Electrocardiography in epilepsy patients without cardiac symptoms

Drake, Miles E.; Reider, Carson; Kay, Amparo

doi:10.1016/s1059-1311(05)80104-9

Cited by 72 publications

(62 citation statements)

References 8 publications

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“…Clinically, it is well established that HERG mutations are responsible for one form of the "long QT" syndrome, an inherited cardiac disorder causing syncope, seizures, and sudden death . In addition, there are several recent reports linking seizure sus- ceptibility to HERG dysfunction or long QT (Drake et al, 1993;Gordon, 1994;Pacia et al, 1994;Yang et al, 1998). Thus, in addition to altered cardiac rhythm, mutated HERG may also affect CNS function by causing hyperexcitability by a mechanism involving astrocytes.…”

Section: Discussionmentioning

confidence: 99%

Do Glia Have Heart? Expression and Functional Role forEther-A-Go-GoCurrents in Hippocampal Astrocytes

et al. 2000

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Potassium homeostasis plays an important role in the control of neuronal excitability, and diminished buffering of extracellular K results in neuronal Hyperexcitability and abnormal synchronization. Astrocytes are the cellular elements primarily involved in this process. Potassium uptake into astrocytes occurs, at least in part, through voltage-dependent channels, but the exact mechanisms involved are not fully understood. Although most glial recordings reveal expression of inward rectifier currents (K IR ), it is not clear how spatial buffering consisting of accumulation and release of potassium may be mediated by exclusively inward potassium fluxes. We hypothesized that a combination of inward and outward rectifiers cooperate in the process of spatial buffering. Given the pharmacological properties of potassium homeostasis (sensitivity to Cs ϩ ), members of the ether-a-go-go (ERG) channel family widely expressed in the nervous system could underlie part of the process. We used electrophysiological recordings and pharmacological manipulations to demonstrate the expression of ERG-type currents in cultured and in situ hippocampal astrocytes. Specific ERG blockers (dofetilide and E 4031) inhibited hyperpolarizationand depolarization-activated glial currents, and ERG blockade impaired clearance of extracellular potassium with little direct effect on hippocampal neuron excitability. Immunocytochemical analysis revealed ERG protein mostly confined to astrocytes; ERG immunoreactivity was absent in presynaptic and postsynaptic elements, but pronounced in glia surrounding the synaptic cleft. Oligodendroglia did not reveal ERG immunoreactivity. Intense immunoreactivity was also found in perivascular astrocytic end feet at the blood-brain barrier. cDNA amplification showed that cortical astrocytes selectively express HERG1, but not HERG2-3 genes. This study provides insight into a possible physiological role of hippocampal ERG channels and links activation of ERG to control of potassium homeostasis.

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Section: Discussionmentioning

confidence: 99%

Do Glia Have Heart? Expression and Functional Role forEther-A-Go-GoCurrents in Hippocampal Astrocytes

et al. 2000

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“…In one study, resting ECGs in 75 patients with epilepsy were compared with normal ECGs recorded in age-matched patients without cardiac or neurological disorders; ventricular rate, Pr interval, QrS duration, and QT interval (corrected for heart rate) were compared 40 . Those with epilepsy had higher heart rates and longer QT durations than the age-matched controls.…”

Section: Sudden Unexpected Death In Epilepsymentioning

confidence: 99%

The mistery of Gustave Flaubert's death: could sudden unexpected death in epilepsy be part of the context?

Albuquerque

Scorza

Arida

et al. 2009

Arq. Neuro-Psiquiatr.

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-Epilepsy is the most common serious neurological condition and sudden unexpected death in epilepsy (SUDEP) is the most important direct epilepsy-related cause of death. Information concerning risk factors for SUDEP is conflicting, but high seizure frequency is a potential risk factor. Additionally, potential pathomechanisms for SUDEP are unknown, but it is very probable that cardiac arrhythmias during and between seizures or transmission of epileptic activity to the heart via the autonomic nervous system potentially play a role. More than two decades ago, temporal lobe epilepsy was suggested as having been the ''nervous disease'' of Gustave Flaubert, one of the most important French novelists. In these lines, as the circumstances of his death were the subject of fabulous and mysterious speculations, we postulated in this paper that Falubert's death could be due SUDEP phenomenon.KEy worDS: epilepsy, Gustave Flaubert, SUDEP, seizure. O mistério da morte de Gustave Flaubert: pode a morte súbita em epilepsia fazer parte o contexto ?Resumo -A epilepsia é a condição neurológica crônica grave mais comum e a morte súbita em epilepsia (SUDEP) é a mais importante causa de morte diretamente relacionada à epilepsia. Informações sobre fatores de risco para SUDEP são conflitantes, porém, a alta freqüência de crises epilépticas é um fator de risco em potencial. Além disso, os mecanismos causais para SUDEP ainda não estão conhecidos, mas é muito provável que arritmias cardíacas durante e entre as crises epilépticas ou a transmissão da atividade epiléptica para o coração via sistema nervoso autônomo desempenhem um importante papel. Mais de duas décadas atrás, foi proposto que a "doença nervosa" de Gustave Flaubert, um dos mais importantes novelistas franceses, era epilepsia do lobo temporal. Nesse sentido, como a morte de Gustave Flaubert ainda seja motivo de misteriosa especulação, nosso artigo propõe que a mesma poderia estar relacionada ao fenômeno de SUDEP.

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“…QTc is higher in epileptic patients as compared to normal subjects, and it appears to be related to disease duration, particularly over the early history of disease. It is unrelated to patient age or recent reported seizure frequency 22 but may be triggered by interictal epileptiform discharges, suggesting that transient dysfunction of cortical networks can interfere with cardiac repolarization 23 .…”

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confidence: 99%

When your child with epilepsy die suddenly: febrile seizures are part of the process?

Machado

Sakamoto

Arida

et al. 2011

Arq. Neuro-Psiquiatr.

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Febrile seizures (FS) affect almost 2-5% of children and factors related to an increase susceptibility of children to FS may involve an imbalance of inflammatory cytokines and genetic factors. FS had low morbidity, but may be associated with the occurrence of late chronic epilepsy. Here we describe factors related to FS and its possible correlation with SUDEP. Key words: epilepsy, sudden death, febrile seizures.Quando seu filho com epilepsia morre subitamente: crises febris fazem parte do processo? RESUMO Crises febris (CF) afetam aproximadamente 2-5% das crianças e os fatores envolvidos com essa maior susceptibilidade das crianças às CF podem estar relacionados com uma ação inadequada de citocinas inflamatórias, além de fatores genéticos. As CF têm baixa morbidade, mas podem estar associadas à ocorrência de epilepsia crônica. Nós

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Electrocardiography in epilepsy patients without cardiac symptoms

Cited by 72 publications

References 8 publications

Do Glia Have Heart? Expression and Functional Role forEther-A-Go-GoCurrents in Hippocampal Astrocytes

Do Glia Have Heart? Expression and Functional Role forEther-A-Go-GoCurrents in Hippocampal Astrocytes

The mistery of Gustave Flaubert's death: could sudden unexpected death in epilepsy be part of the context?

When your child with epilepsy die suddenly: febrile seizures are part of the process?

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