Electronic integration of glottic closure and cricopharyngealrelaxation for the control of aspiration: A canine study

Abstract

Aspiration can result from muscular weakness or paralysis of laryngopharyngeal muscles after lower motor neuron disorders (e.g., stroke) or unchecked gastroesophageal reflux. We submit that rehabilitation of the finely tuned swallowing mechanism should provide at least restoration of the normal dynamic relationships between glottic closure and cricopharyngeal relaxation. In three dogs under general endotracheal anesthesia, the recurrent laryngeal nerves and the pharyngeal musculature were exposed through a midline cervical incision. A tracheotomy was performed to allow unhindered laryngoscopic exposure of the vocal cords. A no. 9 endotracheal tube passed through the upper esophageal sphincter was used as a pressure transducer by saline inflation of its cuff and linked to an oscilloscope. The cricopharyngeus was placed under baseline tension with pulse trains administered by an intramuscular needle with a circuit previously used for agonist/antagonist coupling of reinnervated facial musculature. A second output channel was linked to the contralateral recurrent laryngeal nerve by a bipolar electrode. As the pulse width of the current to the recurrent laryngeal nerve increased, that to the cricopharyngeus was reciprocally decreased, producing snug glottic closure and synchronous cricopharyngeal relaxation. Results were documented on videotape. These findings were highly reproducible. We believe that the novel approach proposed in the current model offers an attractive solution to long-term aspiration problems resulting from an imbalance between vocal cord and cricopharyngeal activities.