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Visceral hypersensitivity is currently the holy grail....it is widely regarded as the reason for the development of functional gastrointestinal diseases, including functional dyspepsia and irritable bowel syndrome.1 Although the field has advanced considerably in the past decade, it is necessary to take stock and realistically appraise our current understanding. Identifying issues of controversy will help address the directions or priorities to advance this field in the future. Thus our objectives are to review the current understanding of the neuroanatomy and physiology of gut sensation, briefly review examples of the relationship between symptoms and sensorimotor dysfunction, and discuss controversies and speculations requiring more thorough study. In pursuing this discussion, we have drawn on experience and data from several regions of the gut as work in a single region does not provide the comprehensive or broad perspectives necessary.
Neuroanatomy and physiology of sensation
Enteroendocrine cells in the lining of the gut serve as chemical and mechanical transducers for local reflexes (for example, peristalsis) or initiation of afferent projections to the central nervous system.1 ,2 As with somatic sensation, gut afferent signals reach conscious perception through a three neurone chain.2 The first order neurone, whose cell body is in the dorsal root ganglion, terminates in the dorsal column laminae of the spinal cord (fig 1). En passant fibres project to noradrenergic neurones in prevertebral ganglia, and this reflex centre results in modulation of viscus functions, including motility. Somatic and visceral afferents converge on dorsal horn neurones and result in viscerosomatic projection or referred pain. Descending modulatory fibres (serotonergic, adrenergic, and possibly others) from brain stem centres such as the periaqueductal grey alter the sensitivity of the dorsal horn neurones and thus serve to centrally control the intensity of perception during visceral stimulation (fig1).1