Gastrointestinal Motility Disorders Part 1

Motility disorders of the stomach, small intestine, and colon are characterized by the acute, recurrent, or chronic presentation of symptoms of stasis or rapid transit in the absence of mucosal disease or any obstruction within the lumen of the gut.

The most common syndromes associated with disorders of motility are nonulcer dyspepsia,2 irritable bowel syndrome (IBS), functional constipation,3 and outlet obstruction to defecation (evacuation disorders)4; the prevalence of gastroparesis and chronic intestinal pseudo-obstruction1 is far lower. These disorders result from impaired neurologic or muscular control of the gut or from incoordination of defecation dynamics. Motility disorders are sometimes caused by a process that influences the extrinsic autonomic nerves that supply the gut. Other disorders infiltrate the GI smooth muscle and extraintestinal organs, particularly the urinary bladder.1


Gastric, small bowel, and colonic motility

GI motor functions are characterized by distinct patterns of contractile activity in the fasting and postprandial periods. The fasting period is characterized by a cyclic motor phenomenon called the interdigestive migrating motor complex [see Figure 1]. In healthy people, it occurs approximately once every 60 to 90 minutes and comprises a period of quiescence (phase I), a period of intermittent pressure activity (phase II), and an activity front, during which the stomach and small intestine contract at their highest frequency (phase III). These contraction frequencies reach three a minute in the stomach and 11 or 12 a minute in the proximal small intestine. The interdigestive activity front migrates a variable distance down the small intestine; there is a gradient in the frequency of contractions during phase III, from 11 or 12 a minute in the duodenum to as low as five a minute in the ileum. The distal small intestine also demonstrates another characteristic motor pattern—a propagated prolonged contraction, or power contraction, that serves to empty residue from the ileum to the colon in bolus transfers.

In the postprandial period, the fasting cyclic activity of the stomach and small intestine is replaced by irregular, fairly frequent contractions in those regions of the stomach and small bowel that come in contact with food [see Figure 1]. The caloric content of the meal is the major determinant of the duration of this so-called fed pattern. The maximum frequency of contractions is below that noted during phase III of the interdigestive migrating motor complex. After meals, segments of the small intestine that are not exposed to digesta may still show the interdi-gestive complex. Thus, there may be simultaneous patterns of interdigestive activity in the distal small bowel at a time when the proximal small bowel is in contact with intraluminal digesta and is responding with the irregular contractile activity that characterizes the fed pattern.

Solid and liquid food empty from the stomach at different rates. Liquids empty from the stomach in an exponential manner. For nonnutrient liquids, the healthy stomach tends to empty liquids with a half-emptying time of 20 minutes or less. On the other hand, solids are initially retained selectively within the stomach until particles have been triturated to a size smaller than 2 mm, at which point they can be emptied in a linear fashion from the stomach. Thus, the gastric emptying of solids consists of an initial lag period, followed by a more linear postlag gastric-emptying phase. The small intestine transports solids and liquids at approximately the same rate. Because there is a separation of the two phases in the stomach, it is clear that liquids may arrive in the colon before the head of the solid phase of the meal. Ileal emptying of chyme is characterized by bolus transfers.

Normal gastrointestinal motility. Note the normal interdigestive migrating motor complex during the fasting phase (a) and the irregular but persistent antral and intestinal phasic pressure activity in the fed phase (b).

Figure 1 Normal gastrointestinal motility. Note the normal interdigestive migrating motor complex during the fasting phase (a) and the irregular but persistent antral and intestinal phasic pressure activity in the fed phase (b).

Normal defecation requires relaxation of the puborectalis and external anal sphincter, straightening of the rectoanal angle, and an increase in intraluminal pressure, usually induced by the Valsalva maneuver. Defecation may be obstructed if any of these functions is impaired.

Figure 2 Normal defecation requires relaxation of the puborectalis and external anal sphincter, straightening of the rectoanal angle, and an increase in intraluminal pressure, usually induced by the Valsalva maneuver. Defecation may be obstructed if any of these functions is impaired.

Another important function of the stomach is the initial relaxation response that occurs after the ingestion of food. This response, also called accommodation, is mediated by the vagus nerves and involves the activation of intrinsic nitrergic inhibitory nerves in the wall of the stomach. Failure of gastric accommodation results in symptoms such as early fullness, satiety, and bloating and may contribute to nausea, indigestion (dyspepsia), or discomfort postprandially.5,6

The colon serves as a reservoir to facilitate absorption of fluids, electrolytes, and short-chain fatty acids produced by bacterial metabolism of unabsorbed carbohydrates. This reservoir function is centered predominantly in the ascending and transverse colonic regions. The descending colon functions as a conduit for the relatively rapid transit of feces to the sigmoid colon, which acts as a second reservoir. Emptying of the sigmoid colon is largely under volitional control. The defecatory process requires the Valsalva maneuver to raise intra-abdominal pressure, which is transmitted to the rectal contents, and relaxation of the pu-borectalis (or pelvic floor) and external anal sphincter,4 which necessitates a coordinated series of functions [see Figure 2]. This facilitates the opening or straightening of the rectoanal angle and expulsion of stool. The control and function of contractions in the colon are not fully understood; some irregular contractions serve to mix its contents, whereas high-amplitude propagated contractions (HAPCs), which occur on average four to six times a day, are sometimes associated with mass movement of colonic residue and lead to defecation. After meals of at least 500 kcal, there is a greater propensity for HAPCs to develop and for the tone (background state of contractility) of the colon to increase and lead to bowel movements in the first 2 hours after meals.

Control of gi motor and sensory functions

Motor function of the gut depends on the contraction of the smooth muscle cells and their integration and modulation by enteric and extrinsic nerves.1 Smooth muscle contraction results from fluxes of ions that alter the electrical potential of the cell membrane. The enteric nervous system—approximately 100 million (108) neurons organized in ganglionated plexi (submucosal and myenteric being the predominant plexi)—is organized in intricate excitatory and inhibitory programmed circuits [see Figure 3]. These circuits play essential roles in controlling peristalsis and the migrating motor complex. Among the enteric plexi, there are also interstitial cells of Cajal, which are thought to serve as pacemakers. Enteric nerves are also important in mediating sensation from the gut. Visceral sensation, as with somatic sensation, is mediated by A-delta fibers (which respond to short, sharp stimuli) and polymodal C-unmyelinated fibers (which tend to respond to more prolonged stimuli). The latter nerves mediate pain as well as the autonomic and emotional responses that are commonly noted in patients with functional GI diseases.8

Extrinsic neural control is subdivided into the craniosacral parasympathetic outflow and the thoracolumbar sympathetic supply. The cranial outflow is predominantly through the vagus nerve, which supplies neural control from the stomach down to the right side of the colon, and the sacral parasympathetic supply, which provides neural control to the left colon and, through ascending intracolonic fibers, the more proximal regions of the colon. Parasympathetic supply is excitatory to nonsphincteric muscle. Sympathetic fibers to the GI tract arise from levels T5 to L1 of the intermediolateral column of the spinal cord. Sympathetic fibers are stimulatory to sphincteric muscle and relaxatory to nonsphincteric muscle. The prevertebral sympathetic ganglia integrate afferent impulses from the gut and sympathetic supply from the central nervous system. Derangement of any of these intrinsic or extrinsic control mechanisms may lead to altered gut motor function [see Gastroparesis and Chronic Intestinal Pseudoobstruction, below].

Structural Diseases and Their Effects on GI Motility

Disturbances of gastric and proximal small bowel motility are frequently observed in symptomatic patients after gastric surgery. Uncoordinated phasic pressure waves occur in the Roux limb after Roux-en-Y partial gastrectomy.9 In these patients, the vagotomized gastric remnant may also contribute to the development of symptoms, because relaxation and contraction of the gastric remnant are deranged after vagotomy and partial gastric resection. In practice, pharmacologic agents are generally ineffective in this situation; further resection of the gastric remnant may relieve the symptoms resulting from upper gut stasis in about two thirds of these patients.

Another frequently encountered postoperative disorder is the postfundoplication syndrome. An excessively tight repair of hi-atal hernia may result in dysphagia; the increase in the use of lap-aroscopic fundoplication has led to a greater appreciation of the frequency with which this procedure results in postprandial upper abdominal pain, gas, bloating, and a dyspeptic condition that seems further aggravated by the patient’s inability to belch as a result of the effective wrap.

In subacute mechanical obstruction, proximal small bowel manometry shows simultaneous prolonged contractions separated by periods of quiescence. This pattern was shown to have a positive predictive value of 80%,12 and patients showing this pattern should undergo further careful assessment with entero-clysis, laparoscopy, or laparotomy to exclude obstruction. The increased availability and experience of laparoscopic surgeons have led to less need for motility tests to diagnose mechanical obstruction.

Small bowel fistulas, diverticula, and postsurgical blind loops are all associated with bacterial overgrowth, but the pathogenic sequence is not always clear. Experimentally, bacterial toxins induce migrating action potential complexes in the rabbit ileum, as well as abnormal motility, rapid transit through the small bowel, diarrhea, and steatorrhea. It has also been suggested that multiple jejunal diverticula may result from abnormal neuromuscular function.

Volvulus of the stomach, small bowel loops, cecum, and sig-moid colon may present as acute or subacute symptoms caused by mechanical obstruction. These need to be differentiated from conditions that primarily affect the motor apparatus, such as gastroparesis and pseudo-obstruction.

Functional Gastrointestinal Disorders

Functional GI disorders are characterized by disturbances of motor or sensory functions in the absence of mucosal or structural abnormality or of known biochemical or metabolic disorders. These syndromes affect one or more regions of the GI tract and include functional dysphagia, nonulcer dyspepsia,2 IBS,3 slow-transit constipation,4 and outlet obstruction to defecation4 (also termed evacuation disorders).

Functional GI disorders share common pathogenetic features, including abnormal motility, heightened visceral sensation, and psychosocial disturbance.2,3 In some patients, these syndromes are preceded by an episode of gastroenteritis. The abnormal motility may be characterized by rapid or slow transit of food or residue through the bowel or abnormal gastric relaxation to accommodate the meal.5,6 Abnormal contractile patterns have been described, but more important, patients perceive a sensation of excessive gut contractions.8 In patients with these conditions, there is frequently evidence of psychological comorbidity, such as anxiety, depression, or obsessive-compulsive disorder.3 These factors appear to influence the decision of patients to consult their physicians.

Control of gut motility. Interactions between extrinsic neural pathways and the intrinsic nervous system (enteric brain) modulate contractions of gastrointestinal smooth muscle. Peptide-receptor interactions alter muscle membrane potentials by stimulating bidirectional ion fluxes. In turn, membrane characteristics dictate whether or not the muscle cell contracts.

Figure 3 Control of gut motility. Interactions between extrinsic neural pathways and the intrinsic nervous system (enteric brain) modulate contractions of gastrointestinal smooth muscle. Peptide-receptor interactions alter muscle membrane potentials by stimulating bidirectional ion fluxes. In turn, membrane characteristics dictate whether or not the muscle cell contracts.

Nonulcer dyspepsia

Dyspepsia (from the Greek term for bad digestion) that is not caused by ulcers is characterized by upper abdominal symptoms in the postprandial period, such as nausea, vomiting, pain, bloating, anorexia, and early satiety. It affects about 20% of the population of the United States.


Factors other than altered gastric emptying, increased gastric sensitivity, and psychosocial distress may contribute to the development of nonulcer dyspepsia, but the pathogenesis remains unclear. A subgroup of patients may suffer nonerosive reflux esophagitis; others may have Helicobacter pylori gastritis. The role H. pylori infection plays in dyspepsia is uncertain, but current epidemiologic evidence and the results of eradication studies do not support a causal relationship.14,15 Dyspepsia is also associated with impaired gastric relaxation or accommodation.5,6


The history usually provides information on the specific symptoms or the spectrum of symptoms experienced by the patient. However, the symptoms have little discriminative value for predicting the physiologic alterations in an individual patient. Studies have suggested that the presence of postprandial fullness or satiation soon after starting the meal may be indicative of delayed gastric emptying and reduced gastric accommodation, respectively.5,6,16 Moreover, weight loss of more than 5 kg is more frequent in patients with reduced gastric accommoda-tion.5 However, weight loss should not be dismissed on the basis of being a functional alteration; it mandates performance of en-doscopy to exclude ulceration or cancer. The physical examination is usually normal. On rare occasions, there may be a succus-sion splash in the epigastrium from the retention of food in the stomach. An epigastric mass, hepatomegaly, or supraclavicular lymphadenopathy may suggest that the dyspepsia is the result of malignancy.

In the presence of alarm features such as dysphagia, bleeding, or weight loss in association with dyspepsia, it is essential to exclude mucosal diseases, such as ulcer or cancer.2 Cancer may still be present, however, even when these alarm features are absent. Patients are reassured by a negative endoscopic examination.

In most cases, the underlying cause of dyspepsia will not be obvious from the history and physical examination. For new-onset dyspepsia, endoscopy and testing for H. pylori infection are generally recommended.

The presence of heartburn suggests a component of gastroe-sophageal reflux. Reflux needs to be differentiated from rumina-tion,17 which results in the effortless regurgitation of undigested food within 30 minutes after oral ingestion; rumination occurs with virtually every meal and is not associated with nausea. The symptoms that appear to be most closely related to impaired gastric relaxation or accommodation are early satiety and weight loss.5 This impairment of accommodation may also contribute to hypersensitivity of the stomach of such patients to intraluminal stimuli. There is great interest in identifying ways to demonstrate this hypersensitivity before therapy is initiated, because such knowledge would have a bearing on choice of therapy. Tests in which the patient drinks water or a nutrient beverage have been devised to evaluate the maximal tolerated volume and the symptoms of fullness, satiety, bloating, nausea, and pain at a defined period after ingestion (typically 30 minutes).5,18,19 These tests are noninvasive and inexpensive, and they have been introduced into clinical practice in some centers. However, they do not necessarily differentiate disturbances in the accommodation response from hypersensitivity per se. Until recently, measurement of accommodation required the placement of an intra-gastric balloon to measure fasting and postprandial volumes.5 Recently, a novel imaging approach was developed to measure accommodation noninvasively by use of single-photon emission computed tomography.6

Algorithm for the treatment of dyspepsia.2 (IBS—irritable bowel syndrome; EGD—esophagogastroduodenoscopy)

Figure 4 Algorithm for the treatment of dyspepsia.2 (IBS—irritable bowel syndrome; EGD—esophagogastroduodenoscopy)

Simple, cost-effective tests for mucosal disease, gastric empty-ing,20-22 and gastric accommodation6 provide a rational alternative to the use of sequential empirical trials for identifying the mechanism causing dyspepsia2 [see Figure 4].


In clinical practice, dyspepsia is often treated with acid-suppressing regimens consisting of proton pump inhibitors or H2 receptor antagonists, though the evidence in favor of this approach is limited, and of all patients treated, a cure is achieved in less than one in 10.23 Temporary acid suppression with a proton pump inhibitor or an H2 receptor agonist may delay diagnosis of cancer.24 In cases of dyspepsia associated with H. pylori infection, eradication of the H. pylori infection results in resolution of the syndrome in only a small minority of patients25,26; the current consensus is that in the absence of erosions or ulcers, eradication of H. pylori is not indicated for treatment of dyspepsia,13 though it is usually treated anyway because of concern with development of atrophy or gastric cancer in the long term.

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