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Handbook of Electrogastrography$
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Kenneth L. Koch and Robert M. Stern

Print publication date: 2003

Print ISBN-13: 9780195147889

Published to Oxford Scholarship Online: November 2020

DOI: 10.1093/oso/9780195147889.001.0001

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PRINTED FROM OXFORD SCHOLARSHIP ONLINE (oxford.universitypressscholarship.com). (c) Copyright Oxford University Press, 2021. All Rights Reserved. An individual user may print out a PDF of a single chapter of a monograph in OSO for personal use. date: 17 June 2021

Tachygastrias

Tachygastrias

Chapter:
(p.149) 7 Tachygastrias
Source:
Handbook of Electrogastrography
Author(s):

Kenneth L. Koch

Robert M. Stern

Publisher:
Oxford University Press
DOI:10.1093/oso/9780195147889.003.0011

Gastric dysrhythmias are abnormal myoelectrical signals originating from the stomach. As recorded from cutaneous or serosal electrodes, bradygastrias range from 0 to 2.5 cycles per minute (cpm). Bradygastrias and mixed gastric dysrhythmias are reviewed in detail in Chapter 8. Tachygastrias range from 3.75 to l0.0cpm. The normal duodenal pacesetter potential ranges from 12 to 14 cpm. In this chapter, tachygastrias are reviewed in detail. Multiple metabolic mechanisms and neural-hormonal pathways influence gastric myoelectrical activity. The normal activities of enteric neurons, smooth muscle, hormones, and extrinsic nerves influence the ongoing activity of the interstitial cells of Cajal (ICCs), the pacemaker cells of the stomach. In healthy subjects, the frequency of gastric myoelectrical activity may vary from approximately 2.5 to 3.7cpm, depending on specific circumstances or provocative tests (Fig. 7.1). Specific diseases and disorders, with their specific pathophysiologies, may adversely affect gastric myoelectrical activity and are associated with gastric dysrhythmias. For example, many patients with type I and II diabetes have gastric dysrhythmias, and in healthy subjects, hyperglycemia itself produces gastric dysrhythmias. Gastric dysrhythmias occur when the ICCs are damaged or dysfunctional or when enteric neurons, circular smooth muscle cells (and perhaps longitudinal muscle activity), and extrinsic nerve activity from the parasympathetic and sympathetic nervous system input to the stomach are abnormal. Endocrine, neurocrine, and paracrine activities may also affect interstitial cells, enteric neurons, and smooth muscle and thereby affect gastric myoelectrical rhythms,21 shifting electrical activity to bradygastrias (0-2.5cpm) or tachygastrias (3.7- l0.0cpm) as shown in Figure 7.1. All of these influences interact to maintain normal gastric myoelectrical activity during baseline periods and in response to meals or other provocative stimuli. Stimuli that provoke stomach neuromuscular activity range from motion and the illusion of motion to emotionally challenging situations (disgust, anger) to the cephalic phase of digestion (vagal activation in the presence of appetizing food) to the relaxation, contraction, and coordination of stomach neuromuscular responses during and after the ingestion of a wide variety of solid and liquid foodstuffs. Thus, there are many gut-brain and brain-gut interactions to consider when evaluating gastric myoelectrical events during EGG recordings at baseline and after provocative stimuli.

Keywords:   Eugastria, Fourier transform (FT), Harmonics, Nervous system, Tachygastria(s), Uncoupling, Vagus nerve

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