UES opening muscle dysfunction

Abstract

The upper esophageal sphincter (UES) is composed of the cricopharyngeus (CP), the inferior pharyngeal constrictor (IPC), and the most proximal segment of the esophagus and maintains a high pressure zone between pharynx and esophagus. UES opening mechanism during deglutition is multifactorial and includes the combination of neural relaxation of tonically contracted crycopharyngeus muscle, traction forces imparted by the suprahyoid (SH) UES opening muscles, intrabolus pressure generated by the oncoming bolus, and distensibility of the UES musculature [1, 2]. Each of the aforementioned factors involved in UES opening can potentially be modified to compensate for deficiency of others in a compensated state allowing complete pharyngeal clearance; failing to do so results in an uncompensated state, diminished deglutitive UES opening resulting in incomplete pharyngeal clearance, and postdeglutitive residue and potentially postdeglutitive aspiration. While the end result of this complex mechanism namely UES opening in health and disease has been extensively studied, the relative contribution of each of the components of this mechanism has received less and variable attention. Abnormal UES opening can be classified as primary, namely those due to (1) lack of neural relaxation and (2) abnormal UES distensibility, or it can be secondary namely due to inadequate traction forces imparted on the sphincter by the contraction of SH muscles. This chapter focuses on the latter topic.