Relating gastric scintigraphy and symptoms to motility capsule transit and pressure findings in suspected gastroparesis.

BACKGROUND: Wireless motility capsule (WMC) findings are incompletely defined in suspected gastroparesis. We aimed to characterize regional WMC transit and contractility in relation to scintigraphy, etiology, and symptoms in patients undergoing gastric emptying testing. METHODS: A total of 209 patients with gastroparesis symptoms at NIDDK Gastroparesis Consortium centers underwent gastric scintigraphy and WMCs on separate days to measure regional transit and contractility. Validated questionnaires quantified symptoms. KEY RESULTS: Solid scintigraphy and liquid scintigraphy were delayed in 68.8% and 34.8% of patients; WMC gastric emptying times (GET) were delayed in 40.3% and showed 52.8% agreement with scintigraphy; 15.5% and 33.5% had delayed small bowel (SBTT) and colon transit (CTT) times. Transit was delayed in ≥2 regions in 23.3%. Rapid transit was rarely observed. Diabetics had slower GET but more rapid SBTT versus idiopathics (P ≤ .02). GET delays related to greater scintigraphic retention, slower SBTT, and fewer gastric contractions (P ≤ .04). Overall gastroparesis symptoms and nausea/vomiting, early satiety/fullness, bloating/distention, and upper abdominal pain subscores showed no relation to WMC transit. Upper and lower abdominal pain scores (P ≤ .03) were greater with increased colon contractions. Constipation correlated with slower CTT and higher colon contractions (P = .03). Diarrhea scores were higher with delayed SBTT and CTT (P ≤ .04). CONCLUSIONS & INFERENCES: Wireless motility capsules define gastric emptying delays similar but not identical to scintigraphy that are more severe in diabetics and relate to reduced gastric contractility. Extragastric transit delays occur in >40% with suspected gastroparesis. Gastroparesis symptoms show little association with WMC profiles, although lower symptoms relate to small bowel or colon abnormalities.

Sympathetic control of lower esophageal sphincter function in the cat. Action of direct cervical and splanchnic nerve stimulation.

The purpose of this study was to determine the effect of direct stimulation of the sympathetic nerves on the lower esophageal sphincter (LES) in the anesthetized cat. Neither unilateral nor bilateral cervical sympathectomy, or splanchnicectomy significantly modified basal LES pressure in animals with intact vagi, or animals having undergone bilateral cervical vagotomy. Electrical stimulation of the cut, peripheral, cervical sympathetic trunk increased mean arterial blood pressure, but had no effect on LES pressure or LES relaxation as induced by vagal stimulation. Stimulation of the central end of the cervical sympathetic trunk had no effect on LES pressure. Stimulation of the central end of the cut splanchnic nerve produced a decrease in LES pressure with a maximal response of 69.1+/-16.0% (mean+/-SEM). This inhibitory response was not modified by either propranolol or bilateral cervical vagotomy. Stimulation of the peripheral end of the cut, greater splanchnic nerve gave an increase in LES pressure with a maximal response of 38.2+/-7.19 mm Hg. Guanethidine, in the presence or absence of the adrenal glands, significantly augmented this excitatory response. This response was also slightly increased by phentolamine alone at 10 V, 1 Hz, but was not altered by propranolol. The excitatory response was completely antagonized by atropine or by trimethaphan camsylate. Stimulation of the peripheral end of the splanchnic nerve inhibited LES relaxation as induced by vagal stimulation. The results of this study suggest that: (a) the LES in the cat is not affected by either central or peripheral stimulation of the cervical sympathetic trunk; (b) the central portion of the splanchnic nerve carries an afferent inhibitory response to the LES through yet unknown pathways; (c) the peripheral splanchnic nerve carries an atropine-sensitive excitatory response to the LES; and (d) the splanchnic nerves may modulate LES relaxation as induced by vagal stimulation.

Mechanism of deoxycholic acid stimulation of the rabbit colon.

Previous studies showed that deoxycholic acid (DCA) stimulated migrating action potential complexes (MAPC) in the colon. The aim of this study was to clarify the mechanism of DCA-stimulated colonic motility. Myoelectrical and contractile activity were measured in New Zealand White rabbits from a loop constructed in the proximal colon. During the control period, slow waves were present at a frequency of 10.8 +/- 0.5 cycle/min and there were 1.5 +/- 0.5 MAPC/ h. After adding DCA (16 mM) to the loop the slow wave activity was unchanged. However, MAPC increased to 15.1 +/- 2.4 MAPC/h (P less than 0.001). MAPC activity was not stimulated in the colonic smooth muscle outside the loop. The intraluminal addition of procaine or tetrodotoxin to the colonic loop inhibited the DCA-stimulated increase in MAPC activity (0.2 +/- 0.2 MAPC/h) (P less than 0.005). Intravenous administration of atropine or phentolamine also inhibited MAPC activity that had been stimulated by DCA (P less than 0.005). Pretreatment with 6-hydroxydopamine also inhibited an increase in MAPC activity. Propranolol, trimethaphan camsylate, or hexamethonium had no effect on DCA stimulation of MAPC activity. Although the concentration of bile salt increased in the mesenteric venous outflow from the colonic loop, the intravenous administration of bile salt did not stimulate colonic MAPC activity. These studies suggest: (a) the action of DCA on smooth muscle activity is a local phenomenon, (b) the increase in MAPC activity is dependent on intact cholinergic and alpha adrenergic neurons, and (c) an increase in the concentration of bile salts in the serum is not associated with an increase in colonic MAPC activity.

Characterization of opiate-mediated responses of the feline ileum and ileocecal sphincter.

Although opioid peptides have been demonstrated immunohistochemically in the feline intestine, the action of these peptides is unknown. The aims of this study were: (a) to determine the distal ileal and ileocecal sphincter (ICS) responses to morphine sulfate (MS), methionine enkephalin (ME) and leucine enkephalin (LE); (b) to determine the mechanism by which exogenous opiates mediate these responses; (c) to determine the type of receptor involved in mediating these responses and (d) to ascertain whether endogenous opiate-mediated responses may be vagally induced. The ICS responded to all three opiate agonists with tonic and phasic contractions, the latter being associated with increased spike activity. The ED(max) for ICS pressure response was 1 mug/kg for ME, 5 mug/kg for LE, and 150 mug/kg for MS. The distal ileum responded with increased spike activity and phasic contractions. The ED(max) for the ileal motility index response was 1.0 x 10(-1) mug/kg for ME, 1 mug/kg for LE, and 150 mug/kg for MS. Thus, both sites demonstrated similar dose-response relationships, both responding to at least 100 times lower doses of enkephalins than MS. The ICS contraction preceded ileal contractions. The ileal and ICS response was not antagonized by atropine, hexamethonium, phentolamine, propranolol, cinanserin, or tetrodotoxin. Naloxone, 600 mug/kg, antagonized the response to the enkephalins while 10 mug/kg antagonized the response to MS. Higher doses of the specific-receptor agonist SKF 10047 and kappa-receptor agonist ketocyclazocine were required before a contractile response was elicited. Electrical stimulation of the cervical vagus induced ICS contraction and a fall in blood pressure. The ICS contractile response but not the blood pressure response was inhibited by naloxone 1 mg/kg. These data indicate: (a) tonic and phasic ICS contraction followed by ileal contraction may be mediated through delta-type opiate receptors located in the muscle membrane and (b) opiate-mediated ICS contraction may be induced during vagal stimulation.

Early satiety and postprandial fullness in gastroparesis correlate with gastroparesis severity, gastric emptying, and water load testing.

BACKGROUND: Early satiety (ES) and postprandial fullness (PPF) are often present in gastroparesis, but the importance of these symptoms in gastroparesis has not been well-described. The aims were: (i) Characterize ES and PPF in patients with gastroparesis. (ii) Assess relationships of ES and PPF with etiology of gastroparesis, quality of life, body weight, gastric emptying, and water load testing. METHODS: Gastroparetic patients filled out questionnaires assessing symptoms (PAGI-SYM) and quality of life (PAGI-QOL, SF-36v2). Patients underwent gastric emptying scintigraphy and water load testing. KEY RESULTS: 198 patients with gastroparesis (134 IG, 64 DG) were evaluated. Early satiety was severe or very severe in 50% of patients. Postprandial fullness was severe or very severe in 60% of patients. Severity scores for ES and PPF were similar between idiopathic and diabetic gastroparesis. Increasing severity of ES and PPF were associated with other gastroparesis symptoms including nausea/vomiting, satiety/early fullness, bloating, and upper abdominal pain and GERD subscores. Increasing severity of ES and PPF were associated with increasing gastroparesis severity, decreased BMI, decreased quality of life from PAGI-QOL and SF-36 physical health. Increasing severity of ES and PPF were associated with increasing gastric retention of a solid meal and decreased volume during water load test. CONCLUSIONS & INFERENCES: Early satiety and PPF are commonly severe symptoms in both diabetic and idiopathic gastroparesis. Early satiety and PPF severity are associated with other gastroparesis symptom severities, body weight, quality of life, gastric emptying, and water load testing. Thus, ES and PPF are important symptoms characterizing gastroparesis. ClinicalTrials.gov number: NCT NCT01696747.

Diabetic and idiopathic gastroparesis is associated with loss of CD206-positive macrophages in the gastric antrum.

BACKGROUND: Animal studies have increasingly highlighted the role of macrophages in the development of delayed gastric emptying. However, their role in the pathophysiology of human gastroparesis is unclear. Our aim was to determine changes in macrophages and other cell types in the gastric antrum muscularis propria of patients with diabetic and idiopathic gastroparesis. METHODS: Full thickness gastric antrum biopsies were obtained from patients enrolled in the Gastroparesis Clinical Research Consortium (11 diabetic, 6 idiopathic) and 5 controls. Immunolabeling and quantitative assessment was done for interstitial cells of Cajal (ICC) (Kit), enteric nerves protein gene product 9.5, neuronal nitric oxide synthase, vasoactive intestinal peptide, substance P, tyrosine hydroxylase), overall immune cells (CD45) and anti-inflammatory macrophages (CD206). Gastric emptying was assessed using nuclear medicine scintigraphy and symptom severity using the Gastroparesis Cardinal Symptom Index. RESULTS: Both diabetic and idiopathic gastroparesis patients showed loss of ICC as compared to controls (Mean [standard error of mean]/hpf: diabetic, 2.28 [0.16]; idiopathic, 2.53 [0.47]; controls, 6.05 [0.62]; P=.004). Overall immune cell population (CD45) was unchanged but there was a loss of anti-inflammatory macrophages (CD206) in circular muscle (diabetic, 3.87 [0.32]; idiopathic, 4.16 [0.52]; controls, 6.59 [1.09]; P=.04) and myenteric plexus (diabetic, 3.83 [0.27]; idiopathic, 3.59 [0.68]; controls, 7.46 [0.51]; P=.004). There was correlation between the number of ICC and CD206-positive cells (r=.55, P=.008). Enteric nerves (PGP9.5) were unchanged: diabetic, 33.64 (3.45); idiopathic, 41.26 (6.40); controls, 46.80 (6.04). CONCLUSION: Loss of antral CD206-positive anti-inflammatory macrophages is a key feature in human gastroparesis and it is associates with ICC loss.

Evaluation of the pylorus with concurrent intraluminal pressure and EndoFLIP in patients with nausea and vomiting.

BACKGROUND: Nausea and vomiting occurs in gastroparesis due to diabetes mellitus or unknown causes. The aim of this study was to compare (i) pyloric distensibility to pyloric manometric pressure in patients with nausea and vomiting and (ii) to correlate distensibility with delays in gastric emptying. METHODS: Sleeve manometry and EndoFLIP were performed sequentially during the same endoscopy on 114 patients with nausea and vomiting (47 with diabetes mellitus and 67 with idiopathic cause) after a standardized gastric emptying study. The sleeve manometer was positioned fluoroscopically, and the EndoFLIP was placed endoscopically. Manometric pressure using a water-perfused catheter and distensibility using an EndoFLIP filled with 40 cc of saline were measured from the pylorus. KEY RESULTS: The basal pyloric pressure was elevated (>10 mmHg) in 34 patients and was normal in 80 patients. The basal and peak pressures were similar in patient with normal and delayed gastric emptying (p > 0.05). There was a significant decrease in distensibility (8.0 ± 1.0 mm(2) /mmHg) in patients with gastric retention (>20% at 4 h) compared with patients (12.4 ± 1.4 mm(2) /mmHg) (p < 0.01) with normal gastric retention (<10%). Pressure measurements from the sleeve manometer and the EndoFLIP correlated (r = 0.29) (p < 0.002), and increased EndoFLIP balloon pressure (19.4 ± 1.4 mmHg) (p < 0.01) was associated with a severe delay in gastric emptying. CONCLUSIONS & INFERENCES: Elevated basal pyloric pressure occurs in 42% of patients with nausea and vomiting and delayed emptying. Decreased pyloric distensibility occurs with nausea, vomiting, and delayed gastric emptying. The EndoFLIP is a useful tool in the evaluation of pyloric function in symptomatic patients.

Baseline features and differences in 48 week clinical outcomes in patients with gastroparesis and type 1 vs type 2 diabetes.

BACKGROUND: In studies of diabetic gastroparesis, patients with type 1 and type 2 diabetes mellitus (T1DM, T2DM) are often combined for analyses. We compared gastroparesis severity, healthcare utilization, psychological function, and quality of life in T1DM vs T2DM gastroparesis patients. METHODS: Questionnaire, laboratory, and scintigraphy data from patients with gastroparesis and T1DM and T2DM from seven centers of the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Registry were compared at enrollment and after 48 weeks. Multiple regression models assessed baseline and follow-up differences between diabetes subtypes. KEY RESULTS: At baseline, T1DM patients (N = 78) had slower gastric emptying, more hospitalizations, more gastric stimulator implantations, higher hemoglobin A1c (HbA1c), and more anxiety vs T2DM patients (N = 59). Independent discriminators of patients with T1DM vs T2DM included worse gastroesophageal reflux disease, less bloating, more peripheral neuropathy, and fewer comorbidities (p ≤ 0.05). On follow-up, gastrointestinal (GI) symptom scores decreased only in T2DM (p < 0.05), but not in T1DM patients who reported greater prokinetic, proton pump inhibitor, anxiolytic, and gastric stimulator usage over 48 weeks (p ≤ 0.03). Gastrointestinal symptoms at baseline and 48 weeks with both subtypes were not associated with HbA1c, peripheral neuropathy, psychological factors, or quality of life. CONCLUSIONS & INFERENCES: Baseline symptoms were similar in T1DM and T2DM patients, even though T1DM patients had worse gastric emptying delays and higher HbA1c suggesting other factors mediate symptom severity. Symptom scores at 48 weeks decreased in T2DM, but not T1DM patients, despite increased medical and surgical treatment utilization by T1DM patients. Defining causes of different outcomes in diabetic gastroparesis warrants further investigation.

Nausea and vomiting in gastroparesis: similarities and differences in idiopathic and diabetic gastroparesis.

BACKGROUND: Nausea and vomiting are classic symptoms of gastroparesis. It remains unclear if characteristics of nausea and vomiting are similar in different etiologies of gastroparesis. The aims of this article were as follows: to describe characteristics of nausea and vomiting in patients with gastroparesis and to determine if there are differences in nausea and vomiting in diabetic (DG) and idiopathic gastroparesis (IG). METHODS: Gastroparetic patients enrolling in the NIDDK Gastroparesis Registry underwent assessment with history and questionnaires assessing symptoms, quality of life, and a questionnaire characterizing nausea and vomiting. KEY RESULTS: Of 159 gastroparesis patients (107 IG, 52 DG), 96% experienced nausea, whereas 65% experienced vomiting. Nausea was predominant symptom in 28% and vomiting was predominant in 4%. Nausea was severe or very severe in 41%. PAGI-SYM nausea/vomiting subscore was greater with increased vomiting severity, but not nausea severity in DG than IG. Nausea was related to meals in 71%; lasting most of the day in 41%. Increasing nausea severity was related to decreased quality of life. Nausea often preceded vomiting in 82% of patients and vomiting often relieved nausea in 30%. Vomiting was more common in DG (81%) compared to IG (57%; p = 0.004). Diabetic patients more often had vomiting in the morning before eating, during the night, and when not eating. CONCLUSIONS & INFERENCES: Nausea is present in essentially all patients with gastroparesis irrespective of cause and associated with decreased quality of life. In contrast, vomiting was more prevalent, more severe, and occurred more often in DG than IG. Thus, characteristics of vomiting differ in IG vs DG.

The pathophysiology and treatment of gastroesophageal reflux disease: new concepts.

In summary, the recent understanding of the pathogenesis of gastroesophageal reflux disease as owing to LES incompetence has led to improvement in both the diagnosis and the treatment of this disorder. Diagnosis now dependent on demonstrating the presence of reflux, an incompetent sphincter mechanism, or some complication of reflux. Treatment is focused on reducing the endogenous factors that contribute to reflux, or actually restoring the sphincteral barrier to reflux by pharmacologic or surgical means.

Abnormal gastrocolic response in patients with intestinal pseudo-obstruction.

Gastrointestinal motility disturbances after endogenous stimuli have been demonstrated only in the esophagus and small intestine in patients with chronic idiopathic pseudo-obstruction. The 1,000-calorie meal stimulated a significant increase in spike and contractile activity in normal subjects. No increase in colonic spike or contractile activity occurred in patients with chronic idiopathic pseudo-obstruction even though colonic motility increased normally following the administration of neostigmine methylsulfate. These findings suggest that the normal response to eating is absent in patients with chronic idiopathic intestinal pseudo-obstruction even though their smooth muscle has been shown to be responsive to cholinergic stimulation. This loss of a gastrocolic response is further evidence for a disorder of the neurohumoral control mechanisms in patients with chronic idiopathic intestinal pseudo-obstruction.

Long-term safety of tegaserod in patients with constipation-predominant irritable bowel syndrome.

BACKGROUND: Tegaserod is a 5-hydroxytryptamine-4 receptor partial agonist. Oral administration causes gastrointestinal effects resulting in increased gastrointestinal motility and attenuation of visceral sensation. AIM: : To determine the long-term safety and tolerability of tegaserod in patients suffering from irritable bowel syndrome with constipation as the predominant symptom of altered bowel habits. METHOD: A multicentre, open-label study with flexible dose titration of tegaserod in out-patients suffering from constipation-predominant irritable bowel syndrome. RESULTS: A total of 579 patients with constipation-predominant irritable bowel syndrome were treated with tegaserod. Of these, 304 (53%) completed the trial. The most common adverse events, classified as related to tegaserod for any dose, were mild and transient diarrhoea (10.1%), headache (8.3%), abdominal pain (7.4%) and flatulence (5.5%). Forty serious adverse events were reported in 25 patients (4.4% of patients) leading to discontinuation in six patients. There was one serious adverse event, acute abdominal pain, classified as possibly related to tegaserod. There were no consistent differences in adverse events between patients previously exposed to tegaserod and those treated de novo. No pattern-forming tegaserod-related abnormalities in haematological and biochemical laboratory tests, urinalysis, blood pressure, pulse rate or electrocardiograms were found. CONCLUSIONS: Tegaserod appears to be well tolerated in the treatment of patients with constipation-predominant irritable bowel syndrome. The adverse event profile, clinical laboratory evaluations, vital signs and electrocardiogram recordings revealed no evidence of any unexpected adverse events, and suggest that treatment is safe over a 12-month period.

The role of a colonic motility disturbance in ulcerative colitis.

Alterations in colonic motility appear to exacerbate the symptom of increased frequency of bowel movements in patients with ulcerative colitis. Decreased segmenting contractions allow rapid forward movement of luminal contents accentuating the diarrhea. The decrease in segmenting colonic motility is further exacerbated by increased numbers of propagating contractions. The rapid transport of intraluminal contents with a propagating contractions into a nondistensible rectum may be one explanation for the relative high incidence of fecal incontinence in these patients. The pathogenesis of the decreased segmenting contractions appears due to an electromechanical dissociation resulting from inhibition of myosin light chain phosphorylation. It is possible that several inflammatory mediators including free oxygen radicals decrease smooth muscle cell function.

Comparison of transit times in the J-shaped and the isoperistaltic lateral ileal reservoir--using isotope technique in rabbits.

An ileal reservoir appears to reduce stool frequency and urgency in conjunction with endorectal ileal pull-through operations. The optimal type of reservoir construction has not been determined. In a rabbit model, the isotope transit time, measured as a percentage of isotope remaining in a segment of intestine one hour after injection, was 79% for the J-shaped reservoir (JR) and 57% for the lateral isoperistaltic reservoir (LR). Transit times in ileal segments longitudinally incised and closed and control segments were 49% and 63%, respectively. The mean reservoir volume three months after operation was 53 mL for LR, 101 mL for JR, 20 mL for longitudinally incised and closed ileal segments, and 25 mL for control segments. Although reservoir function between the LR and JR may be similar at six to nine months postoperatively, it appears that the JR empties more slowly and becomes more distended during the first three months after construction in the rabbit model studied.

Mechanism of neurotensin depolarization of rabbit colonic smooth muscle.

The aims of this study were (1) to measure the effect of neurotensin on the membrane potential of circular muscle of the distal colon of the rabbit and (2) to determine the mechanism by which neurotensin affects the membrane potential of this tissue. The membrane potential was measured with microelectrodes placed intracellularly and the double sucrose gap. Neurotensin (10(-11) M to 10(-7) M) dose-dependently decreased the membrane potential. The maximum decrease in membrane potential occurred with 10(-9) M neurotensin. The ED50 of neurotensin depolarization of the membrane potential was 0.87 +/- 0.33 X 10(-10) M. The frequency of the slow waves was unchanged after neurotensin. The voltage response to a constant current pulse decreased as the concentration of neurotensin increased. The amplitude of the voltage response after a 0.6 microA current pulse decreased by 6 +/- 0.5 mV after neurotensin (10(-7) M) compared to the Krebs control (P less than 0.05). Decreasing the [Na+]o to 0-23 mM did not affect the decrease in membrane potential after neurotensin. However, perfusion with a test solution containing no added Ca2+ or verapamil (10(-5) M) inhibited neurotensin depolarization of the tissue. Evidence was found that neurotensin depolarizes colonic circular smooth muscle, and the decrease in membrane potential is associated with an increase in conductance which is dependent on influx of Ca2+.

The effect of methylcellulose on symptoms of constipation.

The efficacy of methylcellulose was evaluated in 538 patients with a history of constipation. The patients were seen both by primary care physicians and by consultants. Patients were selected on the basis of passage of fewer than three stools per week. Frequency, consistency, and ease of passage of the stools were measured before and after one to three tablespoonsful per day of methylcellulose. The frequency of bowel movements as well as the consistency and ease of passage of the stools returned to normal with methylcellulose treatment; 61% of the patients were judged to have less constipation. The response to methylcellulose was not altered by the sex or age of the patients nor by the presence of colonic diverticular disease. This study suggests that methylcellulose is beneficial for the treatment of chronic and acute constipation.

Clinical considerations in GERD (gastroesophageal reflux disease) therapy: focus on cisapride.

Heartburn, the major symptom of gastrointestinal reflux disease (GERD), is a common condition that is usually self-treated with over-the-counter products. For patients with severe or recurrent symptoms of GERD, pharmacologic therapy includes acid suppression with H2-receptor antagonists and proton pump inhibitors, and, alternatively, the use of prokinetic agents. While all of these are efficacious, given its high efficacy in nonerosive and mild-to-moderate erosive esophagitis, the prokinetic agent cisapride deserves significant consideration in this patient population.

Comparison of the myoelectrical activity of the lateral and J-shaped ileal reservoirs.

Ileal myoelectrical activity was studied in ten 10-cm J-shaped and ten lateral ileal reservoirs (IR) in rabbits. Electrodes and a strain gauge were placed on both ileal segments of the reservoirs as well as the proximal and distal ileum entering and leaving the reservoirs. In three additional rabbits without reservoirs (controls), electrodes and a strain gauge were sutured to the distal ileum in a similar manner. Myoelectrical activity was recorded as (1) short spike burst complexes (SSBC) lasting greater than 25 seconds but less than three minutes, and (2) long spike burst complexes (LSBC) lasting more than three minutes. SSBC propagated through the lateral IR two weeks after its construction and were synchronous with intestinal contraction. In contrast, SSBC did not become organized or propagate distally through the J-shaped IR until eight weeks after reservoir construction. LSBC occurred infrequently in control rabbits and in those after construction of the J-shaped and lateral IRs. Propagation of LSBC in control rabbits was synchronous with prolonged propulsive intestinal contraction. In both the J-shaped and lateral reservoirs, LSBC occurred randomly and did not propagate from proximal to distal ileum through the IR until three months after reservoir construction. The frequency and duration of LSBC remained diminished for the J-shaped IR at three months when compared with the lateral IR. It is concluded that the return of normal propulsive activity occurs earlier in the lateral iso-peristaltic IR than in the J-shaped IR but that both are effective at three months.(ABSTRACT TRUNCATED AT 250 WORDS)

Current concepts in the management of the irritable bowel syndrome.

In the irritable bowel syndrome gastrointestinal tract motility is disturbed from the esophagus to the colon, causing pain and altered function. When colonic motility is abnormal, the patient can experience either constipation or diarrhea in addition to abdominal pain and bloating. In constipated patients the postprandial colonic motility can increase normally after eating or the colon can remain motionless. Generally propagating contractions are absent in patients with constipation predominant irritable bowel syndrome. Propagating contractions are increased in frequency in patients with diarrhea, although the phasic contractions are decreased. Questionnaires discriminate between patients with structural disease such as ulcerative colitis and patients with functional disease, however they cannot differentiate between the different subgroups of patients with constipation predominant irritable bowel syndrome. Treatment strategies are beginning to focus on the underlying pathophysiologic abnormality.

Myoelectric and motor activity of the colon in normal and abnormal states.

The nature of colonic motility in normal subjects is discussed. Colonic myoelectrical control is disturbed in certain diseases: slow-wave activity may be affected, or the postprandial gastrocolonic spike response may be altered. Due to these changes in contractile activity, abnormal movement of materials through the colon takes place. These phenomena are reviewed with reference to the irritable colon syndrome, idiopathic constipation, diverticular disease, diabetes mellitus, peripheral systemic sclerosis, and chronic idiopathic intestinal pseudo-obstruction. The treatment of hypermotile states requires the use of agents that diminish colonic motility. If the colon is inert, however, stimulating drugs, e.g. metoclopramide or prostigmine, are indicated.