Dorsal Frontal, Orbital and Mesial Frontal Cortical Lesion and Amygdaloid Kindling in Cats

Abstract

Bilateral anteromesial or orbital cortical lesions do not affect sequential pattern of amygdaloid seizure development. However, orbital cortex lesions appear to significantly participate in the elaboration of a Stage 6 seizure pattern. Amygdaloid kindling ipsilateral to the side of anterodorsal cortical lesion or in animals with the same bilateral lesion appears to predispose them for the development of spontaneous, nonconvulsive (partial complex) seizures. It also significantly modifies clinical ictal patterns with practical ommission of Stages 2, 3 and 5, and largely lateralizes AD propagation to the stimulated hemisphere. The latter two features are strikingly reminiscent of the electroclinical manifestations of secondary site AM kindling in intact animals or AM kindling in animals with forebrain commissure bisection. Nonconvulsive (partial complex) status epilepticus was readily arrested by placement of electrolytic lesions ipsilateral to the AM stimulation, suggesting that MRF is essential for the perpetuation of the recurrent spontaneous seizure. Finally, the presence and absence of positive and negative aftereffects respectively, in animals with anterodorsal cortical lesion is consistent with the view that transfer and interference effects are mediated through the brain stem and forebrain commissures respectively.