Stages in development of high-pressure neurological syndrome in the mouse

Abstract

The development of the high-pressure neurological syndrome (HPNS) in the CD-1 mouse is characterized by 2 discrete and successive seizure events, which are described. Manipulation of the compression profile, and suitable premedication, affect the threshold pressure eliciting the 2 seizure events in different ways. The 1st seizure is far more susceptible to changes in compression rate than the 2nd seizure. Phenytoin depresses 1st-seizure thresholds at dosages that markedly increase 2nd-seizure thresholds. Reserpine lowers 1st-seizure thresholds without markedly affecting 2nd seizures. Electrocorticographic changes associated with the 1st seizure are minimal, whereas the 2nd seizure is characterized by generalized paraoxysmal 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.