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February 1967

Control Mechanisms in Cortical Epileptogenic Foci*: "Surround" Inhibition

Author Affiliations

Palo Alto, Calif
From the Neurophysiology Laboratories, Division of Neurology, Stanford University School of Medicine, Palo Alto, Calif. Dr. Wilder's present address is Department of Neurology. University of Florida School of Medicine, Gainesville, Fla.

Arch Neurol. 1967;16(2):194-202. doi:10.1001/archneur.1967.00470200082007

ELECTROPHYSIOLOGICAL investigations of cellular activities in cortical epileptogenic foci produced by strychnine,2,3 local freeze lesions,4,5 and penicillin application6-9 have 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.2,3,5,8,9 The 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

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