Review of autonomic dysfunction, cardiac arrhythmias, and epileptogenic activity
Lathers CM and Schraeder PL(1987) Review of autonomic dysfunction, cardiac arrhythmias, and epileptogenic activity. J Clin Pharmacol 27:5 346–56.
Abstract: Similarities in autonomic dysfunction associated with arrhythmias and death in animal models for digitalis toxicity, myocardial infarction, psychotropic toxicity, and epileptogenic activity are reviewed. When intravenous (IV) pentylenetetrazol was given to anesthetized cats, autonomic dysfunction was associated with both interictal and ictal epileptogenic activity. The autonomic dysfunction was manifested by the fact that autonomic cardiac nerves did not always respond in a predictable manner to changes in blood pressure, the development of a marked increase in variability in mean autonomic cardiac nerve discharge, and the appearance of a very large increase in the variability of the discharge rate of parasympathetic nerves first and then secondly in sympathetic discharge. The altered autonomic cardiac nerve discharge was associated with interictal epileptogenic activity and arrhythmia, which may contribute to sudden unexplained death in patients with epilepsy. Since phenobarbital (20 mg/kg, IV 60 min prior to pentylenetetrazol) exhibited anticonvulsant, but not antiarrhythmic and neural depressant activity, phenobarbital does not appear to be the ideal agent to prevent the autonomic dysfunction associated with epileptogenic activity in this animal model.
Lathers and Schraeder reviews various possible outcomes from epileptic activity within the cat model. The two main models they discuss are the Digitalis Toxicity model which used ouabiain. Studies showed that when this drug was injected into a cat model they saw decreased neural discharges win the sympathetic system. They also discuss the epilepsy model in the cat when given PTZ. They describe autonomic dysfunction during the interictal and ictal period. Their research also showed changes to the QRS complex with premature atrial and ventricular contractions. These results were similar to Schraeder's 1985 original work inducing epileptic activity within the cat model.