Abstract
Current understanding of the fundamental mechanisms of epilepsy is largely based on experimental animal studies. In these studies, the intrinsic difference between chronic epileptic brain and intact non-epileptic brain must be considered. The use of normal brain is important for understanding the capacity of cerebral structures to produce electroclinical manifestations of epilepsy. However, chronic or acquired epileptic brain in animal models such as kindling has now been shown to be significantly different from normal brain in terms of synaptic function with certain alteration of morphology.1 The presence of comparable morphological changes has also been confirmed in temporal lobe specimens removed for therapeutic purposes in medically refractory epilepsy. 2–7 To study the pathophysiology of epilepsy, it would therefore be desirable to use a chronic animal model having a potential of developing a recurrent spontaneous seizure with persistent epileptogenic susceptibility either acquired or genetically dictated. In this regard, kindling8 is an ideal model of partial epilepsy with secondarily generalized seizures. Kindling causes permanent reorganization of brain function leading to spontaneous emission of partial or generalized seizures.9–11 In this model, interaction of acquired and genetically dictated factors may be studied by comparing the pattern and outcome of kindling between animal species with or without predisposition to epileptic seizures such as Senegalese baboons, Papio papio and Rhesus monkeys, respectively.12,13
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Wada, J.A. (1995). Midline Subcortical Structures for Transhemispheric Ictal and Interictal Transmission. In: Reeves, A.G., Roberts, D.W. (eds) Epilepsy and the Corpus Callosum 2. Advances in Behavioral Biology, vol 45. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1427-9_7
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