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AND C. ERICKSON Department Neurology and Neurosurgery of McGill University, Montreal Neurological Institute, Montreal (Received for publication June and 24, 1940) INTRODUCTION THE FUNDAMENTAL MECHANISM involved in the initiation of paroxysmal excessive s of the cortex has been investigated recently from several avenues of approach. Epileptiform s of the cortex, either experimentally induced by electrical stimulation or by convulsant drugs in animals, or as associated with epileptic seizures in man are accompanied by an increase in circulation through the discharging area, as shown by Gibbs (1933), Gibbs, Lennox, and Gibbs (1934), and Penfield, von Santha and Cipriani (1939). The change in circulation appears, however, to be secondary to the increase in neuronal . Since a change in circulation has never been observed to precede the onset of excessive neuronal , but always to follow evidence of a convulsion, Penfield, von Santha and Cipriani conclude that circulatory changes probably do not play a part in the immediate initiation of epileptiform activity. No direct evidence has been given pertaining to the mechanism of this increase in but the release of CO2 or acid metabolites of activity has been suggested as well as a possible local accumulation of acetylcholine. Simultaneous records
Journal of Neurophysiology – The American Physiological Society
Published: Jul 1, 1941
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