Esophageal motility is a complex and multifactorial process that functions to pass food and liquid through the esophagus. Using systematic contractions in the esophageal body, combined with an appropriately timed relaxation of the lower esophageal sphincter (LES), the bolus is able to pass from the esophagus into the stomach. Errors in the process can occur anywhere along this chain of events and can lead to significant morbidity for patients. The constellation of presenting symptoms includes dysphagia, chest pain, and reflux. Due to these often vague symptoms, many patients undergo multiple other therapies prior to being diagnosed with an esophageal motility disorder and ultimately go on to further treatment. It is reasonable to start with a short course of acid suppression therapy in patients; however, when their symptoms fail to improve, this should prompt additional workup.
Achalasia is by far the most commonly diagnosed disease of esophageal motility; however, numerous other dysmotility patterns exist. The advent of high-resolution manometry has led to new understanding of esophageal function. In addition, the information obtained from advanced diagnostics has led to improved patient selection for the various management options available. This chapter will review the common esophageal motility disorders, their diagnosis, and their management.
NORMAL ESOPHAGEAL FUNCTION
A normal esophagus varies from 18 to 25 cm in length and serves to transport food from the oropharynx to the stomach. Structurally, the esophagus is made up of 4 primary layers, including the innermost mucosa, submucosa, muscularis propria, and adventitia. The muscle layer includes the innermost circular fibers and the outer longitudinal fibers, of which the upper third consists mostly of striated muscle, whereas the lower two-thirds are primarily smooth muscle. In addition to the circular and longitudinal muscles, the esophagus also contains 2 muscular sphincters. The upper esophageal sphincter controls the entrance of food to the esophagus from the oropharynx, whereas the LES prevents reflux of acid contents into the esophagus from the stomach.
Normal esophageal function is a complicated and well-choreographed event. When food is swallowed, the epiglottis moves backward to prevent aspiration and to direct food into the esophagus all while the upper esophageal sphincter relaxes. Primary peristalsis transfers the bolus down the esophagus by rhythmic contractions, which are controlled by excitatory activity in the vagal nucleus ambiguous, which releases acetylcholine.1 In coordination and prior to the excitatory signal, inhibitory neurons (which release nitric oxide and vasoactive intestinal peptide) are activated by the preganglionic neurons and provide deglutitive inhibition. As one moves further down the esophagus toward the stomach, there is an increased inhibitory action called the latency gradient.2 This delays contractions and allows the bolus to move forward toward the stomach. In contrast to primary peristalsis, secondary peristalsis is elicited by esophageal distension and is a local reflex that independently causes contraction of the esophagus. It is the relationship of inhibitory and excitatory signals along the esophagus ...