In an attempt to know whether the existing anticonvulsants act on epileptogenic focus, the effect on SA induced by freezing of the visual cortex was examined in gallamine-immobilized cats. The SA was localized in the neighbor or ipsilateral cortex of the freezing area; little epileptiform activity was produced in the contralateral anterior cortex, and ipsilateral thalamus and hippocampus. Spike frequency and its amplitude were stable over 8 hr. Diazepam suppressed SA and decreased spike frequency and its amplitude. Dipropylacetate and acetazolamide also suppressed SA. On the other hand, phenobarbital, carbamazepine, and a high dose of phenytoin enhanced SA and increased the spike frequency. Low doses of phenytoin and trimethadione were without effect in this aspect. Taurine suppressed SA and changed the spikes to wave-like forms. The EEG arousal response was depressed with phenobarbital, carbamazepine, diazepam, and a high dose of phenytoin, but not with the other drugs examined. From these results, it is suggested that diazepam, dipropylacetate, acetazolamide, and taurine depress the epileptogenic focus activity itself without relation to the activating system.
Effects of zonisamide (AD-810, CI-912) were examined on tungstic acid gel-induced thalamic generalized seizures and conjugated estrogen-induced cortical spike-wave discharges in gallamine-immobilized cats. Zonisamide prolonged the interictal periods of the generalized seizures by thalamic (centralis lateralis) application of tungstic acid gel (50 microliters) and, at the higher doses, abolished the seizures; its potency was near that of phenobarbital. Zonisamide abolished the spike-wave discharges by cortical (posterior lateralis) application of 2% conjugated estrogens (CE); its potency was stronger than that of dipropylacetate or trimethadione, but slightly less than that of phenytoin, phenobarbital, or carbamazepine. Zonisamide did not affect the posttetanic potentiation of the monosynaptic reflexes (ventral root potentials) in urethane-chloralose-anesthetized spinal rats. From these results, it is suggested that zonisamide suppresses both seizures originating from the thalamus and the cortex through the mechanism differing from that of phenytoin. Zonisamide appears to be effective in primary generalized seizures, especially the grand mal epilepsies, in addition to being effective in cortical epilepsies.
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