الفهرس 
Anatomy of the esophagus.Only 14 pages are availabe for public view
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Abstract
Normal esophageal motility is dependant on intact neural control mechanisms and normal function of the esophageal muscle. Motor disorders present when defects in the neuromuscular apparatus are present. Motor disorders can be primarily focused in the esophagus or secondary related to a systemic disease and can affect specific regions of the esophagus or multiple regions. The most distinctive as well as the longest recognized and best understood motor disease of the esophagus is achalasia.
Achalasia is uncommon esophageal motor disease, with an estimated annual incidence of 1 per 100000 persons. Achalasia has been described from infancy to the ninth decade, with the majority of patients presenting between the ages of 20 to 40 years with no sex prediction.
More recent studies have demonstrated that primary achalasia is a result of one or more neural defects, although the inciting factor remains elusive. Proposed mechanisms for the pathogenesis of the neuromuscular abnormalities observed include autoimmune disease, primary degeneration of neurons centrally and/or peripherally, and/or neuropathic infectious agent.
Patients commonly present with liquid dysphagia with variable degrees of solid dysphagia. Regurgitation, chest pain, heartburn, weight loss, and recurrent chest infections may occasionally the presenting complaints. The most serious complication of the esophageal achalasia is the development of carcinoma of the esophagus.
Crucial to the diagnoses of idiopathic achalasia is exclusion of secondary achalasia syndromes (pseudo-achalasia). Achalasia is best detected by functional studies, either fluoroscopy during a barium swallow or esophageal manometery. The radiographic features are aperistalsis, esophageal dilatation, and minimal LES opening with a bird-beak appearance; defining manometric features are aperistalsis and incomplete LES relaxation. The amplitude of pressure at the LES is found to be 2 or 3 times higher than normal in the body of the esophagus and resting pressures are higher than fundic pressures because of dilatation and retention, whereas pressure at the UES is within the normal range.
One therefore may consider two patho-physiological components for achalasia. First, a functional barrier to esophageal emptying located at the LES level, and secondly, lack of propulsive forces that are important for pushing the bolus through the esophagus.