Botulinum toxin treatment of upper esophageal sphincter hyperfunction

Abstract

Hyperfunction of the upper esophageal sphincter can cause severe dysphagia and appears to be the cause of Zenker’s diverticulum. This condition may occur in the context of a number of neurologic conditions, such as stroke, postpolio syndrome, Parkinson’s disease, and amyotrophic lateral sclerosis, or it may be idiopathic. Upper esophageal sphincter hyperfunction may also develop after laryngectomy, interfering with swallowing and, more commonly, preventing the successful use of a tracheoesophageal speech prosthesis, which depends on passage of air through the sphincter as a sound source. Botulinum toxin (BTX)* treatment offers a nonsurgical treatment alternative for upper esophageal sphincter (UES) hyperfunction, which is useful because affected patients are often debilitated or may have had radiation treatment to the neck. BTX treatment may also be used as a diagnostic maneuver to identify patients who would benefit from a myotomy. 1 THE UES The UES is a 2- to 4-cm section of high intraluminal pressure separating the hypopharynx from the esophagus. Its most prominent component is the cricopharygeus (CP) muscle, making up approximately its lower-most third. 2,3 For that reason, the UES is sometimes called the CP sphincter. The balance of the UES comprises the lower portion of the inferior pharyngeal constrictor and the cricoid cartilage anteriorly. The fibers of the CP originate and insert into the dorsolateral aspect of the cricoid cartilage, forming a semicircle that encompasses the esophageal lumen. Innervation of the CP muscle remains a matter of debate. It is principally supplied by the vagus, via the superior laryngeal nerve and the pharyngeal plexus, with contributions from the recurrent laryngeal nerve. It also appears to receive input from the glossopharygeal nerve and sympathetic nerve