It is now increasingly recognized that the brain plays an important role in modulating gut function. For example, alterations in emotional state can lead to disturbed gastrointestinal symptoms such as diarrhea, dyspepsia and even abdominal pain. Furthermore, alterations in gastrointestinal motility have been described after lesions to the central nervous system, for instance symptoms such as dysphagia after stroke, anal incontinence in cerebrovascular disease and multiple sclerosis and even alterations in small bowel motility following brainstem damage.

In this chapter I will describe current knowledge of human brain–gut interactions both in health and disease in relation to three specific areas: mechanisms of swallowing, mechanisms of anal continence and mechanisms of visceral perception. Particularly, I aim to bring the reader up to date with some newer concepts in relation to the neurophysiology of human cortical swallowing and anal motor function as well as touching on the newer areas of visceral sensitivity and functional bowel disorders. Finally, I will look at future directions specifically looking at potential therapies which may help in disease states that disrupt the human brain–gut axis.

Basic anatomy and physiology of the brain–gut axis

The enteric nervous system

The human brain–gut axis is a complex sensory motor system which has both extrinsic and intrinsic neural elements. At the intrinsic level the enteric nervous system represents an integrative system of neurons and interneurons with structural complexity and functional heterogenicity similar to that of the brain and spinal cord (Gershon, 1981). The principal role of the enteric nervous system (ENS) is to control and coordinate gut functions, including motility, secretion, mucosal transport and blood flow as necessary for normal digestive processes. These functions are mediated by the ENS via motor neurons located within enteric ganglia which form the final common pathway to the effector cells of the GI tract. The ENS houses a matrix of differing cell populations, which each play a role in maintaining intrinsic gastrointestinal sensory motor activity and include mast cells, smooth muscle cells, interstitial cells of Cajal, enteric enteroenteric cells and motor neurons. These also are subject to the release of various neurotransmitters, growth factors and cytokines which result in an enteric micro-environment that controls GI motility in an autonomous manner.