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European Congress Proceedings Epilepsicl, 35(Suppl 7):l-100, 1994 Raven Press, Ltd., New York 0 International League Against Epilepsy European Congress Proceedings European Congress of Epileptology Oporto, Portugal, September 6-10, 1994 Topic I: Epileptogenesis Epileptic discharges represent a pathologic extreme of the emergent properties of neuronal networks. Excitatory connec- tions between the pyramidal cells of neocortex and hippocampus Main Session (1OOOa-1OOOc) play a key role in initial synchronization of neuronal activity into epileptic discharges. Combined experimental studies and realis- Ionic Mechanisms of Epileptogenesis. U we Heinemann, A. Dra- tic computer simulations of a range of acute experimental epi- lepsies has led to detailed understanding of the necessary fea- guhn, and H. Luhmann (Department of Neurophysiology, Phys- iological Institute of the Charite, Humboldt University, Berlin, tures of the hippocampal CA3 region (J Physiol (Lond) 1993;461: 525-47): The divergence and efficacy of the connections between Germany)-lOOOa. pyramidal cells. Acute convulsants generally increase efficacy. For ictogenesis, the balance between excitation and inhibition Chronic models more closely parallel clinical epilepsies. One must be disturbed. This is organized on two levels: the synaptic such is the tetanus toxin model. lnitially (<4 weeks), synaptic and the cellular. On the cellular level, depolarizing inward cur- inhibition is disrupted by block of y-aminobutyric acid (GABA) rents must be balanced by hyperpolarizing outward currents. release. Subsequently, GABA release recovers, but the tissue Similarly, on the synaptic level, excitatory postsynaptic poten- remains epileptogenic (Neuroscience 1993;57:235-9; J Physiol tials (EPSPs) must be counteracted by inhibitory postsynaptic (Lon4 1993;465:595-614). During this late phase, inhibitory in- potentials (IPSPs). Consequently, changes in intrinsic membrane terneurons appear disconnected from the excitatory network, properties or synaptic organisation can contribute to epileptoge- consistent with the “dormant” interneuron hypothesis. Dormant nesis. Interfering with this balance induces epileptiform activity interneurons and the sprouting of new excitatory connections both in vivo and in vitro. Although interictal and absence type have each appeared in several chronic epilepsies, suggesting that seizures are not associated with major ionic changes in the ex- they have general significance for epileptogenesis. (Supported by tracellular microenvironment, such changes occur during sei- The Wellcome Trust.) zurelike events. The observed ionic changes are themselves ca- pable of inducing epileptiform activity and thus provide for feed- Molecular and Morphologic Changes in Epilepsy: A Process Lead- back mechanisms supporting seizure development. ing From Seizures to Neosynaptogenesis. A. Represa, H. Pollard, If an ictogenic agent is applied for some time to a cortical slice C. Marlangue, M. Khrestchatisky, J. Niquet, K. Bugra, and Y. such as the entorhinal cortex (EC) slice, the epileptiform activity Ben-Ari (INSERM U. 29, Paris, France)-lOOOc. may change both its appearance and drug sensitivity. This was particularly well documented for low Mg2+-induced seizurelike Seizures set in motion a cascade of complex molecular and events in EC. The transition from seizurelike events to late re- genomic changes, which may contribute to abnormally increased current discharges which are no longer sensitive to clinically neuronal excitability and be involved in maintenance of the ep- used anticonvulsants, and the transition to late recurrent dis- ileptic process. These changes may also be responsible for de- charges, is facilitated by K+ channel blockers such as TEA and velopment of seizure-induced neuronal lesions. Such modifica- by GABA receptor antagonists. Because in EC Kf channels tions have been well analyzed in experimental models of tempo- sensitive to TEA are metabolically regulated, increased energy ral lobe epilepsy in rats, but recent data already suggest that consumption and consequent downregulation of K currents may similar changes develop in human epilepsy. contribute to the transition from seizurelike events to late recur- Seizure-induced changes may be rapid and transient (from 30 rent discharges. With respect to GABA, we noted that the GABA min to 24 h after seizure onset). These changes include increased uptake blocker nipocotic acid blocked late recurrent discharges expression of transcription factors (i.e., c-fos and zif268), whereas barbiturates and benzodiazepines were ineffective. trophic factors (i.e., basic fibroblast growth factor), and neuro- Between seizures, brain, although predisposed to ictogenesis, transmitter receptors (glutamatergic receptors of the AMPA is stabilized, and a momentary disregulatory event will start the type). Such changes may also be delayed and long-lasting (from actual seizure. Such disregulation may occur under emotional 24 h after seizures; they may last for the life of the animal). conditions in which steroids interact with brain. Seizure onset During this phase, a persistent change in glutamate receptor ex- may be related to certain stimuli and to release of neuromodu- pression, development of neuronal death (by both necrotic and lators such as serotonin, norepinephrine, and histamine. The ef- apoptotic mechanisms), glial proliferation and hypertrophy, ac- fects of some of these agents were determined in our study. tivation of cytoskeletal proteins and, finally, reactive sprouting Through IA receptors, serotonin blocked epileptiform activity and neosynaptogenesis have been observed. Study of such pro- both in rat hippocampal slices and in EC. cesses may lead to better understanding of the consequences of The processes that underlie epileptogenesis are multifold. Im- seizures in brain as well as of the mechanisms underlying focal pairment of circuitry formation, hypoxia, and status epilepticus, epilepsy. as well as infection, induces lesions in brain; tumors and seizure- induced alterations in neuronal properties are most common. Evidence €or changes in cellular and synaptic properties can be Platform Presentation 1 (1001-1006) obtained in preparations from hypoxia-lesioned animals and in animals with a kindled as well as a tetanus focus. Whether changes in neuromodulatory activity can produce epileptiform activity in Effect of Cycloheximide Intraventricular Administration on Epi- these prelesioned animals still has not been well investigated. leptic Focus Development in Amygdala-Kindled Cats. J. Maj- kowski, A. Sobieszek and Jerzy Majkowski (Department of Neu- rology and Epileptology, CMKP, Warsaw, Poland)-1001 . Basic Mechanisms of Partial Epilepsies. John G.R. Jefferys (St. Mary’s Medical School, Imperial College, London, England)- Epileptic focus formation in a kindling model is an expression 1000b. of permanent synaptic plastic modification, which in turn is a 1 2 EUROPEAN CONGRESS PROCEEDlNGS result of neuronal protein synthesis. We studied the inhibitory ence between MAM-treated and control rats. The results suggest effect of the protein synthesis inhibitor cycloheximide on epilep- that some types of NMDs are not associated with a greater de- togenesis. Electrodes for kindling stimulation were implanted in gree of seizure-induced hippocampal damage in developing different cat brain structures, including amygdala. An osmotic brain. Alzet pump (2 ML4) containing 2 ml cycloheximide solution 50 pg/ml was then implanted subcutaneously. The pump was con- nected by a polyethylene tube to a cannula inserted in the lateral ventricle of the hemisphere. Cycloheximide was infused at a Pathogenic Clinical Mechanisms in Temporal Seizures. Gary W. constant rate for 28 days (2.5 pl/h). After pump insertion, Mathern, Thomas L. Babb, James K. Pretorius, and Barbara G. amygdala kindling was started. The control group of animals Vickrey (Division of Neurosurgery, RNRC, UCLA Medical received physiologic saline. Center, Los Angeles, CA, U.S.A.)-1004. Preliminary results show that epileptic focus formation in amygdala was decreased in animals receiving cycloheximide. In temporal lobe epilepsy (TLE), prolonged first seizures and Moreover, no epileptic seizures occurred. In contrast, control head trauma, termed initial precipitating injuries (IPI), have been cats receiving saline infusion developed seizures during a com- suggested to cause hippocampal sclerosis (HS). We determined parable time period. The protein synthesis inhibitor cyclohexi- the clinicopathologic associations between IPIs, HS, and seizure mide may have some inhibitory effect on amygdalar epileptoge- outcome in a cohort of 215 surgically treated TLE patients. The nesis in the kindling model of epilepsy. presence and type of iPI (independent variable) was compared with hippocampal (HC) neuron losses, mossy fiber (MF) sprout- ing, and seizure outcome (three dependent variables). For non- lesional TLE (n = 163), patients with IPis had greater HC loss (p Implication of Chemical Kindling for Drug-Resistant Epilepsy. = 0.0001), more MF sprouting (p = 0.0005), and better outcome Andrey Mazarati, Alexei Shandra, Leonid Godlevsky, and Val- (p = 0.0001) as compared with No-IPI patients. Of the IPi types, entin Kresyun (Department of Normal Physiology, Medical In- those with prolonged first seizures and head trauma had signifi- stitute, Odessa, Ukraine)-1002. cantly better outcome than types with birth injury or nonseizure cerebral infections (p = 0.0043). Of those with lesional TLE (n Antiepileptic drug (AED) resistance
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