Shaker Reza
Division of Gastroenterology and Hepatology, Department of Medicine, MCW Digestive Disease Center, Medical College of Wisconsin, Milwaukee, WI 53223, USA.
J Clin Gastroenterol. 2007 Jul;41 Suppl 2:S160-2. doi: 10.1097/MCG.0b013e318042d660.
Emerging information on physiology and pathophysiology of gastroesophageal reflux disease raises the question of whether our thought process should go beyond mucosal injury and consider 2 parallel tracks that may cross each other at some time, but at other times they may indeed remain parallel, that is, neurally mediated effects of reflux events beyond the esophageal wall and inflammation mediated effect of reflux within the esophageal wall. In this process, intraesophageal events with and without causing mucosal injury may induce changes in the neural function on a temporary or long-term basis resulting in symptoms at different organs and various levels not completely in lock-step with esophageal mucosal injury. Emerging data also suggest the influence of liminal and subliminal esophageal acid exposure on cerebral cortical networks involved in motor function such as swallowing in addition to its effect on sensory centers. These observations suggest the existence of a more extensive influence of esophageal sensory input to the cerebral cortical processing mechanisms than previously thought and may provide new avenues for research in pathophysiology of reflux disease.
