Esophageal perception and noncardiac chest pain.
Symptoms arising from the esophagus are produced generally in one of two ways: through stimulation of chemosensitive-nociceptors (eg, through excess esophageal exposure to refluxed gastric acid or the resulting inflammation arising in acid-damaged tissue) or through stimulation of mechanosensitive nociceptors (eg, through repeated deformation or distension of the esophageal wall resulting from peristaltic or lower esophageal sphincter dysfunction). These symptoms are usually attributed in most patients to such well recognized conditions as reflux esophagitis, achalasia,etc. that subsequently result in the delivery of specific and effective treatment.However, a subset of patients exists in which the etiology of "similar-sounding symptoms" remains obscure and their responses to standard specific treatments poor. Now recognized as among this group of patients are those with visceral hypersensitivity. Visceral hypersensitivity is not itself a disease but a definable aberrant sensory response (allodynia or hyper-algesia) to end-organ stimulation. Such an aberrant sensory response is neither specific for nor limited to the esophagus, and the etiopathogenesis for its development within this organ is unknown. Nonetheless, esophageal symptoms as a manifestation of visceral hypersensitivity are increasingly recognized and worthy of attention because they identify a disorder that responds to treatment aimed at the end organ's nociceptors or their neuroanatomic pathways within the CNS.
Orlando
Roy C
RC
Tulane University Medical School, 1430 Tulane Avenue, New Orleans, LA 70112-2699, USA. rorland@tmcpop.tmc.tulane.edu
D002637:Chest Pain / Q000209:etiology / Q000503:physiopathology*; D004947:Esophagus / Q000294:innervation* / Q000503:physiopathology*; D006801:Humans; D006930:Hyperalgesia / Q000503:physiopathology; D009619:Nociceptors / Q000503:physiopathology; D010465:Perception / Q000502:physiology*; D014781:Viscera / Q000503:physiopathology