T. Hiyoshi et al., EVIDENCE OF SECONDARY EPILEPTOGENESIS IN AMYGDALOID OVERKINDLED CATS - ELECTROCLINICAL DOCUMENTATION OF SPONTANEOUS SEIZURES, Epilepsia, 34(3), 1993, pp. 408-415
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.