Key points

Overview

Glottal closure occurs during the normal swallow as part of the mechanism that prevents aspiration of the bolus of foods. It also protects the airway from aspiration of respiratory secretions produced by the salivary glands of the upper aerodigestive tract.

Glottal competence is aided by a series of events that begin in the oral cavity and end with closure of the glottis and opening of the upper esophageal sphincter (UES). The oral cavity and oropharynx are responsible for oral propulsion forces that advance the bolus into the pharynx, whereas the esophagus acts as a “suction pump” that propels the bolus further into the UES. Oral competence and velopharyngeal closure are crucial to maintain oronasal separation and thus necessary for bolus propulsion by a series of pressure gradients created.

The pharyngeal phase of the swallowing begins as the bolus of food touches the anterior tonsillar pillars. A series of sensory-mediated events that are triggered in the pharynx and the supraglottic larynx occurs that translate into airway protection: the false and true vocal folds close, the pharyngeal constrictors contract, the larynx and the hyoid elevate anteriorly, the epiglottis tilts posteriorly covering the glottic inlet, and the cricopharyngeus muscle relaxes. The fine-tuned interplay of all of these involuntary mechanisms prevents aspiration/penetration of food into the larynx. The risk of dysphagia in the presence of glottal insufficiency is thus heightened by inability of the bolus to have the adequate speed or consistency, by loss of the pressure gradient from oral incompetence or velopharyngeal insufficiency, or because of an inability to pass the bolus into the esophagus.

The primary mechanisms by which glottal incompetence occurs are unilateral vocal fold immobility (UVFI), bilateral vocal fold atrophy, and postintubation phonatory insufficiency (PIPI) ( Box 1 ).

Overview

Glottal closure occurs during the normal swallow as part of the mechanism that prevents aspiration of the bolus of foods. It also protects the airway from aspiration of respiratory secretions produced by the salivary glands of the upper aerodigestive tract.

Glottal competence is aided by a series of events that begin in the oral cavity and end with closure of the glottis and opening of the upper esophageal sphincter (UES). The oral cavity and oropharynx are responsible for oral propulsion forces that advance the bolus into the pharynx, whereas the esophagus acts as a “suction pump” that propels the bolus further into the UES. Oral competence and velopharyngeal closure are crucial to maintain oronasal separation and thus necessary for bolus propulsion by a series of pressure gradients created.

The pharyngeal phase of the swallowing begins as the bolus of food touches the anterior tonsillar pillars. A series of sensory-mediated events that are triggered in the pharynx and the supraglottic larynx occurs that translate into airway protection: the false and true vocal folds close, the pharyngeal constrictors contract, the larynx and the hyoid elevate anteriorly, the epiglottis tilts posteriorly covering the glottic inlet, and the cricopharyngeus muscle relaxes. The fine-tuned interplay of all of these involuntary mechanisms prevents aspiration/penetration of food into the larynx. The risk of dysphagia in the presence of glottal insufficiency is thus heightened by inability of the bolus to have the adequate speed or consistency, by loss of the pressure gradient from oral incompetence or velopharyngeal insufficiency, or because of an inability to pass the bolus into the esophagus.

The primary mechanisms by which glottal incompetence occurs are unilateral vocal fold immobility (UVFI), bilateral vocal fold atrophy, and postintubation phonatory insufficiency (PIPI) ( Box 1 ).

Cause and diagnosis

Vocal fold immobility is most commonly caused by iatrogenic injury to the recurrent laryngeal nerve, idiopathic neural injury (usually related to viral illness), or tumors affecting the vagus nerve ( Box 2 ). The term is generally used to describe vocal fold paresis or paralysis.

Vocal atrophy occurs with age because there is loss of vocal fold mass. PIPI occurs with prolonged intubation that leads to medial arytenoid cartilage erosion and vocal fold scarring with subsequent glottic insufficiency.

Glottal insufficiency caused by UVFI, vocal atrophy, or PIPI can be confirmed with laryngeal video stroboscopy. Aspiration, penetration, and reduced laryngeal clearance during the swallow are diagnosed with the aid of different testing tools. The role of each of these testing modalities in dysphagia is further discussed in other articles in this publication ( Box 3 ) (see articles Dysphagia Screening and Assessment Instruments by Speyer and The Modified Barium Swallow and Functional Endoscopic Evaluation of Swallowing by Brady).

Pathophysiology

Inability to achieve glottal closure leads to valvular incompetence that causes a constant pressure leak into the airway that can make the production of voice and swallowing more difficult. Glottal insufficiency can lead to voice, respiratory, and swallowing symptoms. Cough and choking with liquids or saliva are the most common manifestations of dysphagia in glottal insufficiency. Choking with solids is less frequent, but may also occur in some patients, especially those with high vagal paralysis.

Patients with high vagal paralysis exhibit decreased velopharyngeal closure, decreased and discordant pharyngeal constriction, UVFI, decreased laryngeal sensation, and cricopharyngeal dysfunction. These patients usually present with more severe symptoms of aspiration as these result in decreased bolus propulsion, impaired glottal sensory protection, and decreased esophageal opening. Many of these patients are at risk of becoming tracheostomy- or gastrostomy-dependent to manage secretions and avoid aspiration of food, and some may even require laryngectomy.

The goal of surgical treatment of patients with glottal insufficiency is to restore valve closure to re-establish airway protection during the swallow. The role of injection laryngoplasty and medialization thyroplasty with or without arytenoid repositioning is to re-establish glottal closure. In high vagal paralysis patients, Cricopharynx (CP) myotomy and pharyngoplasty can also be used in the management of glottal insufficiency to decrease the risk of aspiration by increasing the transit time of the pharyngeal bolus.