Gastrointestinal Motor Abnormalities Research Articles

Mechanism, Pathophysiology and Herbal Management-A Review on Irritable Bowel Syndrome

Background: The global distribution of IBS is surprisingly uniform, affecting men and women of all ages. Its deep-rooted character, symptoms that fluctuate from moderate to extreme, have several detrimental effects on the sufferer's standard of living; consequently, proper treatment of these patients is necessary. The etiology of IBS is unknown. Although several explanations were also proposed, the specific etiology of irritable bowel syndrome remains unknown. Clinical trials using stabilized therapies and new active medications have shown symptom reduction over placebo. Objective: IBS has long been linked to visceral sensitivity and gastrointestinal motor abnormalities. The pathophysiology of IBS appears to be multifaceted. However, several of the following elements are vital in forming IBS. This paper aims to provide a complete, scientific proof assessment of the prognosis, pathogenesis, and therapy choices to assist clinicians in successfully treating their patients. Method: The report's information was compiled by combining numerous review articles and research papers from multiple sources, including Hindawi, Elsevier, NCBI [National Centre for Biotechnology Information], and Research Gate, from 1981 to 2021, using keywords such as IBS, Brain-gut axis, postinfectious IBS, Microbiota, low-grade inflammation, and so on. Conclusion: The acute symptom influences the selection of medical techniques and therapy (IBS with diarrhoea, IBS with constipation, or mixed IBS). Current research demonstrates both pharmaceutical and non-pharmaceutical treatment has a positive impact (in comparison to a placebo) on irritable bowel syndrome (IBS) problems, discomfort relief, and improved health status.

Evaluating Action of Homoeopathy by using Gastrointestinal Symptom Rating Scale (GSRS) in Gastro Intestinal Disorders- A Case Series

Gastrointestinal disorders are the one of the attention seeking conditions in day to day life which affects 10- 15% of total population. Gastrointestinal Symptom Rating Scale (GSRS) is a tool used to measure the severity and gradation of dyspepsia. Infections, gastrointestinal motor abnormalities, brain-gut interaction, visceral hypersensitivity, inflammation, central neural dysregulation, altered gut flora are main reasons for gastrointestinal disorders. Common presentations of gastro intestinal disorders are nausea, vomiting, heart burn, dyspepsia, pain abdomen, flatulency, bowel movement alteration (constipation, diarrhoea) and bleeding per rectum.Homoeopathy is asystem of medicine which is based on “Similia Similibus Curentur” and with the combination of constitutional prescription and law of similars the normal harmonious health will be maintained in all the patients.

Toll-Like Receptor 4 Modulates Small Intestine Neuromuscular Function through Nitrergic and Purinergic Pathways.

Objective: Toll-like receptors (TLRs) play a pivotal role in the homeostatic microflora-host crosstalk. TLR4-mediated modulation of both motility and enteric neuronal survival has been reported mainly for colon with limited information on the role of TLR4 in tuning structural and functional integrity of enteric nervous system (ENS) and in controlling small bowel motility.Methods: Male TLR4 knockout (TLR4-/-, 9 ± 1 weeks old) and sex- and age-matched wild-type (WT) C57BL/6J mice were used for the experiments. Alterations in ENS morphology and neurochemical code were assessed by immunohistochemistry whereas neuromuscular function was evaluated by isometric mechanical activity of ileal preparations following receptor and non-receptor-mediated stimuli and by gastrointestinal transit.Results: The absence of TLR4 induced gliosis and reduced the total number of neurons, mainly nNOS+ neurons, in ileal myenteric plexus. Furthermore, a lower cholinergic excitatory response with an increased inhibitory neurotransmission was found together with a delayed gastrointestinal transit. These changes were dependent on increased ileal non-adrenergic non-cholinergic (NANC) relaxations mediated by a complex neuronal-glia signaling constituted by P2X7 and P2Y1 receptors, and NO produced by nNOS and iNOS.Conclusion: We provide novel evidence that TLR4 signaling is involved in the fine-tuning of P2 receptors controlling ileal contractility, ENS cell distribution, and inhibitory NANC neurotransmission via the combined action of NO and adenosine-5′-triphosphate (ATP). For the first time, this study implicates TLR4 at regulating the crosstalk between glia and neurons in small intestine and helps to define its role in gastrointestinal motor abnormalities during dysbiosis.

Current Status of Translational Research on Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder. The pathophysiology of IBS is not completely understood. Genetic, immune, environmental, inflammatory, neurological and psychological factors contribute to the risk of this condition. Traditional research explored gastrointestinal motor abnormalities, central neural dysregulation, abnormal psychological features, and visceral hypersensitivity. More recent investigations consider bacterial overgrowth, abnormal serotonin pathways, altered gut flora, immune activation and mucosal inflammation. The purpose of this article is to review recent translational research concerning the pathophysiology, biomarker and genetic factors of IBS and to encourage IBS research in Korea.

Evaluation of gastrointestinal transit after infection with different loads of Strongyloides venezuelensis in rats

The aim was to correlate the gastrointestinal transit profile in rats, evaluated by a biomagnetic technique, in response to infection with different loads of Strongyloides venezuelensis. Eggs per gram, intestinal number of worms and fecundity, and also gastric emptying time, cecum arrival time, small intestinal transit time and stool weight were determined. Assessments occurred at 0 (control), 3, 6, 9, 12, 15, 18 and 21 days post infection (dpi) with three infective loads (400, 2000, and 10,000L). Gastric emptying was faster (p=0.0001) and the intestinal transit was significantly slower (p=0.001) during the infection time course. Also, linear mixed-effects models showed significantly changes in small intestinal transit after three parasite load over time. Cecum arrival was not influenced by infection time course or parasite load. As indirect effect, stool weight decreased accompanied a strong oviposition peak at 9dpi in 400L and 2000L. In several motor function instances, neuromuscular dysfunction persists after mucosal inflammation has decreased. Our approach could be very helpful to evaluate gastrointestinal motor abnormalities in vivo after parasite infection. Despite parasitological data progressively decreased after 15 dpi, small intestinal transit worse over time and according to burden.

Tissue ghrelin level and gastric emptying rate in adult patients with celiac disease

Celiac disease (CD) patients show a number of gastrointestinal motor abnormalities. Ghrelin, a gastric peptide implicated in short-term feeding control and long-term body weight regulation, has been recently considered a key regulator of gastric motility. The aim of this study was to evaluate the gastric emptying rate of solids and the density of ghrelin-immunopositive cells in adult CD patients before and at least 1 year after starting a gluten-free diet. Twenty CD patients (M 8/F 12; mean age 36 years) and 10 controls underwent endoscopy with gastric and duodenal biopsies and 13C-octanoic acid breath test to measure gastric emptying of solids. Celiac disease patients repeated the protocol at least 1 year after starting gluten-free diet. Ghrelin tissue levels were evaluated by immunohistochemistry on gastric mucosa specimens. Gastric emptying time was normal in all control subjects (t(1/2) = 89 +/- 16 min) while it was delayed in CD patients prior to gluten-free diet (t(1/2) = 252 +/- 101 min; P < 0.005). The mean number of ghrelin-positive cells/field (x 400) was 14.4 +/- 2.7 in controls and 25.3 +/- 5.7 in CD patients respectively (P < 0.0001). Gluten withdrawal was effective in normalizing gastric emptying time in all CD patients (97 +/- 14 min; P < 0.0001) and resulted in a significant reduction of the density of ghrelin-immunopositive cells (19.8 +/- 5.4; P < 0.0001). The density of ghrelin-positive cells correlated directly with the degree of duodenal damage (P < 0.001) and inversely with the body mass index of CD patients (P < 0.0001). However, in neither CD patients nor controls, a correlation between tissue ghrelin levels and gastric emptying rate was detected. In conclusion, tissue ghrelin level does not correlate with gastric emptying rate in adult CD patients and in controls.

Clinical Presentation and Patterns of Slow Transit Constipation Do Not Predict Coexistent Upper Gut Dysmotility

Slow transit constipation (STC) is associated with upper gastrointestinal tract motor abnormalities in a subset of patients. This could influence the clinical approach, particularly in those rare cases where surgical management is considered. To identify factors that predict proximal gut dysmotility in patients with STC. Esophageal and small bowel motor function were evaluated in 77 patients with STC. Severity and pattern of colonic transit delay, prevalence of a co-existent rectal evacuatory disorder, and type (if present), and duration, and onset of constipation symptoms were compared. Of the 77 patients studied, 43% exhibited altered motor function in the esophagus and/or small bowel. Frequency of defecation was lower in these patients than in those without upper gastrointestinal dysmotility (0.5 +/- 0.1 vs. 1.3 +/- 0.3 bowel movements/per week, respectively; P = 0.04). Severity and patterns of colonic transit delay and the mechanism associated with the onset of constipation symptoms or with their duration were similar in subjects with or without upper gastrointestinal tract dysmotility. Small bowel but not esophageal motor dysfunction was more frequently associated with a co-existent rectal evacuatory disorder (P = 0.01). Upper gastrointestinal tract dysmotility in patients with STC is frequent, but prediction on the basis of clinical history and characteristics of colonic transit is problematic.

Gastrointestinal motor activity associated with postoperative ileus and emesis

The gastrointestinal motor activity associated with post-operative ileus and emesis has not been fully elucidated. This study has evaluated gastric and small-bowel motility in six patients before and after cholecystectomy and in six healthy volunteers, by solid-state manometry. Nausea and vomiting were recorded post-operatively. After surgery, fasting motor abnormalities including (a) total gastric quiescence and (b) small-bowel ‘phasic-bursts’ of contractions were observed in all patients. Phasic bursts (PB) resembled phase III of the migrating motor complex (MMC) on initial visual inspection, but further analysis revealed that they were of shorter duration (3.4 ±.2 min [PB] vs 6.4 ± 0.8 min [MMC], [mean ± SEM] P < 0.01), lower contraction frequency (6.4 ± 0.1 contractions min −1 [PBj vs 10 ± 0.3 contractions min−1 [MMC] [mean ± SEM] P < 0.01) and shorter periodicity (36.4 ± 3 min [PB] vs 70.0 ± 6 min [MMC] [mean ± SEM] P < 0.01). Four patients experienced nausea during phasic burst activity. Vomiting was only observed in association with retrograde phasic-bursts, which migrated through the duodenum to the stomach. This study has shown consistent gastrointestinal motor abnormalities in the immediate post-operative state.

Enteric glial cells and their role in gastrointestinal motor abnormalities: Introducing the neuro-gliopathies

The role of enteric glial cells has somewhat changed from that of mere mechanical support elements, gluing together the various components of the enteric nervous system, to that of active participants in the complex interrelationships of the gut motor and inflammatory events. Due to their multiple functions, spanning from supporting elements in the myenteric plexuses to neurotransmitters, to neuronal homeostasis, to antigen presenting cells, this cell population has probably more intriguing abilities than previously thought. Recently, some evidence has been accumulating that shows how these cells may be involved in the pathophysiological aspects of some diseases. This review will deal with the properties of the enteric glial cells more strictly related to gastrointestinal motor function and the human pathological conditions in which these cells may play a role, suggesting the possibility of enteric neuro-gliopathies.

Reassessment of functional dyspepsia: A topic review

Dyspepsia itself is not a diagnosis but stands for a constellation of symptoms referable to the upper gastrointestinal tract. It consists of a variable combination of symptoms including abdominal pain or discomfort, postprandial fullness, abdominal bloating, early satiety, nausea, vomiting, heartburn and acid regurgitation. Patients with heartburn and acid regurgitation invariably have gastroesophageal reflux disease and should be distinguished from those with dyspepsia. There is a substantial group of patients who do not have a definite structural or biochemical cause for their symptoms and are considered to be suffering from functional dyspepsia (FD). Gastrointestinal motor abnormalities, altered visceral sensation, dysfunctional central nervous system-enteral nervous system (CNS-ENS) integration and psychosocial factors have all being identified as important pathophysiological correlates. It can be considered as a biopsychosocial disorder with dysregulation of the brain-gut axis being central in origin of disease. FD can be categorized into different subgroups based on the predominant single symptom identified by the patient. This subgroup classification can assist us in deciding the appropriate symptomatic treatment for the patient.

Gastrointestinal motility disturbances in celiac disease.

It is quite frequent to recognize celiac patients who show gastrointestinal motor abnormalities in clinical practice. In fact, in 30 to 60% of patients, physical examination and dyspeptic symptoms (epigastric discomfort, early satiety) suggest a gastrointestinal motility disorder. Consistent data are now available on the presence of a disturbed motility of the esophagus, stomach, small intestine, gallbladder, and colon of untreated celiac patients. Gastrointestinal abnormalities differ in different gastrointestinal districts. In fact, esophageal transit, gastric and gallbladder emptying, and orocecal transit time are delayed, while colonic transit is faster. These findings are related to the complex interactions among reduced absorption of food constituent (in particular, fat), neurologic alteration, and hormonal derangement. Motility disorders of the gut are also a predisposing factor in the development of small intestinal bacterial overgrowth and may contribute both to development of symptoms in some untreated celiacs and to the persistence of symptoms after gluten-free diet in some of them. All these alterations fortunately disappear after gluten-free diet, and patients return to well being status. Whatever the initial event in the pathogenesis of the celiac lesions may be, we know for certain at this time that gastrointestinal disturbances play an important role in the genesis of gastrointestinal symptoms in celiac disease and that surveillance for celiac disease in patients complaining of dysmotility-like dyspeptic symptoms should be increased.

Immunological features of idiopathic myenteric ganglionitis associated with severe gastrointestinal motor abnormalities

Immunological features of idiopathic myenteric ganglionitis associated with severe gastrointestinal motor abnormalities

Effect of rectal distension on gallbladder emptying and circulating gut hormones

Abnormalities of upper gut motility, including a delay of gastric emptying and small bowel transit, found in patients with constipation may be secondary to factors originating in the colon or rectum as a result of faecal stasis. The aim was to determine if stimulation of mechanosensory function by rectal distension affects postprandial gallbladder emptying and release of gastrointestinal peptides participating in control of upper gut motility. Eight healthy volunteers were studied with an electronic barostat and a plastic bag positioned in the rectum. Intrabag pressure was maintained at minimal distension pressure + 2 mmHg on one occasion and on a pressure that induced a sensation of urge on the other. Gallbladder volume and plasma concentrations of cholecystokinin (CCK), pancreatic polypeptide (PP) and peptide YY (PYY) were measured before and after ingestion of a 450-kcal mixed liquid meal. Rectal distension enhanced maximum gallbladder emptying from 66 +/- 7% to 78 +/- 5% (P < 0.05). Distension tended to increase integrated plasma PYY from 77 +/- 30 pM min to 128 +/- 40 pM min in the first hour after the meal (P = 0.08) and it suppressed integrated plasma PP from 1133 +/- 248 pM min to 269 +/- 284 pM min in the second hour (P < 0.05). Integrated plasma CCK concentrations were not significantly affected. Mechanosensory stimulation of the rectum enhances postprandial gallbladder emptying and influences postprandial release of gut hormones involved in the regulation of gastrointestinal motility in healthy subjects. These mechanisms may play a role in the pathogenesis of the upper gastrointestinal motor abnormalities observed in constipated patients.

Effect of rectal distension on gallbladder emptying and circulating gut hormones

Abnormalities of upper gut motility, including a delay of gastric emptying and small bowel transit, found in patients with constipation may be secondary to factors originating in the colon or rectum as a result of faecal stasis. The aim was to determine if stimulation of mechanosensory function by rectal distension affects postprandial gallbladder emptying and release of gastrointestinal peptides participating in control of upper gut motility. Eight healthy volunteers were studied with an electronic barostat and a plastic bag positioned in the rectum. Intrabag pressure was maintained at minimal distension pressure + 2 mmHg on one occasion and on a pressure that induced a sensation of urge on the other. Gallbladder volume and plasma concentrations of cholecystokinin (CCK), pancreatic polypeptide (PP) and peptide YY (PYY) were measured before and after ingestion of a 450-kcal mixed liquid meal. Rectal distension enhanced maximum gallbladder emptying from 66 ± 7% to 78 ± 5% (P < 0·05). Distension tended to increase integrated plasma PYY from 77 ± 30 pM min to 128 ± 40 pM min in the first hour after the meal (P = 0·08) and it suppressed integrated plasma PP from 1133 ± 248 pM min to 269 ± 284 pM min in the second hour (P < 0·05). Integrated plasma CCK concentrations were not significantly affected. Mechanosensory stimulation of the rectum enhances postprandial gallbladder emptying and influences postprandial release of gut hormones involved in the regulation of gastrointestinal motility in healthy subjects. These mechanisms may play a role in the pathogenesis of the upper gastrointestinal motor abnormalities observed in constipated patients.

Gastric emptying of solids is delayed in celiac disease and normalizes after gluten withdrawal.

Several gastrointestinal motor abnormalities have been detected in patients with celiac disease, but it is unclear whether they are able to influence the gastric emptying rate. The aim of this work was to evaluate the gastric emptying rate of solids in children with celiac disease before and after a gluten-free diet. Nine children with celiac disease and nine healthy controls (age range 4-16 y) underwent a 13C-octanoic acid breath test to measure gastric emptying. Half emptying time (t1/2) and lag phase (t(lag)) were calculated. After 6 mo of a gluten-free diet, all celiac children underwent a repeat 13C-octanoic acid breath test. The gastric motility parameters, t1/2 and t(lag), were significantly longer in patients than in controls. No significant correlation between abnormal gastric emptying and specific symptom patterns or severity of histological damage was found. On a gluten-free diet, the gastric emptying rate normalized in all celiac patients. This finding supports the hypothesis that gluten-driven mucosal inflammation might determine motor abnormalities by affecting smooth muscle contractility or impairing the release of neurotransmitters. Alternatively, nutrient malabsorption might determine significant changes in intraluminal milieu, which, in turn, may affect intestinal motor functions. patients affected by celiac disease have a markedly delayed gastric emptying of solids, which returns to normal after gluten withdrawal.

Gastric emptying of solids is delayed in celiac disease and normalizes after gluten withdrawal

Several gastrointestinal motor abnormalities have been detected in patients with celiac disease, but it is unclear whether they are able to influence the gastric emptying rate. The aim of this work was to evaluate the gastric emptying rate of solids in children with celiac disease before and after a gluten‐free diet. Nine children with celiac disease and nine healthy controls (age range 4‐16 y) underwent a 13C‐octanoic acid breath test to measure gastric emptying. Half emptying time (t1/2) and lag phase (tlag) were calculated. After 6 mo of a gluten‐free diet, all celiac children underwent a repeat 13C‐octanoic acid breath test. The gastric motility parameters, t1/2 and tlag, were significantly longer in patients than in controls. No significant correlation between abnormal gastric emptying and specific symptom patterns or severity of histological damage was found. On a gluten‐free diet, the gastric emptying rate normalized in all celiac patients. This finding supports the hypothesis that gluten‐driven mucosal inflammation might determine motor abnormalities by affecting smooth muscle contractility or impairing the release of neurotransmitters. Alternatively, nutrient malabsorption might determine significant changes in intraluminal milieu, which, in turn, may affect intestinal motor functions. Conclusion: patients affected by celiac disease have a markedly delayed gastric emptying of solids, which returns to normal after gluten withdrawal.

Gastric Emptying and Plasma Neurotensin Levels in Untreated Celiac Patients

Upper gastrointestinal motor abnormalities could account for some of the dyspeptic symptoms of celiac patients. However, the data on gastric emptying time are conflicting, and the pathophysiology of motor disturbances is still unclear. Neurotensin modulates upper gastrointestinal motor activity, and its postprandial increase is a reliable index of nutrient delivery to the ileum. We therefore assessed both plasma neurotensin levels and gastric emptying in untreated celiacs. The gastric antral area of nine untreated celiac patients and nine controls was measured with ultrasound at base line and every 30 min after a fatty meal (227 kcal, 45% fat); the base-line and postprandial neurotensin plasma levels were determined by means of radioimmunoassay. The data are mean values +/- standard deviation and were analyzed by using non-parametric tests. The overall and half gastric emptying time were significantly longer in the patients (203+/-32 versus 133+/-15 min, P = 0.0117, and 137+/-32 versus 78+/-11 min, P = 0.0001). The pattern of the changes in antral area was similar in both groups during the observation period as a whole but differed significantly in the first 120 min (P = 0.0343). Base-line neurotensin levels were significantly higher in the patients (41.6+/-23.9 versus 18.2+/-5.5 pg/ml, P = 0.0214) and their net postprandial increase was lower than in controls (15.0+/-15.9 versus 29.8+/-13.0 pg/ml, P = 0.046). In both groups the base-line neurotensin levels were related to the half gastric emptying time (P = 0.023). In untreated celiac patients gastric emptying time is longer than in controls and is concomitant with an increase in base-line plasma neurotensin levels.

8 Relevance of gastrointestinal motor disturbances in functional dyspepsia

Gastrointestinal motor abnormalities are frequent findings in patients with functional dyspepsia. However, these abnormalities are rather non-specific and seem to be restricted to a proportion of patients. Furthermore, they are not necessarily time-linked to symptom perception. The relationship of digestive motor derangements and symptoms in functional dyspepsia remains, therefore, unsettled. A variety of methodological and conceptual shortcomings characterize many of the studies investigating the relationship between gastrointestinal motility disorders and dyspeptic symptoms, and this obviously contributes to a higher level of uncertainty in the field. Recent reports suggest that gastrointestinal dysmotility is associated with perception of some dyspeptic symptoms, at least in a subset of patients. Well-conducted studies using appropriate methodology are needed to verify whether gastrointestinal motor disorders play a causal role in functional dyspepsia and whether this is of clinical relevance.

Oesophageal motility in adult coeliac disease

Coeliac sprue is a relatively frequent disease with protean clinical manifestations. Recent studies suggest that gastrointestinal motor abnormalities may explain some symptoms complained of by such patients. We investigated whether coeliac patients have oesophageal motor abnormalities from both a clinical and a physiological point of view. Thirty-six consecutive adult sprue subjects (14 during the florid phase and 22 on gluten-free diet) were studied. A clinical questionnaire on gastrointestinal symptoms (with emphasis on those of oesophageal origin) was administered. Moreover, 18 patients (13 on free and five on gluten-free diet) gave their consent for oesophageal manometry and eight subjects for pH-metry also. Oesophageal clinical symptoms were compared with those of 144 age- and sex-matched controls from a general population sample, and manometry with that of 34 healthy volunteers. Of coeliac patients 50% complained of dysphagia (P < 0.001 vs. controls) and 14% noncardiac chest pain (P = NS vs. controls). Manometric examination showed motor abnormalities in 67% of the subjects examined, consisting of nutcracker oesophagus, hypotonic lower oesophageal sphincter associated with simultaneous contractions, and frequent repetitive (> 3 peaks) contractions. These abnormalities were equally distributed among free and gluten-free diet patients. pH-metry showed only one pathological reflux out of eight subjects studied. We conclude that patients with coeliac sprue may display abnormal oesophageal motility. This confirms previous studies suggesting that gastrointestinal motor abnormalities should probably be added to the clinical spectrum of the disease.

Upper Gastrointestinal Motor Abnormalities in Children with Active Celiac Disease

Summary: Although from the clinical point of view a Gl motor disorder can be suspected in celiac disease, objective evidence for this is still lacking. We therefore conducted a study on children with active celiac disease to detect possible Gl motor abnormalities in this disease. Fourteen children (age range, 1–13 years) were studied; they underwent fasting and fed manometric recordings in the gastroduodenojejunal area. Four patients were re‐studied after a 6‐month gluten‐free diet. Data were compared with those obtained in eight control children. As compared with controls, celiac disease patients showed a shorter duration of activity fronts (p &lt; 0.01) and a significant (p &lt; 0.01) reduction of the postprandial antral motility index; furthermore, &gt; 90% of the patients displayed marked fasting and/or fed motor abnormalities, suggesting a neuropathic disorder. Interestingly, gut dysmotilities disappeared in the four subjects, reassessed after the gluten‐free diet. It is concluded that celiac disease frequently affects the motor behavior of the gut and that its effects may be reversed by appropriate diet.