Prokinetics in Treatment of Gastric Motility Disorders

Abstract

Congenital abnormalities, postsurgical and medical conditions such as gastroparesis, gastric arrhythmias, myenteric neuropathies, functional dyspepsia and Parkinson’s diseases to name a few have the common manifestation of altered gastric movements in the form of either atony, hypo- or hypermotility. These are a result of pathological changes in the anatomical structure of the organ, the central and myenteric nervous system, interstitial cells of Cajal and the coordinated interplay between them. For example, the enhanced apoptosis of the enteric neurons and ICC, the decrease in NO synthase protein expression, the damage to the vagus nerve, and marked stromal fibrosis have been identified in the pathogenesis of gastroparesis (Grover et al. 2011; Ördög et al. 2009; Zaráte et al. 2003; Chen et al. 2003; Gibbons et al. 2009; Lin et al. 2010; Badyánszki and Bódi 2012; Harberson et al. 2010; Kim et al. 2012; Stevens et al. 2013); truncal and/or selective vagotomy, antrectomy, pyloroplasty and Roux-en-Y reconstruction, as well as partial gastrectomy (Bilroth I and II procedures) have been attributed to the development of postsurgical dysmotility and dumping syndrome (Dong et al. 2006); degenerative dysplasia and paraneoplastic syndromes associated with inflammatory neuropathic abnormalities have been shown to play a role in hypomotility (Di Nardo et al. 2008; De Giorgio et al. 2000; Yarandi and Srinivasan 2014); cholinergic downregulation of ICC-IM and irregular initiation, aberrant conduction, and low amplitude electrical activity in SIP could contribute to gastric arrhythmogenesis (O’Grady and Abell 2015); peptic ulcer and indomethacin could lead to hypermotility (Liebermann-Meffert et al. 1982; Takeuchi et al. 1990).

Each problem that I solved became a rule which served afterwards to solve other problems.

Rene Descartes