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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: Advances in epilepsy in recent years are reviewed with an emphasis on therapeutics and underlying mechanisms, including status epilepticus, drug and surgical treatments, and lessons from rarer epilepsies regarding the relationship between epilepsy type, mechanisms and choice of antiepileptic drugs are explored.
Abstract: This paper reviews advances in epilepsy in recent years with an emphasis on therapeutics and underlying mechanisms, including status epilepticus, drug and surgical treatments. Lessons from rarer epilepsies regarding the relationship between epilepsy type, mechanisms and choice of antiepileptic drugs (AED) are explored and data regarding AED use in pregnancy are reviewed. Concepts evolving towards a move from treating seizures to treating epilepsy are discussed, both in terms of the mechanisms of epileptogenesis, and in terms of epilepsy's broader comorbidity, especially depression.

144 citations

Journal ArticleDOI
TL;DR: It is suggested that, within a certain concentration range, DA and 5‐HT contribute independently to the prevention of hippocampal epileptogenesis via, respectively, D2 and 5-HT1A receptor activation.
Abstract: The present microdialysis study evaluated the anticonvulsant activity of extracellular hippocampal dopamine (DA) and serotonin (5-HT) with concomitant assessment of the possible mutual interactions between these monoamines. The anticonvulsant effects of intrahippocampally applied DA and 5-HT concentrations were evaluated against pilocarpine-induced seizures in conscious rats. DA or 5-HT perfusions protected the rats from limbic seizures as long as extracellular DA or 5-HT concentrations ranged, respectively, between 70-400% and 80-350% increases compared with the baseline levels. Co-perfusion with the selective D(2) blocker remoxipride or the selective 5-HT(1A) blocker WAY-100635 clearly abolished all anticonvulsant effects. These anticonvulsant effects were mediated independently since no mutual 5-HT and DA interactions were observed as long as extracellular DA and 5-HT levels remained within these protective ranges. Simultaneous D(2) and 5-HT(1A) receptor blockade significantly aggravated pilocarpine-induced seizures. High extracellular DA (> 1000% increases) or 5-HT (> 900% increases) concentrations also worsened seizure outcome. The latter proconvulsive effects were associated with significant increases in extracellular glutamate (Glu) and mutual increases in extracellular monoamines. Our results suggest that, within a certain concentration range, DA and 5-HT contribute independently to the prevention of hippocampal epileptogenesis via, respectively, D(2) and 5-HT(1A) receptor activation.

144 citations

Journal ArticleDOI
TL;DR: The effects of seizures on somatostatin‐containing neurons, somatstatin mRNA and immunoreactivity, the release of this peptide and its receptor subtypes in the CNS are reviewed, providing new directions for the development of novel anticonvulsant treatments.
Abstract: Recent evidence shows that neuropeptide expression in the CNS is markedly affected by seizure activity, particularly in the limbic system. Changes in neuropeptides in specific neuronal populations depend on the type and intensity of seizures and on their chronic sequelae (i.e. neurodegeneration and spontaneous convulsions). This paper reviews the effects of seizures on somatostatin-containing neurons, somatostatin mRNA and immunoreactivity, the release of this peptide and its receptor subtypes in the CNS. Differences between kindling and status epilepticus in rats are emphasized and discussed in the light of an inhibitory role of somatostatin on hippocampal excitability. Pharmacological studies show that somatostatin affects electrophysiological properties of neurons, modulates classical neurotransmission and has anticonvulsant properties in experimental models of seizures. This peptidergic system may be an interesting target for pharmacological attempts to control pathological hyperactivity in neurons, thus providing new directions for the development of novel anticonvulsant treatments.

144 citations

Journal ArticleDOI
TL;DR: It is found that in response to muscarinic activation, pools of EC interneurons discharge synchronously by a mechanism not necessarily involving principal cell activation, and their robust epileptogenic character may be of major importance in temporal lobe epilepsy.
Abstract: Oscillation and synchronization of neural activity is important in normal brain function but is also relevant to epileptogenesis. One of the most frequent forms of epilepsy originates in temporal lobe circuitry of which the entorhinal cortex (EC) is crucial. Because muscarinic receptor activation promotes oscillatory dynamics in EC neurons, we investigated in a brain slice preparation the effects of carbachol (CCh) on oscillatory population activity in the EC. We found that CCh produced epileptiform activity in EC, which according to field profile and current source density analysis was usually driven by layer V. In addition, localized CCh application and surgical isolation experiments demonstrated that EC layer II, but not layer III, can also independently generate synchronous population activity. Intracellular recordings from EC principal cells during epileptiform activity demonstrated large-amplitude, synaptically driven depolarizing events and bursts of action potentials synchronized to the field spikes. In layer II neurons, the depolarizing events had a multiphasic reversal potential that suggested concurrent glutamatergic and GABAergic synaptic input. Interestingly, although the epileptiform activity required activation of AMPA but not NMDA receptors, small-amplitude field spikes persisted during block of fast excitatory neurotransmission. These field spikes were correlated to large-amplitude IPSPs in layer II neurons, and both activities were abolished by GABAA-receptor antagonism. Thus, in response to muscarinic activation, pools of EC interneurons discharge synchronously by a mechanism not necessarily involving principal cell activation. Given the differential projection pattern of EC layers V and II toward the neocortex and hippocampus, respectively, their robust epileptogenic character may be of major importance in temporal lobe epilepsy.

143 citations

Journal ArticleDOI
TL;DR: Patients with temporal lobe epilepsy with chronic and postictal psychoses show similar profiles of clinical and seizure variables, suggesting shared etiologic factors.
Abstract: Objective This study sought to elucidate the relation of clinical, neuropsychological, and seizure variables to chronic and postictal psychoses in patients with temporal lobe epilepsy. Method Forty-four patients with treatment-refractory temporal lobe epilepsy were given formal psychiatric evaluations; 29 patients had no psychiatric disorder or a nonpsychotic disorder, eight patients had postictal psychoses, and seven patients had chronic psychoses. Comparisons of clinical, neuropsychological, magnetic resonance imaging, and seizure variables were made between the nonpsychotic and the psychotic patients and, secondarily, between the patients with transient postictal psychoses and those with chronic psychoses. Results Bitemporal seizure foci, clustering of seizures, and absence of febrile convulsions were associated with both postictal psychoses and chronic psychoses. Younger age at onset of epilepsy and lower verbal and full-scale IQs differentiated the patients with chronic psychoses from those with postictal psychoses. Conclusions Patients with temporal lobe epilepsy with chronic and postictal psychoses show similar profiles of clinical and seizure variables, suggesting shared etiologic factors. These factors may increase the propensity to develop psychotic symptoms, while other factors, such as time of onset of epilepsy and underlying neuropathology, may determine whether transient or chronic psychotic symptoms develop. Even among patients with treatment-refractory temporal lobe epilepsy, a specific subgroup of patients, characterized by bitemporal seizure foci, an absence of febrile convulsions, and a history of clustering of seizures, appears to be particularly prone to develop psychotic disorders. A process similar to secondary epileptogenesis may be involved in the development of the psychoses.

143 citations


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