With the aid of chronic subdural electrodes we have been able to record from the posterior banks of the sylvian fissure, auditory evoked potentials (AEPs) that had morphologies and peak latencies compatible with the primary AEPs described by Celesia and Puletti (1969). These AEPs had amplitudes that were not only affected by the side of stimulus presentation but were maximal in an area close to the primary auditory cortex. The AEPs also displayed an extremely steep spatial gradient and were not altered by pentobarbitone sodium and nitrous oxide anaesthesia. Together, these properties suggest that these subdurally recorded potentials are near-field evoked potentials from the primary auditory cortex. The focal nature of these potentials also allows them to be used as effective electrophysiological tools for localization of the primary auditory cortex in patients.

SUMMARY We performed electrophysiologic studies before and after oral administration of disopyramide phosphate, 200 mg every 6 hours, in 20 patients with atrioventricular (AV) reentrant tachyeardia using a retrogradely conducting accessory pathway. Disopyramide markedly depressed retrograde accessory pathway conduction by increasing the mean ventricular paced cycle length that produced ventriculoatrial block (a2 287 4 to ¢ 392 22 msec, p < 0.01); it also depressed antegrade normal pathway AV conduction by increasing the atrial paced cycle length that produced AV block (287 9 to 328 7 msec, p < 0.01).In 14 patients, tachycardia could not be induced or sustained after disopyramide phosphate. In 13 patients, this reflected depression of the retrograde limb with either absence of atrial echoes (nine patients) or induction of nonsustained tachycardia that terminated after the QRS complex (four patients), and in one, it reflected depression of the antegrade limb with induction of a single atrial echo not followed by a QRS response. In six patients, sustained tachycardia could still be induced after disopyramide.Oral disopyramide phosphate is effective in preventing induction of sustained AV reentrant tachyeardia in most patients. This effect is achieved primarily by depression of the retrograde limb of the reentrant circuit.EFFECTIVE DRUG THERAPY for reentrant tachycardia in patients with the Wolff-Parkinson-White syndrome can be achieved by eliminating atrial or ventricular premature complexes responsible for induction of tachycardia, or by modifying the conduction properties of the reentrant circuit. l1 The former is difficult to achieve and hard to evaluate, while the latter can be evaluated with electrophysiologic studies in the catheterization laboratory.3 6 Procainamide and quinidine increase the retrograde effective refractory period of the accessory pathway;2 3 5 digitalis,1 3 '3' proprano1o13 and verapamil4 8 " increase the antegrade effective refractory period of the atrioventricular (AV) node. These agents may prevent the induction or sustenance of tachycardia. The limited data available suggest that disopyramide increases refractoriness of the retrograde accessory pathway and can suppress reentrant tachycardia.12-14In this study, we evaluated the effects of oral disopyramide on induction and sustenance of AV reentrant tachycardia incorporating a retrogradely conducting accessory pathway in a large group of patients. These effects are examined in terms of the measurable properties of the components of the reentrant circuit. Materials and MethodsThe study group consisted of 20 patients, six females and 14 males, ages 17-70 years (mean 43 ± 17 years F ± SD]). All 20 patients had electrocardiograph- ic documentation of recurrent paroxysmal supraventricular tachycardia, electrophysiologic demonstration of AV reentrant tachycardia incorporating a retrogradely conducting accessory pathway, and induction of sustained tachycardia necessitating termination with electrical stimulation on the day of control study. Pat...