by bursts of hypersynchronized neural network activity that afflict about 1% of the global population. Unfortunately, roughly 30% of people with drug-resistant epilepsy (DRE) continue to experience seizures despite three anti-seizure drugs. In most cases, resective surgery, as the first-line treatment for DRE, is considered a curative therapy for achieving long-term seizure-free status, but about half of patients are not candidates for surgery due to a variety of factors such as multiple/diffuse/widespread seizure foci, epileptic foci arising from eloquent, primary generalized epilepsy, or patients unwilling to undergo surgery. Neuromodulation, albeit palliative, is an important alternative treatment for these individuals to prevent or decrease ictal episodes, which can affect the nervous system in a variety of ways.
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