Experimental Absence Versus Amygdaloid Kindling

Abstract

Neural mechanisms underlying convulsive events are believed to be distinctly different from those of absence seizures.1 Typical absence epilepsy has been suggested to be related to a predominance of inhibitory activity, in contrast to generalized or focal convulsive seizures where an excess of excitatory activity is present.2 Likewise, drugs that exacerbate seizure activity, clinically and in animal models, support the hypothesis concerning distinct differences between convulsive and non-convulsive epileptic events. It has long been known that carbamazepine, oxcarbazepine and phenytoin are successfully used in the treatment of partial and secondary generalized seizures, whereas typical absence seizures are clearly exacerbated by carbamazepine and phenytoin.3, 4 Similarly, despite the fact that vigabatrin is a highly effective anticonvulsive agent against partial seizures,5 two patients with idiopathic generalized absence epilepsy in whom vigabatrin increased the frequency and severity of absence and absence status were reported by Panayiotopoulos et al.6 On the other hand, absence seizures in both animal models and humans respond to ethosuximide and trimethadion, which are ineffective against partial seizures.3, 7 Models of convulsive events as well as non-convulsive seizures offer several unique opportunities to understand the pathophysiology of epileptogenesis in animals and perhaps, by extrapolation, in humans.