Introduction
A normal gastrointestinal function requires the capability of adjusting rapidly or dramatically shifting volumes to food intake, mixing and movement of chyme, and expelling the residuals from the gut. This entire task depends on the forces that are formed by the smooth muscle cells in the gut. Abnormalities of the gastrointestinal tract either acquired or inherited or induced by medications, have a significant impact on nutrient absorption and fecal output. Hypomotility treatment is more focused on clinical features rather than the physiological and molecular mechanisms.
What Is Hypomotility Disorder?
Hypomotility disorder is an inherited or acquired state where changes occur with decreased contractile forces. Along with its symptoms, it also compromises the nutritional status of the individual with other associated complications.
Mechanism of Hypomotility:
The role of muscle activity and disorders of muscle function like inherited abnormalities of contractile protein can contribute to hypomotility development. Detailed physiological and molecular effects potentially lead to more complications in addition to these individuals with acquired changes in ion channels, contractile proteins, and other molecules showing diabetic gastroparesis.
What Causes Hypomotility Disorder?
The following are the causes associated with hypomotility disorder:
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Acquired or inherited connective tissue disorder manifests gastrointestinal motility. This connective tissue provides scaffolding for muscle cells. Systemic conditions like systemic sclerosis or inherited conditions like Marfan or Ehlers-Danlos syndrome can highlight more importance of the condition.
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Less severe phenotypes like hypermotility syndrome are more commonly associated with a high prevalence of gastrointestinal disorders.
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Innervation plays a key role in the regulation of gastrointestinal motility. The enteric and intrinsic nervous system forms the myenteric plexus, with ganglia located between the longitudinal and circular portions of the muscle layer.
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Inherited aganglionosis of the rectum or acquired loss of ganglion cells may delay or even a deadly pattern of activity and block the passage of luminal contents.
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Rarely performed surgeries like vagotomy (surgical removal of a part of the vagus nerve to remove gastric secretions). Unintentional vagal injury during an autonomic neuropathy or foregut surgery can contribute to motility disorders, like dyspeptic symptoms, after antireflux surgery.
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Hypomotility disorders can also be affected by the use of medications. Agents like over-the-counter drugs, antihistamines or Loperamide, prescription medications like poods, nitrates, anticholinergic substances, antidepressants, calcium channel blockers, antiemetics, and antipsychotic drugs may be common culprits.
What Are the Signs and Symptoms of Motility Disorder?
Most frequent hypomotility reveals symptoms similar to that of gastroesophageal reflux disease (GERD) and dysphagia (difficulty in swallowing food). The other symptoms include:
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Regurgitation.
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Chest pain.
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Belching or burping.
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Difficulty in swallowing food.
Esophageal hypomotility is more prevalent in smooth muscle disorders like scleroderma and connective tissue disorders. Phosphodiesterase inhibitors, non-benzodiazepine antispasmodic agents, and calcium channel blockers reduce esophageal contraction vigor and have to be avoided in individuals with hypomotility disorders.
How Is the Diagnosis Made for Hypomotility Disorder?
The diagnosis of hypomotility disorder is made by many methods, including:
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Manometric studies of the esophagus, stomach, and small intestine in which flexible catheters are used and positioned at different levels of the upper gastrointestinal tract. Recording the contractions of the muscles, coordination, and strength is done and further characterized.
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Manometric studies of the colon help in identifying muscle strength and coordination. It is particularly applicable in individuals with severe constipation.
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Gastrointestinal transit is a non-invasive method, possibly measured by scintigraphy or radiopaque marker techniques and this material leaves the stomach. These tests give an overview of the functions of the entire gastrointestinal tract.
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Anorectal manometry or balloon expulsion which is the final step of rectal evacuation. Complementing approaches are muscle coordination, neural innervation, pelvic floor function, anal sphincters and electromyography of pelvic muscles, assessment of evacuation with state-of-the-art magnetic resonance imaging (MRI) techniques, and defecating proctography.
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Assessment of autonomic denervation and innervation.
What Is the Treatment for Hypomotility Disorder?
The treatment of hypomotility disorder includes pharmacological interventions to improve esophageal smooth muscle contractility. Lifestyle modifications, diet, and GERD management remain the cornerstone of the therapy. Acid-suppressive medications are used to improve esophageal motor function by suppressing acid reflux-related symptoms. Proton pump inhibitors (PPI) therapy and prokinetic agents are used in individuals with GERD and esophageal motility to enhance clearance of the reflux contents.
The medical intervention treatment provided are:
1. Dopamine 2 Receptor Blockers: Drugs like Metoclopramide and Domperidone are used that cause significant increases in lower esophageal sphincter (LES) pressure and are also associated with severe adverse effects.
2. Serotonin Modulating Agents:
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Mosapride: Mosapride is more effective than a placebo in decreasing reflux episodes. High doses help in improving motor function and acid reflux.
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Buspirone: It is an anxiolytic drug, partial agonist, as well as antagonist for dopamine D2 receptors.
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Prucalopride: It is an enterokinetic agent. A single dose of Prucalopride enhances primary and secondary peristalsis.
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Sumatriptan: It is a 5-HT1D receptor agonist used to treat migraine. In hypomotility individuals with dysphagia and chest pain on manometry, a subcutaneous injection of Sumatriptan is given.
3. Motilin Receptor Agonists:
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Erythromycin: It is an old macrolide antibiotic with prokinetic properties. It helps in activating motilin receptors on smooth muscle fibers. Oral Erythromycin is effective in improving esophageal motility in diabetic individuals. Though it has many benefits, it is also accompanied by disadvantages like tachyphylaxis, cardiac dysrhythmia, and microbial resistance.
4. Muscarinic Receptor Modulating Agents:
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Bethanechol: It is a direct-acting muscarinic receptor agonist used as a promotility agent in the treatment of GERD. They mimic the effect of acetylcholine directly and increase lower esophageal sphincter (LES) pressure and improve peristaltic pressure. More than a quarter of individuals discontinue treatment due to intolerance to cholinergic side effects, like somnolence, nausea, and increased urinary frequency.
Conclusion
Novel diagnostic approaches may change this apparent paradox and enable more comprehensive information on mechanical forces, electric activity, wall stiffness, motions, and pattern of the flow of luminal contents. New drugs with more effects that are selective and specific delivery can improve the benefits and restrict adverse effects. Complex regulation of motility disorders involves the brain-gut axis as a reciprocal pathway for efferent and afferent signaling. Also, targeting hypomotility with medicinal intervention can alter gut motor function but does not consistently improve symptoms.
