Abstract
Esophageal pain manifests as symptoms of heartburn, chest pain, or both. It shares features with other types of visceral pain in that it is poorly characterized and not well localized, owing to the divergence of visceral afferents. The esophagus is innervated by vagal and visceral spinal afferents, both of which are activated by noxious stimuli and convey information to specific centers within the central nervous system. Many stimuli can induce heartburn and chest pain; broadly, they can be divided into chemical stimuli (acid and others) and mechanical stimuli (distention and muscle spasm). The relationship between muscle spasm and chest pain has been an area of considerable controversy because of a poor temporal correlation between chest pain events and abnormal contractions in the esophagus. Recent studies suggest that spasm of the longitudinal muscles, rather than of circular muscle, may cause esophageal pain. Molecular mechanisms that link noxious stimuli with pain are not totally clear: the two leading contenders are vanilloid receptor 1 (VR1) and anion-sensing ion channels at the peripheral level. The role of esophageal hypersensitivity and psychiatric and psychological factors in the pathophysiology of esophageal pain remains an active area of investigation.
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