Characteristics of postischemic seizures in hyperglycemic rats

Abstract

Normoglycemic animals subjected to 10–20 min of transient ischemia survive without major neurological symptoms, but incur delayed neuronal damage selectively affecting vulnerable neuronal populations. If the animals are hyperglycemic before ischemia is induced, cell damage develops 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 epileptogenic activity which ‘matures’ into clinical seizures, or if the seizures arise as a result of secondary events occurring after many hours of recirculation. EEG activity during 20–24 h of postischemic recirculation was recorded from electrodes implanted in the neocortex and hippocampus of freely moving rats which had been subjected to 10 min of ischemia under normoglycemic or hyperglycemic conditions. Normoglycemic animals showed a transient postischemic reduction of EEG amplitude and frequency, and sparse and temporary epileptiform activity. In contrast, hyperglycemic animals showed a more pronounced reduction of EEG amplitude and frequency, and early appearing epileptiform activity which was sustained, and ultimately transformed into overt electrographic seizures. The EEG changes were more pronounced in the neocortex than in the hippocampus. The results thus demonstrate that the initial ischemic insult, and not the secondary damage appearing many hours after the initiation of recirculation, triggers epileptiform activity that ‘matures’ into status epilepticus.