CHARACTERISTICS OF POSTISCHEMIC SEIZURES IN HYPERGLYCEMIC RATS

Normoglycemic animals subjected to 10-20 min of transient ischemia sur vive without major neurological symptoms, but incur delayed neuronal d amage selectively affecting vulnerable neuronal populations. If the an imals are hyperglycemic before ischemia is induced, cell damage develo ps more rapidly, and postischemic seizures appear after a delay of 18- 24 h. This study was designed to assess whether the primary insult, i. e., transient ischemia in hyperglycemic animals, triggers early epilep togenic activity which 'matures' into clinical seizures, or if the sei zures arise as a result of secondary events occurring after many hours of recirculation. EEG activity during 20-24 h of postischemic recircu lation was recorded from electrodes implanted in the neocortex and hip pocampus of freely moving rats which had been subjected to 10 min of i schemia under normoglycemic or hyperglycemic conditions. Normoglycemic animals showed a transient postischemic reduction of EEG amplitude an d frequency, and sparse and temporary epileptiform activity. In contra st, hyperglycemic animals showed a more pronounced reduction of EEG am plitude and frequency, and early appearing epileptiform activity which was sustained, and ultimately transformed into overt electrographic s eizures. The EEG changes were more pronounced in the neocortex than in the hippocampus. The results thus demonstrate that the initial ischem ic insult, and not the secondary damage appearing many hours after the initiation of recirculation, triggers epileptiform activity that 'mat ures' into status epilepticus.