We perfomed the specific [³H] GTP binding assay to the cerebral cortical membrane in the amygdaloid kindled rats to elucidate the biochemical bases of epileptogenesis.
Crude membrane fractions of bilateral cerebral cortex obtained from kindled and sham-operated control rats were incubated with [³H] GTP in the presence or absence of isoproterenol (IPN), a β-agonist. The data were analyzed by Scatchard analysis.
There were no differences in B_maxand K_dvalues in basal (without IPN) binding, between kindled and control groups. In the presence of IPN, B_maxvalues increased in the control, but did not increase in the stimulated (left) and unstimulated (right) side of the kindled group. The attenuation of IPN effect on B_maxin GTP binding assay was observed at 24h after the last generalized seizure and persisted for two weeks.
These results suggest that decrease in the ability of Gs to bind GTP may be concerned with the generation of the epileptic seizure and the aquisition mechanisms of the long-lasting epileptogenesis in the kindling model of epilepsy.

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In the early stage of a certain group of the progressive myoclonus epilepsy (PME), several salient clinico-electroencephalographic features lead easily to confusion with juvenile myoclonic epilepsy (JME): 3-4 Hz irregular polyspike-wave complex, combination of myoclonic and generalized tonic clonic seizures, and photosensitivity. Wetried to prevent this confusion in this early stage of the illness by elucidating differences between PME and JME. Thirteen PME-as well as twenty JME-patients werechosen among all the 3165 out-patients refered to us as having epilepsies. In the current study, only the first EEG of each case was analysed because this study was concentrated on improving the initial diagnosis among out-patients. The comparison betweenthe two groups revealed following characteristics of the PME-group with statistically significant difference: lack of GTC on awakening, slowing of the basic rhythm, and abundance of bursts of spike & wave complexes. The last feature was measured by a number of the bursts of spike & wave complex within thirty seconds from the onset of the first spike & wave in a given record. These points of differential diagnosis confirmed here would be useful in preventing the misdiagnosis of PME as JMEespecially in the early stage of the developing PME.

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We classified 95 patients (49 boys, 46 girls) with epilepsies that began at less than four years of age, according to the International Classification of Epilepsies and Epileptic Syndromes (ICE). In 55.8% of all patients, the onset was before one year of age. Localization-related epilepsies were observed in 73.7% of patients, generalized epilepsies in 23.2%, and 2.1% were undetermined whether focal or generalized. Very few patients had idiopathic epilepsies, namely, only 5.3% of all patients manifested idiopathic generalized epilepsies. Symptomatic localization-related epilepsies were more common among the patients with seizures beginning at between three and four years of age. On the other hand, symptomatic generalized epilepsies were morecommon in the younger group, especially among the patients with seizures beginning at less than one year of age. The onset of all seven patients who showed evolutional change to other type of epilepsies was under one year of age. Their transition was related to West syndrome or EME. We could classify 99% of all patients with ICE. This fact proved the usefulness of ICE in infancy. However, only 40% of patients were classifiable into epileptic syndromes. In particular, syndrome classification was difficult in localization-related epilepsies.

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The relationship between NOS (nitric oxide Synthase) activity and the susceptibility to epilepsy/convulsion was investigated in the brain of Mongolian gerbils and Sprague-Dawley rats. The NOS activity in the seizure sensitive group of Mongolian gerbils is significantly lower than that in the seizure resistant group.
The NOS activity and the susceptibility to epilepsy/convulsion were inversely correlated.

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