By Ronnie Fass
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Fortyseven (50%) were GERD positive, and 47 (50%) were GERD negative. Only nine patients (19%) in the GERD-positive group and ﬁve (11%) in the GERD-negative group had a positive SI. The authors concluded that a positive SI is relatively uncommon in NCCP patients, regardless of whether GERD is present or absent. This is primarily due to lack of chest pain symptoms during the pH test. In North American studies, most patients with GERD-related NCCP have typical reﬂux symptoms in addition to their chest pain .
It is therefore not surprising why the localization of NCCP to esophagus, heart, trachea, bronchi, or lungs may not be possible in many situations . Esophageal pain modulation Esophageal nociceptor impulses transmitted to the brain eventually ascend to and activate neurons of the anterior cingulate cortex, somatosensory cortex, and insula (Fig. 3) [8–10]. From these areas, aﬀerent pain-inhibitory impulses are transmitted through descending ﬁbers. These impulses, coupled with the descending pain-inhibitory impulses arising from neurons within the periventricular and periaqueductal gray matter, pons, and medullary nuclei, constitute the endorphin-mediated analgesia system (EMAS).
The role that altered autonomic function plays in the pathogenesis of NCCP remains speculative. In most cases in which central and autonomic factors are involved, it is the eﬀect of the former that most likely leads to the occurrence of the latter . A study by Fass et al  demonstrated that chest pain and heartburn may be provoked in normal subjects and in GERD patients during esophageal balloon distention of the esophagus. Volume thresholds for heartburn and chest pain in the proximal or distal esophagus were similar; additionally, they did not diﬀer signiﬁcantly at each esophageal location or between locations.