Functional chest pain of esophageal origin: Hyperalgesia or motor dysfunction

OBJECTIVE: Many patients with functional (noncardiac) chest pain exhibit bo th hypersensitivity and motor dysfunction of the esophageal wall. We aimed to determine whether the sensory or motor dysfunction plays an important ro le in the pathogenesis of chest pain. METHODS: We performed graded balloon distentions of the esophagus using imp edance planimetry in 16 consecutive patients with chest pain and otherwise normal cardiac and esophageal evaluations and in 13 healthy controls. In th ose patients who experienced chest pain with balloon distention, the test w as repeated after atropine was given. Sensory and biomechanical parameters were measured. RESULTS: Balloon distention reproduced typical chest pain in 13/16 patients (81%) and at lower (p < 0.01) sensory thresholds than controls. Pain was r eproduced in all 13 patients and at lower (p < 0.05) sensory thresholds aft er atropine. Also, after atropine, the esophageal cross-sectional area and wall tension increased (p < 0.05), the tension/strain association shifted t o the right (p < 0.05), and reactivity decreased (p < 0.002) relative to re sults before atropine or in healthy controls (i.e., the esophageal wall rel axed and became more deformable). CONCLUSIONS: Even after relaxing the esophageal wall, most patients experie nced chest pain and at lower sensory thresholds. Hence, hyperalgesia rather than motor dysfunction appears to be the predominant mechanism for functio nal chest pain of esophageal origin. (Am J Gastroenterol 2001;96:2584-2589. (C) 2001 by Am. Coll. of Gastroenterology).