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  Vol. 16 No. 2, February 1967 TABLE OF CONTENTS
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Control Mechanisms in Cortical Epileptogenic Foci*

"Surround" Inhibition

David A. Prince, MD; B. Joe Wilder, MD

Arch Neurol. 1967;16(2):194-202.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]


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.


Footnotes

Submitted for publication Sept 26, 1966; accepted Oct. 8.

*Read in part before the 91st Annual Meeting of the American Neurological Association, Washington, DC, June 13, 1966.1

Reprint requests to Division of Neurology, Stanford University School of Medicine, Palo Alto, Calif 94304 (Dr. Prince).



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