Our understanding of the sequence of physiological events that leads to the perception of a gastrointestinal sensation remains limited. What is it that determines whether acid in the oesophagus results in the sensation of heartburn? Why is it that some patients with extensive gastrointestinal inflammation are asymptomatic while others with functional gastrointestinal disorders report severe symptoms in the absence of any apparent biomedical abnormality?

These are questions that we are still some way from adequately addressing. For many years, researchers have attempted to design experiments with the aim of identifying robust biological markers of gastrointestinal pain hypersensitivity.^1,2 Ultimately, the sensitivity and specificity of such approaches, which predominantly rely on subjective reporting of symptomatic episodes, have been generally poor.^3,4 Moreover, even if such provocation tests produce a “positive” result, these data still reveal little about the underlying pathophysiology of the condition.

The primary reason that sensory testing alone is not the answer to solving these clinical conundrums is that this type of approach limits us to examining the gastrointestinal tract in isolation. However, there is a body of evidence which dates back more than a century that tells us that sensory information arising from the gastrointestinal tract comprises one component of a complex neurobehavioral system involved in homeostasis, pain, and emotional-motivational processes.^5,6 Therefore, it is clear that new approaches are needed if progress is to be made in this field.

NEUROPHYSIOLOGY AND BRAIN-GUT SIGNALLING

In the past 10–15 years, gastrointestinal researchers have turned to their neuroscience colleagues in order to develop the investigative tools needed to study brain-gut signalling in more detail.⁷ Neurophysiologists have used evoked potentials (EP) to study somatosensory, visual, auditory, and pain pathways for over half …