Limbic epileptogenesis: a model study using kindling from the amygloid cortical nucleus.

Abstract

The dynamics of limbic epileptogenesis was studied using a model of electrical kindling from different rostrocaudal segments of the cortical nucleus of the amygdala (CoA). Statistically significant relationships were found between the rostrocaudal location of the site of focal stimulation of the CoA and the behavioral and electrographic manifestations of seizure activity. The data obtained suggest that different rostrocaudal segments of the CoA play different roles in the genesis of limbic epilepsy. Temporal lobe epilepsy (or limbic epilepsy) is the most common form of this disease in humans [3, 10, 11]. Patients with this form of epilepsy suffer from complex partial (focal) and secondarily generalized seizures. In most cases, pharmacological resistance develops that makes it difficult to efficiently control seizures or significantly decrease their frequency using anticonvulsant drugs [13]. Because of the high incidence of temporal lobe epilepsy, difficulties in its pharmacotherapy, and the diversity of associated structural and functional brain lesions, of particular interest are experimental studies in which the pathogenetic mechanisms of temporal epilepsy are analyzed using various animal models [9, 10]. Electrical kindling (low-level stimulation that causes a progressively increasing response when applied repeatedly) [8] is the most adequate chronic model of temporal epilepsy that closely follows the natural course of its development with respect to a number of parameters [3‐6, 9, 10]. The role of the CoA in initiating the epileptiform activity of the amygdaloid complex (AC) and of the entire brain remains largely obscure. Our early studies [4, 5] and a recent study by Pitkanen et al. [11] implicated the CoA in spreading the seizure activity, especially in generating mirror foci in the amygdala of the contralateral hemisphere. In contrast, Cain [7] presents evidence that the CoA is of little significance in the epileptogenic process. However, taken together, the fact that the CoA is morphologically closely related to the piriform cortex and to some other structures of the AC in the ipsi- and contralateral hemispheres, and the clinical data indicating that the mediobasal temporal lobe is involved in the genesis of human temporal lobe epilepsy put in doubt Cain’s point of view. In the rat AC, the CoA lies medial to the piriform cortex, being partially exposed on the basal surface of the brain [1, 2]. The CoA is elongated rostrocaudally. This makes it possible to perform separately microstimulation of its anterior and posterior subniclei, which are known for their complex and heterogeneous structure [2]. The CoA can be divided into the anterior CoA (CoAa), the periamygdaloid cortex (PAC), and the posterior CoA (CoAp), based on the differences in their neuron composition, cytoarchitectonics, histochemistry, afferentation, and involvement in the main conducting systems of the AC [1]. The purpose of this study was to determine whether the behavioral and electrographic manifestations of epileptogenesis depend on the rostrocaudal location of the site of focal stimulation.