Abstract

Ingestion and digestion of food as well as expulsion of residual material from our gastrointestinal tract requires normal propulsive, i.e. motor, function. Hypomotility refers to inherited or acquired changes that come with decreased contractile forces or slower transit. It not only often causes symptoms but also may compromise nutritional status or lead to other complications. While severe forms, such as pseudo-obstruction or ileus, may have a tremendous functional impact, the less severe forms of hypomotility may well be more relevant, as they contribute to common disorders, such as functional dyspepsia, gastroparesis, chronic constipation, and irritable bowel syndrome (IBS). Clinical testing can identify changes in contractile activity, defined by lower amplitudes or abnormal patterns, and the related effects on transit. However, such biomarkers show a limited correlation with overall symptom severity as experienced by patients. Similarly, targeting hypomotility with pharmacological interventions often alters gut motor function but does not consistently improve symptoms. Novel diagnostic approaches may change this apparent paradox and enable us to obtain more comprehensive information by integrating data on electrical activity, mechanical forces, patterns, wall stiffness, and motions with information of the flow of luminal contents. New drugs with more selective effects or more specific delivery may improve benefits and limit adverse effects. Lastly, the complex regulation of gastrointestinal motility involves the brain-gut axis as a reciprocal pathway for afferent and efferent signaling. Considering the role of visceral input in emotion and the effects of emotion on visceral activity, understanding and managing hypomotility disorders requires an integrative approach based on the mind-body continuum or biopsychosocial model of diseases.

Highlights

  • Normal gastrointestinal (GI) function requires a system capable of adjusting to, at times, rapidly or dramatically shifting volumes due to food intake, fragmentation of larger ingested particles, and mixing and movement of chyme to bring nutrients to the absorptive sites and to expel residual materials from the gut. Many of these tasks depend on forces generated by the smooth muscle cells found in the mammalian gut

  • Consequences of hypomotility Considering the important role of normal GI motility in assuring entry into and transit through the gut with mixing and fragmentation facilitating absorption, hypomotility should compromise normal GI function and nutritional status and/or cause symptoms

  • Consistent with these theoretical considerations and the previously mentioned role of medications as a cause of motor dysfunction, blunting contractile amplitudes through antimuscarinics, opioids, and L-type calcium channel blockers delays orocecal transit and alters meal-induced changes in colonic activity, likely contributing to the development of constipation that is often seen with these agents[32,33,34,35,36]

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Summary

Introduction

Normal gastrointestinal (GI) function requires a system capable of adjusting to, at times, rapidly or dramatically shifting volumes due to food intake, fragmentation of larger ingested particles, and mixing and movement of chyme to bring nutrients to the absorptive sites and to expel residual materials from the gut. Consequences of hypomotility Considering the important role of normal GI motility in assuring entry into and transit through the gut with mixing and fragmentation facilitating absorption, hypomotility should compromise normal GI function and nutritional status and/or cause symptoms Consistent with these theoretical considerations and the previously mentioned role of medications as a cause of motor dysfunction, blunting contractile amplitudes through antimuscarinics, opioids, and L-type calcium channel blockers delays orocecal transit and alters meal-induced changes in colonic activity, likely contributing to the development of constipation that is often seen with these agents[32,33,34,35,36]. Grant information The author(s) declared that no grants were involved in supporting this work

17. Sjogren RW
64. Bielefeldt K
99. Lisi DM
PubMed Abstract
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