Topic
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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TL;DR: It is suggested that normal developmental features of synaptic development make the immature brain more excitable than the adult brain and may contribute to epileptogenesis.
Abstract: Several factors may contribute to the propensity for the developing brain to have seizures and develop epilepsy. Hypersynchrony of neuronal circuits contributes to the seizure potential and several neurobiological features of the immature brain may support synchronized neuronal firing. The immature cerebral cortex and hippocampus have an increased density of synapses compared to adults and also a higher density of gap junctions and of excitatory amino acid receptors. Enhanced regenerative responses to injury in the developing brain may also contribute to the formation of abnormal hippocampal connections that support epilepsy. Molecular mechanisms that contribute to enhanced synaptic plasticity in the child's brain can also contribute to epileptogenesis in certain circumstances. The phenomenon of kindling, where repeated electrical stimulation of neuronal circuits leads to the development of epileptic seizures, is easily elicited in young animals. Long-term potentiation (LTP), where repeated synaptic stimulation leads to a reduced threshold for activation of that pathway and enhanced postsynaptic potentials, is much more robust in the immature cerebral cortex and may contribute to kindling and epileptogenesis. Age related enhancement of N-methyl-D-aspartate-type glutamate receptors, which are important for the activity dependent plasticity in the developing brain, appears to participate in LTP. This information suggests that normal developmental features of synaptic development make the immature brain more excitable than the adult brain and may contribute to epileptogenesis.
86 citations
TL;DR: Investigation of the long-term expression profiles of NKCC1 and KCC2 in CA1 region in the mice model of lithium-pilocarpine induced status epilepticus and their relationship with epileptogenesis found some expressional changes, which may provide new drug targets for development of new antiepileptic medicine.
86 citations
TL;DR: The mechanisms of mossy fiber sprouting are reviewed and its potential contribution to epileptogenesis is considered and the possibility that prevention of the abnormal sprouting might be a new strategy for medical treatment with temporal lobe epilepsy is focused on.
Abstract: Hippocampal mossy fibers, axons of dentate granule cells, converge in the dentate hilus and run through a narrow area called the stratum lucidum to synapse with hilar and CA3 neurons. In the hippocampal formation of temporal lobe epilepsy patients, however, this stereotyped pattern of projection is often collapsed; the mossy fibers branch out of the dentate hilus and abnormally innervate the dentate inner molecular layer, a phenomenon that is termed mossy fiber sprouting. Experimental studies have replicated this sprouting in animal models of temporal lobe epilepsy, including kindling and pharmacological treatment with convulsants. Because these axon collaterals form recurrent excitatory inputs into dendrites of granule cells, the circuit reorganization is assumed to cause epileptiform activity in the hippocampus, whereas some recent studies indicate that the sprouting is not necessarily associated with early-life seizures. Here we review the mechanisms of mossy fiber sprouting and consider its potential contribution to epileptogenesis. Based on recent findings, we propose that the sprouting can be regarded as a result of disruption of the molecular mechanisms underlying the axon guidance. We finally focus on the possibility that prevention of the abnormal sprouting might be a new strategy for medical treatment with temporal lobe epilepsy.
85 citations
TL;DR: Different stages of epileptogenesis of neurons in deep temporal lobe structures have been studied with fine wire microelectrodes chronically implanted in patients with drug-refractory psychomotor epilepsy, including sub-clinical EEG seizures when EEG abnormalities did not propagate contralaterally and during clinical seizures, involving both hemispheres.
85 citations
TL;DR: It is found that P450scc, the rate-limiting enzyme in steroid synthesis, is upregulated in hippocampal glia during the latent period after pilocarpine-induced SE in rats, suggesting that enhanced steroid synthesis retards epileptogenesis.
85 citations