SUMMARY The relationship between disturbed upper gastro-intestinal motility and symptoms of heartburn and dyspepsia varies. For example, in some symptomatic patients abnormal motor events are not detected, whereas, conversely, impaired motor patterns may be recorded in patients who are asymptomatic. Nociceptive visceral afferents arising in the gut transmit peripheral sensations to the brain. It has been postulated that variations in sensory afferent activity are responsible for the inconsistent expression of disturbed upper gastrointestinal motility. Several studies have demonstrated that patients with so-called functional symptoms, which appear to arise from normal gut regions, exhibit a lower perception threshold to stimuli that distend the gut. Such visceral hypersensitivity could explain the occurrence of symptoms in the absence of demonstrable physiological or morphological abnormalities. Evidence that variations in visceral sensory afferent activity constitute an important disease mechanism is not conclusive. In certain conditions such as non-cardiac chest pain and functional dyspepsia, visceral hypersensitivity provides a useful hypothetical framework. Not only has this framework established a basis for previously unexplained symptoms, but perhaps more importantly it has stimulated research to develop novel pharmacological agents to modulate nociception. The challenge is now to establish putative pathogenetic links between aberrant sensory activity and disturbed upper gastrointestinal motility, and also to locate the neural abnormalities along the gut-brain axis.