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The Role of Extracellular Potassium in Hippocampal Epilepsy
Robert S. Fisher;
Timothy A. Pedley, MD;
William J. Moody, Jr;
David A. Prince, MD
Arch Neurol. 1976;33(2):76-83.
Abstract
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It has been proposed that the notable capacity for epileptogenesis in the hippocampus may be related to potassium accumulation in extracellular spaces. To investigate this hypothesis more directly, we measured changes in extracellular potassium concentration ([K+]o) during focal hippocampal epilepsy using potassiumsensitive microelectrodes. Interictal and ictal electroencephalographic events were accompanied by increases in [K+]o that varied systematically with depth from the ependymal surface and lateral distance from the focus. Maximal [K+]o changes during interictal and ictal discharges occurred in the stratum pyramidale. Initiation of ictal activity did not correlate with a particular "threshold" [K+]o. Comparing these results with similar data from neocortex, we observed that interictal K+ responses in hippocampus lasted longer and had slower rise times, and that peak interictal and ictal [K+]o values were consistently lower. Increases in [K+]o cannot be the sole explanation for regional variations in seizure susceptibility, interictal-ictal transitions, or termination of ictal episodes.
Author Affiliations
From the Department of Neurology, Stanford University Medical Center, Stanford, Calif.
Footnotes
Accepted for publication Dec 26, 1974.
Read in part before the 99th annual meeting of the American Neurological Association, Boston, June 10, 1974.
Reprint requests to Department of Neurology, Stanford University Medical Center, Stanford, CA 94305 (Dr Pedley).
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