The relationship 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 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.
Normally, ingestion of a meal induces a relaxation of the proximal stomach to accommodate the meal volume, and the magnitude of the relaxation is regulated by a complex net of reflexes.90,91 Hence, this partial relaxation prevents wall tension increments and symptoms, but the residual contraction of the proximal stomach still gently forces gastric content distally into the antrum and initiates gastric emptying. As the relaxatory input decreases, the proximal stomach regains tone and emptying progresses. A gastric hyporeactivity to relaxatory reflexes would predictably result in a defective volume accommodation of the proximal stomach and antral overload. In patients with functional dyspepsia, gastric tone and compliance are normal during fasting.25,53,92,93 However, the reactivity of the stomach to regulatory reflexes is abnormal, and the proximal stomach does not relax properly in response to reflexes arising from the antrum and the small intestine.53,94,95 Consequently, accommodation of the proximal stomach to a meal is impaired,92,93,96 which results in antral overload.97,98 Antral distension may release symptoms in these patients, because this area is hypersensitive to increases in wall tension.94 Furthermore, some experimental data indicate that increased intragastric pressure after a meal, simulating a defective gastric accommodation, produces dyspeptic-type symptoms without disturbing gastric emptying,90 a condition that resembles most patients with functional dyspepsia.17 Hence, it is plausible that the gastric hyporeflexia exacerbates the poor tolerance of dyspeptics to intragastric volumes, and thus, contributes to generation of clinical symptoms in the absence of major motor dysfunctions. Some data further suggest that specific symptoms, such as early satiety and postprandial epigastric pain, may be related to impaired accommodation.92,93
It has been reported that rectal hypersensitivity in IBS patients is associated with motor hyperactivity in response to gut stimuli.21 Again, both hypersensitivity and hyperreactivity could contribute to perception of rectal tenesmus and faecal urgency, which is a common symptom in these patients. Recent studies using a gas challenge test further substantiated the role of combined sensory–reflex disturbances in IBS. Whereas healthy subjects propulse and evacuate as much gas as infused into the jejunum, IBS patients have a poor tolerance to gas loads, and develop gas retention and abdominal symptoms.99,100 Gas transit is normally regulated by gut reflexes, and these control mechanisms are altered in IBS patients.101,102 Whether or not intestinal gas is a real problem in IBS remains unclear,103 but the important contribution of the gas challenge studies is the demonstration of abnormal control of gut motility in these patients, which, together with increased gut sensitivity, may produce their symptoms. These data together suggest that altered reflex activity and altered conscious perception of gut stimuli may combine to different degrees in patients with various functional gut syndromes, and their interaction may explain the origin of clinical symptoms.