Tracheostomized cats and piglets demonstrate respiratory stimulation during experimental seizures, whereas airway intact piglets demonstrate hypoventilation and increased subglottic resistances. The purpose of this study was to characterize the role of the vocal folds in contributing to these increased subglottic resistances during experimental seizures. A controlled animal study was performed in six anesthetized, spontaneously breathing, hyperoxic piglets who had subglottic pressure and airflow measured. A fiberoptic video scope directed into the cephalad trachea recorded subglottic images of the vocal folds. Glottal area patency (GAP) was evaluated at inspiratory onset (Io), peak inspiratory pressure (Ip), and expiratory onset (Eo) for four to five consecutive breaths under baseline control, ictal, interictal, and anticonvulsant conditions. Seizures were induced with i.v. pentylenetetrazol or bicuculline. Normalized GAP was greatest at Ip under all conditions, except anticonvulsant. During ictal periods, piglets demonstrated significant reductions in mean GAP throughout the respiratory cycle (Io, 98%; Ip, 78%; Eo, 98%), compared with baseline (p < 0.001, repeat measures analysis of variance). During ictal discharges, hypoventilation and glottal obstruction resulted in significant reductions in mean arterial pH (-0.35) and PaO2 (-39 kPa) and elevations in PaCO2 (+8.1 kPa), compared with baseline conditions. During interictal conditions mean GAP at Ip was increased, whereas at Eo (-66%) GAP was reduced, compared with control. These data demonstrate that the vocal folds are tonically adducted throughout the respiratory cycle during ictal phases and have increased expiratory adduction during interictal phases of seizures induced with standard i.v. convulsants in hyperoxic piglets.