Showing papers on "Epileptogenesis published in 1967"

Control Mechanisms in Cortical Epileptogenic Foci*: Surround Inhibition

Abstract: ELECTROPHYSIOLOGICAL investigations of cellular activities in cortical epileptogenic foci produced by strychnine,2,3local freeze lesions,4,5and penicillin application6-9have revealed that the population of neurons in the area of focal surface epileptiform discharge is a heterogeneous one in terms of its behavior during surface paroxysmal discharges. (In order to avoid confusion in terminology, surface epileptiform discharge or surface paroxysmal discharge will be used throughout to refer to interictal focal epil-eptiform spikes. The term spike or unit spike will always refer to the neuronal action potential.) Intracellular records in such foci show that in most neurons excitatory events, ie, large depolarization shifts (DSs) and repetitive unit firing, accompany surface epileptiform activity; some neurons, however, are inhibited during the surface discharge.2,3,5,8,9The role of inhibited neurons in a region of focal epileptogenesis and the relationship of such cells to the neuronal population responsible for generation of the surface

Secondary epileptogenesis in the frog forebrain

Abstract: SECONDARY OR MIRROR EPILEPTIC LESIONS are common in clinical experience.1-3 Such lesions are encountered in the symmetrical homotopic regions of the hemisphere contralateral to the primary epileptogenic focus. Animal studies have demonstrated the involvement of contralateral homotopic areas following the initiation of focal paroxysmal epileptiform dischargeS4-l1 Such studies have further suggested that secondary epileptogenesis can be expected in a shorter time and with greater predictability in those animals who cerebral cortices represent a more primitive state of evolutionary development or diff erentiationlo and in animals whose central nervous systems are in an early stage of maturation.12 In a search for a model in which one could predictably reproduce secondary epileptogenesis in a brief time span, the frog was selected. The forebrain of this amphibian represents a primitive stage in the evolution of the cerebral hemispheres, while at the same time there exist structures which are readily recognizable in the brains of advanced mammals.13 The primordia of the hippocampus, piriform cortex, and strioamygdaloid complex are clearly defined, and the neural pathways which characterize higher mammals are present. This communication reveals the manner in which secondary epileptogenesis may be induced in the frog forebrain, confirming similar data described from experimental work in the rhinencephalic structures of the higher mammals. This primitive vertebrate model has further enabled .us to incorporate a microelectrodc analysis of secondary epileptiform activity in the acute experiment in which secondary epileptogenesis was induced.