EVIDENCE OF SECONDARY EPILEPTOGENESIS IN AMYGDALOID OVERKINDLED CATS - ELECTROCLINICAL DOCUMENTATION OF SPONTANEOUS SEIZURES

Citation
T. Hiyoshi et al., EVIDENCE OF SECONDARY EPILEPTOGENESIS IN AMYGDALOID OVERKINDLED CATS - ELECTROCLINICAL DOCUMENTATION OF SPONTANEOUS SEIZURES, Epilepsia, 34(3), 1993, pp. 408-415
Citations number
24
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00139580
Volume
34
Issue
3
Year of publication
1993
Pages
408 - 415
Database
ISI
SICI code
0013-9580(1993)34:3<408:EOSEIA>2.0.ZU;2-H
Abstract
Twenty-four spontaneously occurring convulsive seizures were documente d by closed-circuit TV (CCTV)-EEG monitoring in 3 cats subjected to un ilateral amygdaloid overkindling for less-than-or-equal-to 2 years. El ectroclinical manifestations suggested that the seizures originated in the kindled amygdala (AM) (10 seizures in 3 cats), contralateral AM ( 7 seizures in 3 cats), or ipsilateral frontal cortex (7 seizures in 1 cat). All seizures of AM origin except one occurred during sleep 23 h to 20 days after the last stimulation-induced kindled seizure and culm inated in secondarily generalized seizures. The seizures of frontal co rtical origin occurred during waking within 1 h of a kindled seizure a nd remained partial in nature. In seizures of AM origin, ictal pattern s at the primary and secondary sites were mirror images of each other, but latency of onset of each seizure stage in seizures of secondary s ite AM origin was longer than that in seizures of primary site AM orig in in 2 of the 3 animals. We conclude that the secondary epileptogenic functional alterations capable of producing clinical seizures do occu r in AM-overkindled cats, but the seizures are not entirely independen t of the primary kindled site.