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April 1960

Experimental Assessment of Epileptogenesis in the Monkey Cerebral Cortex: II. Development of Chronic Epileptic Foci

Author Affiliations

Long Beach, Calif.
Department of Anatomy, University of California at Los Angeles School of Medicine, and the Veterans Administration Hospital, Long Beach, Calif.
Postdoctoral Trainee, Mental Health Training Program (Dr. White); present address: Division of Neurology, Jefferson Medical College, Philadelphia.

AMA Arch Neurol. 1960;2(4):384-390. doi:10.1001/archneur.1960.03840100022004

Evidence is accumulating which indicates that the capacity of cortical neurons to exhibit seizure discharge is related directly to distorted function of cellular structures mediating the direct cortical response.7,8 Current proposals hold that such distortion of function involves primarily the cortical dendrites.7,8,17 Direct cortical responses (DCR) evoked by a brief single stimulus applied to any cortical locus in the immediate vicinity of the recording electrodes3 are found to be of greatest amplitude in those areas which are most easily caused to discharge by repetitive electrical excitation and are poorly developed in loci which are resistant to after-discharge.7 Additionally, test conditions, such as light sleep or the administration of pentylenetetrazol (Metrazol), which enhance seizure susceptibility in the cortex cause an increase in the amplitude of the DCR, while other induced states, such as deep sedation, known to depress seizure activity result in a diminution or disappearance of

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