Nocturnal Hypermotor Seizures, Suggesting Frontal Lobe Epilepsy, Can Originate in the Insula

Ryvlin, Philippe; Minotti, Lorella; Demarquay, Geneviève; Hirsch, Édouard; Arzimanoglou, Alexis; Hoffman, Dominique; Guénot, Marc; Picard, Fabienne; Rheims, Sylvain; Kahane, Philippe

doi:10.1111/j.1528-1167.2006.00510.x

Cited by 224 publications

(187 citation statements)

References 41 publications

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“…It may be that upstates that originate in these areas are better able to propagate to other cortical areas and manifest on the scalp. This agrees with the observation that the area around the lateral sulcus is important for the initiation and propagation of seizures in many cases of temporal lobe epilepsy (42,43). Intriguingly, patients with insular strokes report significantly more tiredness than patients with similar strokes that do not involve the insula (44).…”

Section: Origins Propagation and Involvement Each Reveal Novel Infosupporting

confidence: 79%

Source modeling sleep slow waves

Murphy

Riedner

Huber

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

419

387

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Slow waves are the most prominent electroencephalographic (EEG) feature of sleep. These waves arise from the synchronization of slow oscillations in the membrane potentials of millions of neurons. Scalplevel studies have indicated that slow waves are not instantaneous events, but rather they travel across the brain. Previous studies of EEG slow waves were limited by the poor spatial resolution of EEGs and by the difficulty of relating scalp potentials to the activity of the underlying cortex. Here we use high-density EEG (hd-EEG) source modeling to show that individual spontaneous slow waves have distinct cortical origins, propagate uniquely across the cortex, and involve unique subsets of cortical structures. However, when the waves are examined en masse, we find that there are diffuse hot spots of slow wave origins centered on the lateral sulci. Furthermore, slow wave propagation along the anterior؊posterior axis of the brain is largely mediated by a cingulate highway. As a group, slow waves are associated with large currents in the medial frontal gyrus, the middle frontal gyrus, the inferior frontal gyrus, the anterior cingulate, the precuneus, and the posterior cingulate. These areas overlap with the major connectional backbone of the cortex and with many parts of the default network.brain mapping ͉ default network ͉ electroencephalography ͉ slow oscillation ͉ traveling wave

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Section: Origins Propagation and Involvement Each Reveal Novel Infosupporting

confidence: 79%

Source modeling sleep slow waves

Murphy

Riedner

Huber

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

419

387

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“…21 Desde este relato, vários tipos de epilepsias têm sido descritos com origem cortical e etiologias variáveis, as quais se apresentam com crises, exclusiva ou predominantemente, durante o sono. 22,23 Uma série de publicações voltou-se para este ponto sugerindo que alguns tipos de malformações do desenvolvimento cortical, mais especificamente displasia cortical focal tipo II, conforme classificação de Palmini e colaboradores, 12 estão mais associadas a anormalidades epilépticas relacionadas ao sono, não somente em função da refratariedade das crises, como também pela presença dos surtos curtos recorrentes pseudoperiodicamente organizados ocorrendo durante o sono de ondas lentas. 24,25 Esta é uma área ainda incipiente e grupos diferentes relataram resultados diferentes, em consequência à inclusão de casos não homogêneos e provavelmente a questões metodológicas envolvidas.…”

Section: Fisiopatologia E Definições: Sono E Epilepsiaunclassified

“…47,48 EPILEPSIA DESENvOLvIMENTAL E SONO O interesse pelas lesões do desenvolvimento, especialmente as malformações corticais, aumentou nas últimas décadas incentivado pelos avanços em neuroimagem e em biologia molecular, tornando o eixo etiológico mais evidente e sugerindo que ao invés da (ou em adição a) topografia, a etiologia pode estar relacionada à probabilidade de ocorrência de epilepsia relacionada ao sono. 23,24,49 Muitas anormalidades estruturais foram reconhecidas e classificadas e as malformações do desenvolvimento cortical são as que mais se relacionam a crises epilépticas. Elas diferem de outras anormalidades estruturais por possuirem diferentes graus de excitabilidade cortical e potencial para gerar crises clínicas associadas à disfunção motora e cognitiva.…”

Section: Microestrutura Do Sono E Epilepsiasunclassified

Avaliação da arquitetura do sono em crianças com epilepsia refratária

Pereira

Kaemmerer

Palmini

et al. 2011

J. epilepsy clin. neurophysiol.

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RESuMOIntrodução: Há um interesse crescente nas relações entre sono e epilepsia incentivado pela compreensão de que existem interações potencialmente relevantes nas duas direções. Embora o papel do sono na hipersincronização e a crescente preocupação na geração de crises sejam bem conhecidos, o grau no qual o sono pode facilitar ou induzir a um fenômeno epileptogênico, nas epilepsias lesionais, permanece indefinido. As epilepsias lesionais parecem apresentar um mecanismo particular de epileptogenicidade e o esclarecimento do papel da macro e microarquitetura do sono pode auxiliar na antecipação e monitorização de fenômenos epilépticos relacionados ao sono, conforme a etiologia da epilepsia. Objetivo: revisar e discutir as relações entre sono e epilepsia na infância e adolescência relacionando as alterações estruturais do sono à etiologia da epilepsia. Métodos: revisão bibliográfica utilizando o banco de dados Medline, abrangendo os estudos publicados nos últimos quinze anos, com as palavras-chave (unitermos) sono e epilepsia. Conclusões: epilepsia refratária durante a infância parece influenciar a organização do sono principalmente naqueles pacientes com etiologia lesional. A definição do tipo de epilepsia pode ser importante na antecipação dos distúrbios de sono nesta população.unitermos: sono, epilepsia, displasia cortical, padrão cíclico alternante. ABSTRACT Evaluation of sleep architecture in children with refractory epilepsyIntroduction: There has been a growing interest in the relations between sleep and epilepsy, kindled by the realization that there are many potentially relevant two-way interactions. Even though the hyper-synchronizing role of sleep and its attending increase in the probability of seizure generation are well known, the degree to which sleep may facilitate or induce epileptogenic phenomena in lesional epilepsies remains unclear. The lesional epilepsies seems to have intrinsic epileptogenic properties and the knowledge about sleep macro and microarchiteture could help clinician to anticipate and monitor sleep-related epileptic phenomena according to the etiology of the epilepsy Objective: Discuss the relationship between sleep and epilepsy in childhood and adolescence. Methods: Literature review in journals indexed through Medline, from the last 15 years. Conclusion: Refractory epilepsy during childhood influences sleep organization mainly in patients with lesional etiology. The definition of the type of epilepsy is important to anticipate sleep disorders in this population.

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“…Paroxysmal arousals, dystonia-like attacks, and epileptic nocturnal wanderings are also part of the phenotype [120]. Ictal video-EEG studies have revealed partial seizures originating from the frontal lobe, but also from parts of the insula and temporal lobe, suggesting a defect of a broader network [121,122]. A mutation in the gene CHRNA4, encoding the α4-subunit of a neuronal nicotinic acetylcholine receptor (nAchR), was the first ion channel mutation found in an DS Dravet syndrome; ID intellectual disability; IS infantile spasms;…”

Section: Autosomal Dominant Nocturnal Frontal Lobe Epilepsymentioning

confidence: 99%

Genetic Epilepsy Syndromes Without Structural Brain Abnormalities: Clinical Features and Experimental Models

2014

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Research in genetics of epilepsy represents an area of great interest both for clinical purposes and for understanding the basic mechanisms of epilepsy. Most mutations in epilepsies without structural brain abnormalities have been identified in ion channel genes, but an increasing number of genes involved in a diversity of functional and developmental processes are being recognized through whole exome or genome sequencing. Targeted molecular diagnosis is now available for different forms of epilepsy. The identification of epileptogenic mutations in patients before epilepsy onset and the possibility of developing therapeutic strategies tested in experimental models may facilitate experimental approaches that prevent epilepsy or decrease its severity. Functional analysis is essential for better understanding pathogenic mechanisms and gene interactions. In vitro experimental systems are either cells that usually do not express the protein of interest or neurons in primary cultures. In vivo/ex vivo systems are organisms or preparations obtained from them (e.g., brain slices), which should better model the complexity of brain circuits and actual pathophysiological conditions. Neurons differentiated from induced pluripotent stem cells generated from the skin fibroblasts of patients have recently allowed the study of mutations in human neurons having the genetic background of a given patient. However, there is remarkable complexity underlying epileptogenesis in the clinical dimension, as reflected by the fact that experimental models have not provided yet results having clinical translation and that, with a few exceptions concerning rare conditions, no new curative treatment has emerged from any genetic finding in epilepsy.

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Nocturnal Hypermotor Seizures, Suggesting Frontal Lobe Epilepsy, Can Originate in the Insula

Cited by 224 publications

References 41 publications

Source modeling sleep slow waves

Source modeling sleep slow waves

Avaliação da arquitetura do sono em crianças com epilepsia refratária

Genetic Epilepsy Syndromes Without Structural Brain Abnormalities: Clinical Features and Experimental Models

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