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==Pathophysiology== | ==Pathophysiology== | ||
=== Pathogenesis === | |||
* The exact pathogenesis of DES is not fully understood. However, current high-resolution manometry studies suggest impairment of inhibitory myenteric plexus neuron. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation. The final result is premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus. |
Revision as of 15:29, 31 October 2017
Diffuse esophageal spasm Microchapters |
Differentiating Diffuse esophageal spasm from other Diseases |
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Diffuse esophageal spasm historical perspective On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Mahmoud Sakr, M.D. [2]
Overview
Historical Perspective
Historical Perspective
Discovery
- DES was first described by Osgood, in 1889 in 6 patients who presented with chest pain and dysphagia.
- Creamer (1954) made the first manometric descriptions of DES.
Landmark Events in the Development of Treatment Strategies
- In 2000, development of high resolution esophageal manometry has led to classification of esophageal motility disorders.
Pathophysiology
Pathogenesis
- The exact pathogenesis of DES is not fully understood. However, current high-resolution manometry studies suggest impairment of inhibitory myenteric plexus neuron. These neurons use nitric oxide (NO) as neurotransmitter. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation. The final result is premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus.