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Showing papers on "Epileptogenesis published in 1976"


Journal ArticleDOI
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


01 May 1976
TL;DR: In this article, the brain's extracellular potassium concentration [K+]0 is increased during focal epileptogenesis, and the changes have particular spatial and temporal profiles that are different in hippocampus and neocortex and in mature and immature animals.
Abstract: Characteristic elevations in the brain's extracellular potassium concentration [K+]0 occur during focal epileptogenesis. These changes have particular spatial and temporal profiles that are different in hippocampus and neocortex, and in mature and immature animals. Increases in [K+]0 cannot be the sole explanation for regional variations in seizure susceptibility, interictal-ictal transitions, or termination of ictal episodes. Excess [K+]0 is cleared primarily by passive diffusion with a small amount taken up into cells and blood vessels. Cortical neuroglia have sensitivities to changes in [K+]0 similar to that observed in glial cells in invertebrates and amphibia. However, discrepancies in the expected relationship between [K+]o and glial membrane potential Vm suggest either a heterogeneous population of glial cell types and/or the presence of a glial syncytium which acts as a spatial buffer to increases in [K+]0.

50 citations


Journal ArticleDOI
TL;DR: It can be concluded that catecholamine inhibits the establishment and activation of the kindled epileptic neuro‐circuits in hippocampal kindled cat brain.
Abstract: SUMMARY Seizure development was examined in amygdaloid (AM), hippocampal (HIPP) and septal (SEPT) “kindled” cats by behavioral and electrographic methods HIPP seizure developed into motor seizure after establishing secondary epileptogenesis in AM and globus paliidus A secondary epileptogenesis in the hippocampus was not necessary for AM seizures to develop into generalized convulsions The SEPT seizure development was almost identical to the hippocampal seizure development This latter finding suggests that psychomotor epilepsy may not only be triggered by the HIPP and AM focus but by the septum and its related structures In the second experiment, the effect of various neuroactive agents on the interictal discharge frequency was studied in AM and HIPP kindled cats Clear antagonistic action of L-Dopa against reserpine or α-MPT induced increase of IID frequency was observed Viewed in conjunction with our previous assay study of catecholamine that showed a marked depletion of both norepi-nephrine and dopamine, in hippocampal kindled cat brain, it can be concluded that catecholamine inhibits the establishment and activation of the kindled epileptic neuro-circuits

28 citations




DOI
01 Jan 1976
TL;DR: It appears that the k i n d l i n g paradigm may provide a v a l u a b l e a d d d i t i o n to the methods of the experimental model of cl i n i c a l e p i l E p t i c syndrome.
Abstract: When p e r i o d i c e l e c t r i c a l s t i m u l a t i o n i s a p p l i e d to any of a number of b r a i n s i t e s there can be a pro g r e s s i v e development and i n t e n s i f i c a t i o n of e l i c i t e d motor s e i z u r e s . This has been termed the k i n d l i n g e f f e c t . Although i t has been repeatedly suggested that the k i n d l i n g paradigm could provide a v a l u a b l e experimental model of c l i n i c a l e p i l e p t o g e n e s i s , i t was only r e c e n t l y found that k i n d l i n g would e v e n t u a l l y l e a d to a bona f i d e e p i l e p t i c syndrome i n r a t s , cats and baboons, c h a r a c t e r i z e d by spontaneous motor s e i z u r e s . The purpose of the present study was to s y s t e m a t i c a l l y describe the development of the e p i l e p t i c syndrome i n k i n d l e d r a t s . In the two experiments animals were s t i m u l a t e d about 15 times per week f o r s e v e r a l months. K i n d l i n g progressed as others have reported, although w i t h continued s t i m u l a t i o n s there were changes i n the e l i c i t e d s e i z u r e s which had not been p r e v i o u s l y described. Almost a l l of the animals, r e g a r d l e s s of whether they were s t i m u l a t e d i n the amygdala, hippocampus, or e n t o r h i n a l c o r t e x , e v e n t u a l l y d i s p l a y e d spontaneous motor s e i z u r e s before the te r m i n a t i o n of the experiment. These s e i z u r e s were found to p e r s i s t i n some animals f o r at l e a s t 7 months. Thus, i t appears that the k i n d l i n g paradigm may provide a v a l u a b l e a d d i t i o n to the methods a v a i l a b l e f o r the experimental i n v e s t i g a t i o n of e p i l e p s y and i t s genesis.