Achalasia

Abstract

AbstractAchalasia is the result of a progressive degeneration process of the ganglion cells of the myenteric plexus, located in the esophageal wall. The disorder motility that characterizes achalasia appears to result primarily from the loss of inhibitory neurons within the wall of the esophagus itself. This loss of the inhibitory innervation in the LOS causes the basal sphincter pressure to rise and renders the sphincter muscle incapable of normal relaxation. The loss of inhibitory neurons from the smooth muscle portion of the esophageal body results in aperistalais [1]. The manifestations of the disease depend on the degree and location of ganglion cell loss [2]. Loss of peristalsis in the distal esophagus and LOS failure to relax with swallowing, both impair esophageal emptying. Most of the signs and symptoms of achalasia are due to the defect in LES relaxation. Esophagogastric junction (OGJ) outflow obstruction. The risk of developing esophageal cancer increases up to 3.3% after a mean symptom duration of 13 years [3].