Cross-device rendering for vector graphics by Worth C.Xr.

By Worth C.Xr.

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In many of these patients a barium tablet is trapped in the proximal or midesophagus and in some is associated with symptoms. Autonomic nerve function tests, which assess parasympathetic vagal nerve function, show that patients with a bolus-specific dysmotility disorder have vagal nerve dysfunction (95). Swallowing initiates an esophageal peristaltic contraction after a brief latency and it is this interplay between inhibitory and contractile neurons that establishes subsequent contraction propagation velocity and amplitude.

Occasionally the upper esophageal sphincter does not relax completely. Abnormal esophageal peristalsis, a delay in opening of the lower esophageal sphincter, and increased gastroesophageal reflux are found in these patients (113). Progressive Supranuclear Palsy Progressive supranuclear palsy, a degenerative extrapyramidal disease, mimics Parkinson’s disease. Dysphagia is common. Uncoordinated lingual movements, excessive oral bolus leakage to the pharynx, vallecular stasis, and abnormal epiglottic motion are common.

Incomplete upper esophageal sphincter relaxation is associated with achalasia—a finding rare in most other motility disorders. In general, the primary abnormality in achalasia is incomplete relaxation of the lower esophageal sphincter, although achalasia patients with a normal lower esophageal sphincter relaxation have been described. Dilation and aperistalsis of the more proximal esophagus develop subsequently. For some reason esophageal bezoars are uncommon in achalasia. Pathologically, patients with achalasia have few or no ganglion cells, but show myenteric inflammation, neural fibrosis, and often a ganglionitis (101); the number of remaining ganglion cells is inversely related to degree of myenteric fibrosis.

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