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 found that febrile status epilepticus, lasting an average of 64 min, increased the severity and duration of subsequent spontaneous seizures compared with FSs averaging 24 min, and this role for this inflammatory mediator in epileptogenesis is confirmed.
Abstract: Whether long febrile seizures (FSs) can cause epilepsy in the absence of genetic or acquired predisposing factors is unclear. Having established causality between long FSs and limbic epilepsy in an animal model, we studied here if the duration of the inciting FSs influenced the probability of developing subsequent epilepsy and the severity of the spontaneous seizures. We evaluated if interictal epileptifom activity and/or elevation of hippocampal T2 signal on magnetic resonance image (MRI) provided predictive biomarkers for epileptogenesis, and if the inflammatory mediator interleukin-1beta (IL-1beta), an intrinsic element of FS generation, contributed also to subsequent epileptogenesis. We found that febrile status epilepticus, lasting an average of 64 min, increased the severity and duration of subsequent spontaneous seizures compared with FSs averaging 24 min. Interictal activity in rats sustaining febrile status epilepticus was also significantly longer and more robust, and correlated with the presence of hippocampal T2 changes in individual rats. Neither T2 changes nor interictal activity predicted epileptogenesis. Hippocampal levels of IL-1beta were significantly higher for >24 h after prolonged FSs. Chronically, IL-1beta levels were elevated only in rats developing spontaneous limbic seizures after febrile status epilepticus, consistent with a role for this inflammatory mediator in epileptogenesis. Establishing seizure duration as an important determinant in epileptogenesis and defining the predictive roles of interictal activity, MRI, and inflammatory processes are of paramount importance to the clinical understanding of the outcome of FSs, the most common neurological insult in infants and children.
248 citations
TL;DR: This review shows that the antiepileptic effects of loop diuretics described in the pertinent literature are based on widely heterogeneous mechanisms ranging from actions on both neuronal NKCC1 and KCC2 to modulation of the brain extracellular volume fraction.
245 citations
TL;DR: This paper presents a review of the literature of glutamate and its role in neurological function and disease and highlights treatment potentials of antagonists to glutamatergic transmission.
Abstract: Glutamate is the principal excitatory neurotransmitter in the brain. Knowledge of the glutamatergic synapse has advanced enormously over the last 10 years, primarily through application of cellular electrophysiological and molecular biological techniques to the study of glutamate receptors and transporters. There are three families of ionotropic glutamate receptors with intrinsic cation permeable channels. There are also three groups of metabotropic, G-protein-coupled glutamate receptors that can modify neuronal excitability. There are also two glial glutamate transporters and three neuronal transporters in the brain. Endogenous glutamate may contribute to the brain damage occurring acutely after traumatic brain injury as well as having a role in the excitatory imbalance present in epileptic conditions and contributing to the pathophysiology of hepatic encephalopathy in animals. Understanding the role of glutamate in these neurological diseases may highlight treatment potentials of antagonists to glutamatergic transmission. This paper presents a review of the literature of glutamate and its role in neurological function and disease.
242 citations
TL;DR: The lack of increased DGC neurogenesis after fewer kindled seizures or at early timepoints following kindling suggests that this process is not involved in kindling development, and newly generated DGCs may be important for maintenance of the kindled state or the increased susceptibility to spontaneous recurrent seizures.
238 citations
01 Jan 1992
TL;DR: It is concluded that the dentate gyrus functions in several modes during seizures, even in the naive brain, and that in chronic epilepsy alterations take place that provide an even greater diversity of functional capabilities.
Abstract: Considerable in vitro work has pointed to a resistance of dentate gyrus granule cells for expressing epileptiform paroxysms. However, in vivo work has shown that these neurons, under appropriate conditions, support and sustain seizure discharges. This range of activity of granule cells, along with their location in the middle of a pathway that connects hippocampal regions with high propensities for generating seizures, allows the dentate gyrus to act as a critical regulator of seizures. In the following report we review experiments on a stereotyped, robust paroxysmal discharge, maximal dentate activation (MDA), that occurs in granule cells, and we examine the role of MDA in reinforcing seizures in hippocampal circuits. In addition, work is presented that indicates MDA regulates seizures at sites beyond the hippocampus and its connections. Other studies that examine morphological and functional changes in the local circuits of granule cells and other neurons in the dentate gyrus in different models of epilepsy are discussed. We conclude that the dentate gyrus functions in several modes during seizures, even in the naive brain, and that in chronic epilepsy alterations take place that provide an even greater diversity of functional capabilities. Explicating these heterogeneous conditions will provide important insight into basic mechanisms of seizures and epileptogenesis.
237 citations