STAGES IN DEVELOPMENT OF HIGH-PRESSURE NEUROLOGICAL SYNDROME IN THE MOUSE

The development of the high-pressure neurological syndrome (HPNS) in the CD-1 mouse is characterized by two discrete and successive seizure events, which are described. Manipulation of the compression profile, as well as suitable premedication, affect the threshold pressure eliciting the two seizure events in different ways. Thus, the first seizure is far more susceptible to changes in compression rate than the second seizure. Phenytoin depresses first seizure thresholds at dosages that markedly increase second seizure thresholds. Reserpine lowers first seizure thresholds without markedly affecting second seizures. Electrocorticographic changes associated with the first seizure are minimal, whereas the second seizure is characterized by generalized paroxysmal irregular spike and wave forms. Deep electrodes have revealed characteristic high-frequency high-voltage discharges associated with type I seizures in the general region of the reticular formation caudal to the pontine level. Type II seizures, but not type I seizures, are associated with a marked transient lowering of heart rate. Mortality is associated with type II but not type I HPNS seizures. The data pose the question of the nature of the HPNS seizures in other mammalian species and suggest a number of criteria to be used in their further exploration.