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Epileptogenesis

About: Epileptogenesis is a research topic. Over the lifetime, 4218 publications have been published within this topic receiving 170809 citations.


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Journal ArticleDOI
TL;DR: Data from animal modelling and laboratory experiments are provided with increased specificity the molecular 'mechanisms, biomarkers, and treatment targets of post-stroke epilepsy in different circumstances, with the aim of modifying epileptogenesis after ischaemic stroke in individual patients without compromising recovery.
Abstract: Summary For about 30% of patients with epilepsy the cause is unknown. Even in patients with a known risk factor for epilepsy, such as ischaemic stroke, only a subpopulation of patients develops epilepsy. Factors that contribute to the risk for epileptogenesis in a given individual generally remain unknown. Studies in the past decade on epilepsy in patients with ischaemic stroke suggest that, in addition to the primary ischaemic injury, existing difficult-to-detect microscale changes in blood vessels and white matter present as epileptogenic pathologies. Injury severity, location and type of pathological changes, genetic factors, and pre-injury and post-injury exposure to non-genetic factors (ie, the exposome) can divide patients with ischaemic stroke into different endophenotypes with a variable risk for epileptogenesis. These data provide guidance for animal modelling of post-stroke epilepsy, and for laboratory experiments to explore with increased specificity the molecular 'mechanisms, biomarkers, and treatment targets of post-stroke epilepsy in different circumstances, with the aim of modifying epileptogenesis after ischaemic stroke in individual patients without compromising recovery.

134 citations

Journal ArticleDOI
TL;DR: In rats, the hypothesis that early postnatal stress, in the form of maternal separation, creates vulnerability to limbic epileptogenesis in adult life is tested and found to be relevant to mesial temporal lobe epilepsy.
Abstract: Summary Purpose: Early life stress has enduring behavioral and neuroendocrine effects, particularly in hippocampus and amygdala. This may be relevant to mesial temporal lobe epilepsy (MTLE) that arises from these structures. In rats, we tested the hypothesis that early postnatal stress, in the form of maternal separation (MS), creates vulnerability to limbic epileptogenesis in adult life. Methods: On postnatal days 2–14, we exposed male and female nonepileptic rats to either MS for 180 min/day, or early handling (EH) and brief separation (15 min/day). At 7 weeks of age, rats of both genders exposed to MS displayed significantly increased anxiety, as evidenced by reduced time spent in the open arms of the elevated plus maze compared with EH rats. For epileptogenesis experiments, separate cohorts of rats, similarly exposed to either early life MS or EH, were implanted with bipolar electrodes into the left amygdala and one week later rapid electrical kindling performed until fully kindled (five Class V seizures, Racine scale). Results: In females, fewer stimulations were required following MS than EH to reach the fully kindled state (39.6 ± 6.4 vs. 67.1 ± 9.4; p < 0.0001); no differences were observed in males (MS: 49.1 ± 5.1; EH: 53.7 ± 6.6 stimulations). Discussion: We conclude that, while postnatal MS stress increases anxiety in both genders, this early life stressor results in persisting vulnerability to limbic epileptogenesis only in females. This has implications for human MTLE and its psychiatric comorbidities, suggesting a common causation model and the involvement of gender-specific factors such as sex hormones.

134 citations

Journal ArticleDOI
TL;DR: The possible role of gap junctions in the manifestation and control of the duration of seizures was tested on the 4‐aminopyridine–induced epilepsy model in rats in vivo by using electrophysiologic, pharmacologic, and molecular biologic techniques.
Abstract: Summary: Purpose: The possible role of gap junctions in the manifestation and control of the duration of seizures was tested on the 4-aminopyridine–induced epilepsy model in rats in vivo, by using electrophysiologic, pharmacologic, and molecular biologic techniques. Methods: In electrophysiologic experiments, the functional states of the gap junctions were manipulated with a specific blocker (carbenoxolone) or opener (trimethylamine) at the already active focus of adult, anesthetized rats, 60 min after the induction of the first seizure, which was repeated spontaneously thereafter. Semiquantitative reverse transcriptase–polymerase chain reaction (RT-PCR) amplification was used to measure the levels of connexin (Cx) 32, 43, and 36 messenger RNAs (mRNAs) prepared from the areas of the already active primary and mirror foci. Results: After repeated seizures, the expression levels of Cx32, Cx43, and Cx36 mRNAs at the epileptic foci were increased significantly. Blockade of the gap junctions with carbenoxolone shortened the duration of seizures and decreased the amplitude of the seizure discharges, whereas their opening with trimethylamine lengthened the duration and increased the amplitude. Secondary epileptogenesis was facilitated when the gap junctions were opened. Conclusions: Our findings support the idea that, in epileptic foci, the gap junctions are involved in the expression of rhythmic ictal discharges and in the control of the duration and propagation of the individual seizures in vivo.

133 citations

Journal ArticleDOI
01 Aug 2012-Glia
TL;DR: This review focuses on the potential roles of the glial water channel aquaporin‐4 (AQP4) in modulation of brain excitability and in epilepsy.
Abstract: Recent studies have implicated glial cells in modulation of synaptic transmission, so it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors, and transporters have all been associated with the epileptic state. This review focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulation of brain excitability and in epilepsy. We will review studies of mice lacking AQP4 (Aqp4(-/-) mice) or α-syntrophin (an AQP4 anchoring protein) and discuss the available human studies demonstrating alterations of AQP4 in human epilepsy tissue specimens. We will conclude with new studies of AQP4 regulation and discuss the potential role of AQP4 in the development of epilepsy (epileptogenesis). While many questions remain unanswered, the available data indicate that AQP4 and its molecular partners may represent important new therapeutic targets.

133 citations

Journal ArticleDOI
TL;DR: This new preparation of electrographic spikes is amenable to moderate-throughput screening, which should accelerate their discovery and may also be of benefit in ameliorating the cognitive dysfunctions associated with epilepsy, to which spike activity may contribute.

133 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023181
2022348
2021245
2020219
2019210
2018209