The relation between the sensory disturbances detected in the laboratory in patients with functional gut disorders and their clinical complaints is still unclear. Sensitivity tests do not allow a clear discrimination between patients and healthy controls, which indicates that altered perception per se may not entirely explain the symptoms. Conceivably, real life situations involve a larger number of stimuli than the testing conditions, and may recruit a wider pool of altered responses, including both altered perception and reflexes. Indeed, an important question in the pathophy-siology of functional gut disorders is whether the neural dysfunction affects exclusively sensory pathways or whether reflex pathways involved in the regulation of motility are also affected.
It has been shown that dyspeptic patients with gastric hypersensitivity also have impaired gastric reflexes (14,48). Physiologically, duodenal distension releases a vagal reflex that induces gastric relaxation. In a group of dyspeptic patients with normal duodenal sensitivity and compliance, duodenal distension induced impaired relaxation of the stomach. It has been suggested that vagal function is impaired in dyspepsia (60), and this could explain the defective duodenogastric reflex. Other studies have shown that IBS patients also display abnormal reflex responses of the gut (40).
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Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.