论文部分内容阅读
Background &Aims: Esophageal hypersensitivity is thought to be important in the generation and maintenance of symptoms in noncardiac chest pain (NCCP). In this study, we explored the neurophysiologic basis of esophageal hypersensitivity in a cohort of NCCP patients. Methods: We studied 12 healthy controls (9 women; mean age, 37.1 ±8.7 y) and 32 NCCP patients (23 women; mean age, 47.2 ±10 y). All had esophageal manometry, esophageal evoked potentials to electrical stimulation, and NCCP patients had 24-hour ambulatory pH testing. Results: The NCCP patients had reduced pain thresholds (PT) (72.1 ±19.4 vs 54.2 ±23.6, P = .02) and increased P1 latencies (P1 = 105.5 ±11.1 vs 118.1 ±23.4, P = .02). Subanalysis showed that the NCCP group could be divided into 3 distinct phenotypic classifications. Group 1 had reduced pain thresholds in conjunction with normal/reduced latency P1 latencies (n = 9). Group 2 had reduced pain thresholds in conjunction with increased (> 2.5 SD) P1 latencies (n = 7), and group 3 had normal pain thresholds in conjunction with either normal (n = 10) or increased (> 2.5 SD, n = 3) P1 latencies. Conclusions: Normal esophageal evoked potential latencies with reduced PT, as seen in group 1 patients, is indicative of enhanced afferent transmission and therefore increased esophageal afferent pathway sensitivity. Increased esophageal evoked potential latencies with reduced PT in group 2 patients implies normal afferent transmission to the cortex but heightened secondary cortical processing of this information, most likely owing to psychologic factors such as hypervigilance. This study shows that NCCP patients with esophageal hypersensitivity may be subclassified into distinct phenotypic subclasses based on sensory responsiveness and objective neurophysiologic profiles.
Background & Aims: Esophageal hypersensitivity is thought to be important in the generation and maintenance of symptoms in noncardiac chest pain (NCCP). In this study, we explored the neurophysiologic basis of esophageal hypersensitivity in a cohort of NCCP patients. Methods: We studied 12 healthy All had esophageal manometry, esophageal evoked potentials to electrical stimulation, and NCCP patients had 24-hour ambulatory (9 women; mean age, 37.1 ± 8.7 y) and 32 NCCP patients Results: The NCCP patients had reduced pain thresholds (PT) (72.1 ± 19.4 vs 54.2 ± 23.6, P = .02) and increased Pl latencies (P1 = 105.5 ± 11.1 vs 118.1 ± 23.4, P = .02). Group 1 had reduced pain thresholds in conjunction with normal / reduced latency P1 latencies (n = 9). Group 2 had reduced pain thresholds in conjunction with increased (> 2.5 SD ) P1 latencies (n = 7), and group 3 had normal pain thresholds in conjunction with either normal (n = 10) or increased (> 2.5 SD, n = 3) P1 latencies. Conclusions: Normal esophageal evoked potential latencies with reduced PT, as seen in group 1 patients, is indicative of increased afferent transmission and therefore increased esophageal afferent pathway sensitivity. Increased esophageal evoked potential latencies with reduced PT in group 2 patients implies normal afferent transmission to the cortex but heightened secondary cortical processing of this information, most likely due to psychologic Factors such as hypervigilance. This study shows that NCCP patients with esophageal hypersensitivity may be subclassified into distinct phenotypic subclasses based on sensory responsiveness and objective neurophysiologic profiles.