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Abstract
Achalasia affects both sexes equally, typically presenting between the ages of 20 and 50, though it can occur at all ages. Ineffective Relaxation of the lower esophageal sphincter (LES) combined with loss of esophageal peristalsis leads to impaired emptying and gradual esophageal dilatation. Dysphagia is the cardinal feature of achalasia, accompanied by varying degrees of aspiration, weight loss, and pain. The anatomic defect appears to be a decrease or loss of inhibitory nonadrenergic, noncholinergic ganglion cells in the esophageal myenteric plexus. Histological analysis of esophagi resected from patients who had end – stage achalasia demonstrates myenteric inflammation, progressive depletion of ganglion cells and subsequent neural fibrosis. There is a significant reduction in the synthesis of nitric oxide and Vasoactive Intestinal polypeptide (VIP), the most important mediators of relaxation in the lower esophageal sphincter.