Reflex Vocal Fold Adduction in the Porcine Model: The Effects of Stimuli Delivered to Various Sensory Nerves

Objectives: The aim of this study was to identify a panel of sensory nerves capable of eliciting an evoked glottic closure reflex (GCR) and to quantify the glottic closing force (GCF) of these responses in a porcine model. Methods: In 5 pigs, the internal branch of the superior laryngeal nerve (iSLN) and the trigeminal, pharyngeal plexus, glossopharyngeal, radial, and intercostal nerves were surgically isolated and electrically stimulated. During stimulation of each nerve, the GCR was detected by laryngeal electromyography and the GCF was measured with a pressure transducer. Results: The only nerve that elicited the GCR in the 5 pigs was the iSLN. The average GCF was 288.9 mm Hg. Conclusions: This study demonstrates that the only afferent nerve that elicits the GCR in pigs is the iSLN, and that it should remain the focus of research for the rehabilitation of patients with absent or defective reflex vocal fold adduction.

Central Facilitation of the Glottic Closure Reflex in Humans

The sphincteric function of the larynx, essential to lower airway protection, is most efficiently achieved through strong reflex adduction by both vocal cords. We hypothesize that central facilitation is an essential component of a bilateral adductor reflex and that its disturbance could result in weakened sphincteric closure. Five patients during supraglottic laryngectomy underwent evoked response laryngeal electromyography under 0.5 and 1.0 minimal alveolar concentration (MAC) isoflurane anesthesia. The internal branch of the superior laryngeal nerve was stimulated through bipolar platinum-iridium electrodes, and recording electrodes were positioned in the ipsilateral and contralateral thyroarytenoid muscles. Consistent threshold responses were obtained ipsilaterally from 0.5 to 1.0 MAC anesthesia. However, the contralateral reflex responses approached 0% in successive trials as anesthetic levels approached 1.0 MAC. In human subjects, alteration of central facilitation by deepening anesthesia abolishes the crossed adductor reflex, predisposing to a weakened glottic closure response. A precise understanding of this effect may improve the prevention of aspiration in patients emerging from prolonged sedation or under heavy psychotropic control.

Glottic Closure Reflex: Control Mechanisms

Reflex glottic closure is a dominant and stable reflex produced by stimulation of the superior laryngeal nerve. Its precise execution is basic to successful sphincteric protection of the lower airway. In exaggerated form, it produces life-threatening laryngospasm. Clearly, reflex glottic closure and laryngospasm are facilitated by: a) expiratory phase; b) decreased arterial partial pressure of carbon dioxide (pCO2); c) increased arterial partial pressure of oxygen (pO2); and d) negative intrathoracic pressure. On the other hand, both reflex glottic closure and laryngospasm are inhibited by: a) inspiratory phase; b) increased arterial pCO2; c) decreased arterial pO2; and d) positive intrathoracic pressure. A clear understanding of laryngeal adductor control is an essential first step in the therapeutic modification of abnormal laryngeal closure and laryngospasm.

Laryngeal Spasm: A Neurophysiologic Redefinition

Within the limits of standard neurophysiologic techniques, we have attempted to redefine laryngeal spasm as distinct from the glottic closure reflex. This distinction is based upon the observation that laryngeal spasm is solely mediated by the superior laryngeal nerve. Stimulation of other afferent nerves, capable of eliciting the glottic closure reflex, produces little adductor after-discharge activity that is characteristic of laryngeal spasm. In this regard, modification of output function from the adductor motoneuron aggregate by means of temporal and spatial summation of sensory input data has been described, and its characteristics further defined in response to varying ventilatory states and barbiturate levels.