Autonomic Visceral Neuropathy and Gastrointestinal Disorders

Abstract

The brain-gut axis is a bidirectional nexus of the sensory input from the gastrointestinal (GI) tract and efferent pathways, which is involved in secretion of digestive hormones, homeostatic regulation and gut motility. This axis comprises among others the autonomic nervous system (ANS), comprising the enteric nervous system (ENS) and parasympathetic and sympathetic branches, which have a delicate regulatory interaction. Therefore, the ANS has an essential role, and any dysfunction leads to impaired mediation of visceral regulation. Consequently, damage to the ANS such as development of diabetic autonomic neuropathy (DAN) is one of the most burdensome complications to diabetes, yet frequently under-diagnosed. These complications cause symptoms in the GI tract such as nausea, vomiting, diarrhoea and constipation; see Fig. 54.1. It is difficult to diagnose DAN, but it may be defined as impaired functions of the involved nerves controlling the involuntary body functions such as the cardiovascular, urinary, pulmonary and digestive systems [1]. Cardiac autonomic neuropathy is a measureable impaired regulation of the heart function, leading to dysrhythmias such as atrial fibrillation, tachycardia and even cardiac arrest [2]. Patients with cardiac autonomic neuropathy develop an impaired adaptability of the heart rate, assessed as reduced heart rate variability [3]; see Chap. 59 for further elaboration. In this chapter we focus upon autonomic gastrointestinal neuropathy in patients with diabetes, explaining the underlying pathophysiology and the symptomatology in the GI tract.