Abstract：
:Chronic epilepsy, as a consequence of status epilepticus, has been studied in animal models in order to analyze the cellular mechanisms responsible for the subsequent occurrence of spontaneous seizures. Status epilepticus, induced by either kainic acid or pilocarpine or by prolonged electrical stimulation, causes a characteristic pattern of neuronal death in the hippocampus; which is followed--after an apparent latent period--by the development of chronic, recurrent, spontaneous seizures. The question most relevant to this conference is the degree to which the subsequent chronic seizures contribute further to epileptogenesis and brain damage. This article addresses the temporal and anatomical parameters that must be understood in order to address this question. (1) How does one evaluate experimentally whether the chronic epileptic seizures that follow status epilepticus contribute to epileptogenesis and lead to brain damage? To answer this question, we must first know the time course of the development of the chronic epileptic seizures, and whether the interval between subsequent individual chronic seizures is a relevant factor. (2) What anatomical parameters are most relevant to the progression of epilepsy? For instance, how does loss of inhibitory interneurons potentially influence seizure generation and the progressive development of epileptogenesis? Does axon sprouting and formation of new synaptic connections represent a form of seizure-induced brain damage? These specific issues bear directly on the general question of whether seizures damage the brain during the chronic epilepsy that follows status epilepticus.
journal_name
Prog Brain Resjournal_title
Progress in brain researchauthors
Dudek FE,Hellier JL,Williams PA,Ferraro DJ,Staley KJdoi
10.1016/S0079-6123(02)35007-6subject
Has Abstractpub_date
2002-01-01 00:00:00pages
53-65eissn
0079-6123issn
1875-7855pii
S0079-6123(02)35007-6journal_volume
135pub_type
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