Abstracts

Treiman et al. (Epilepsy Res 5:49-60, 1990) reported a predictable sequence of EEG changes during status epilepticus (SE) in human generalized convulsive SE and three experimental models of SE. Since then this same sequence has been reported in six other experimental models and in human complex partial SE. All but one report has been in adult humans, rats, or monkeys. Mikati et al. (Epilepsy Res 55:9-19, 2003) found the same sequence in kainate-induced SE in juvenile (P15 and P35) rats. We studied EEG changes during high dose pilocarpine-induced SE in juvenile rats (P25) to see if the same pattern would be observed in this model. Female Sprague-Dawley rats with 14 day old litters were obtained from Charles River Labs. 16 pups were implanted with epidural screw electrodes at age P21. Electrode placements were: Bregma + 1.5 mm [plusmn] 2.3 mm; - 3.0 mm [plusmn] 2.3 mm. At age P25 SE was induced with 400 mg/kg pilocarpine IP. Video/EEG was recorded continuously from 60 minutes prior to the injection until animals exhibited periodic epileptiform discharges (PEDs) on the EEG or died. The sequence and timing of observed EEG patterns was recorded. All of the animals exhibited, sequentially, in the following order, some or all of the five EEG patterns previously described by Treiman et al.: I. Discrete electrographic seizures, II. Waxiing and waning of EEG rhythms, III. Continuous ictal discharges, IV. Continuous discharges punctuated by periods of relative flattening, V. PEDs on a relatively flat background. Quantitative data for each stage are shown in the table.[table1] These results support the hypothesis that the sequence of five EEG patterns described by Treiman et al. represent a fundamental sequence of EEG changes during status epilepticus. Variations in duration of a given pattern, morphological appearance, and time required for progression through the five patterns have been reported, but the fundamental sequence appears to hold true, regardless of the specific type of human SE (GCSE or CPSE), of the species (humans, monkeys, rats), the specific model (kainate, cobalt/homocysteine, LiCl/pilocarpine, high dose pilocarpine, electrical stimulation at various sites, hippocampal slice), or the age of the animal (juvenile rat, adult rats, monkeys, humans). Thus the EEG stage can be used as a marker to study dynamic changes during SE. These results also confirm that pilocarpine induces a severe, frequently lethal, form of SE. (Supported by Barrow Neurological Foundation and St. Joseph[apos]s Hospital [amp] Medical Center, Phoenix, AZ)