Intestinal Motility Disorders

Updated: Jan 18, 2017
  • Author: Luigi Santacroce, MD; Chief Editor: Burt Cagir, MD, FACS  more...
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The phrase intestinal motility disorders applies to abnormal intestinal contractions, such as spasms and intestinal paralysis. This phrase is used to describe a variety of disorders in which the gut has lost its ability to coordinate muscular activity because of endogenous or exogenous causes. [1, 2, 3] Such disorders may be primary or secondary and may manifest in a variety of ways, including the following:

In a broad sense, any alteration in the transit of foods and secretions into the digestive tract may be considered an intestinal motility disorder. The following are considered intestinal motility disorders [4, 5] :

Chronic intestinal pseudo-obstruction

Chronic intestinal pseudo-obstruction (CIP) is a clinical syndrome caused by ineffective intestinal propulsion and characterized by symptoms and signs of intestinal obstruction in the absence of an occluding lesion of the intestinal lumen. [6] CIP is caused by a group of heterogeneous nerve and muscle disorders and results in obstructive intestinal symptoms in the absence of any mechanical obstruction. Usually, CIP occurs in patients with severe comorbid clinical conditions or after traumas (even surgical) or in patients with other underlying medical diseases.

A consensus working group defined CIP as a “rare, severe disabling disorder characterized by repetitive episodes or continuous symptoms and signs of bowel obstruction, including radiographic documentation of dilated bowel with air-fluid levels, in the absence of a fixed, lumen-occluding lesion.” [7] However, this definition is really applicable only to the most severe forms of CIP; air-fluid levels may not always be present.

Thus, the criteria for diagnosis should include definite symptoms and signs of obstruction, with documentation of air-fluid levels on plain radiographs of the abdomen or a dilated duodenum, small intestine, or colon on barium radiographs. Even though severe dysmotility may otherwise be present, the term pseudo-obstruction should not be used when these radiographic findings are absent.



Coordinated movements of the stomach and intestines are required to digest and propel intestinal contents along the digestive tract. The complex patterns of contraction and relaxation necessary for proper motility of the gastrointestinal (GI) tract are generated in the nerves and muscles within the GI walls.

Every day, at any time, many factors can influence GI motility (eg, physical exercise, emotional distress). The pathogenesis of primary intestinal motility disorders probably is multifactorial, but neither biochemical abnormality nor structural abnormality has been demonstrated commonly, except in some forms of intestinal pseudo-obstruction. More recently, there is evidence that low-grade mucosal inflammation and immune activation (particularly with mast cell involvement) in association with impaired epithelial barrier function and aberrant neuronal sensitivity may play a role in functional gastrointestinal disorders. [8]

Although the overall structural organization is similar throughout the digestive tract, each part has distinct motor activities. The musculature of the digestive tract has either extrinsic innervation (both sympathetic and parasympathetic) or intrinsic innervation (Auerbach plexus or myenteric plexus).

Intrinsic innervation is fundamental to coordinating GI motor activity. A neural network branching between longitudinal and circular muscle layers of the GI tract constitutes intrinsic innervation. Another nervous intrinsic plexus in the GI tract (Meissner plexus or submucosal plexus) helps to modify mucosal absorption and secretion without influencing motility.

Random, unorganized motor activity with occasional peristaltic and antiperistaltic complexes occurs during feeding, and this allows gastric remixing of foods. After this, another motor activity occurs, which is more regular, and this begins the peristaltic waves (ie, contractions of the circular musculature of the small intestine) that allow progression of undigested food through the intestines.

These events happen because the gastric pacemaker area, which originates electric slow waves with a frequency of 3 cycles per minute, occurs at the junction between the body and the antrum of the stomach. These electric waves, called migrating myoelectric complexes, determine the frequency of muscular contractions in the antral and pyloric areas through electromechanical coupling.

Migrating myoelectric complexes regulate gastric emptying and move gastric contents distally. Every 90 minutes, a cluster of migrating myoelectric complexes arises in the stomach and migrates distally beyond the ileum. Vagal function and the release of nitric oxide, vasoactive intestinal polypeptide, motilin, and nutrients of the meal and other enterohormones also affect GI motility.

Knowles and Martin attempted to define a novel classification for intestinal motility disorders, [9] in which these conditions are categorized as well-defined entities, entities with a variable dysfunction-symptom relation, questionable entities, and entities associated with behavioral disorders.

Well-defined entities in the Knowles-Martin classification include the following:

  • Delayed colonic transit - Slow transit constipation (eg, enteric neuropathy, enteric myopathy, Parkinson disease, endocrine disorders, spinal injury); the impairment of gastric motility in Parkinson disease patients, particularly in those with motor complications (42%), may be due in part to the effect of L-dopa on gastric dopaminergic receptors [10] ; in patients with spina bifida and spinal cord injuries, altered histology of the enteric nervous system as well as myenteric plexus neuronal loss and decreased nerve fiber density may play a major role in intestinal motility [11]

  • Dilated colon (diffuse or segmental) - Ogilvie syndrome, megacolon

  • Absent rectoanal inhibitory reflex - Hirschsprung disease

Entities with a variable dysfunction-symptom relation include the following:

  • Abnormally low anal canal pressure fecal incontinence (eg, diabetes mellitus, spinal injury)

Questionable entities include the following:

  • Accelerated transit bile salts

  • Short bowel

  • Rare endocrine and metabolic disorders

Entities associated with behavioral disorders include the following:

  • Impaired pelvic floor relaxation, prolonged storage in the rectosigmoid, outlet delay, anismus

  • Avoidance of defecation, functional fecal retention (eg, poor pelvic floor training, poor diet, fear of pain, learned suppression)



Causes of intestinal motility disorders seem to be multifactorial, and only a few have been detected.

Degenerative disorders cause pseudo-obstruction along with other problems; however, in patients with pseudo-obstruction, only changes in the nervous and muscular systems have been observed.

Many drugs that are commonly used (eg, tricyclic antidepressants, diuretics, laxatives) or have specific indications (eg, lithium salts, vinca alkaloids, and other chemotherapy agents) may interfere with intestinal motility. Stypsis may be related to drug abuse. Drugs such as benzodiazepines, lithium salts, laxatives, and codeine cause secondary stypsis. The latter can produce narcotic bowel syndrome, which is usually observed in patients who abuse opiates for chronic pain.

Endocrine disorders (eg, myxedema) can also cause pseudo-obstruction.

IBS, the more commonly diagnosed disorder of intestinal motility, has been considered a disease of the colon for decades, but research on GI motility has demonstrated that underlying motility disturbances can occur in the small bowel.

Irritable bowel syndrome

The causes of irritable bowel syndrome (IBS) remain unknown. According to some reports, the small intestine and colon of patients with IBS are more sensitive and reactive to mild stimuli than usual. IBS could be related to immature status of muscles and nerves in the intestinal wall of these persons.

Fecal incontinence

Aging, dementia, stroke, Parkinson disease, spinal cord injuries, rectal tears during birthing, diabetes, surgical complications, and neuromuscular disorders (eg, myasthenia gravis) may cause fecal incontinence.

Occasionally, fecal incontinence may occur after ingestion of certain foods. Sugars, insoluble fibers, and starches (except rice) are broken down in the intestines, forming a variable amount of gas that must be expelled. Most people who have lactase deficiency cannot digest lactose, a sugar common in several foods (eg, milk, cakes). People who have lactose deficiency may experience uncontrolled liquid diarrhea after lactose ingestion.


Constipation commonly has several causes, either primary or secondary. The most frequent of these are the following:

  • Diet that is very poor in fiber and high in animal fats and refined sugars

  • Pregnancy

  • Psychological constipation related to lifestyle changes (eg, travel, a new job, or divorce), in which the patient ignores the urge to defecate

  • Hypothyroidism

  • Electrolyte imbalance, especially if it involves Ca++ or K+

  • Tumors producing mechanical compression on an intestinal tract, either internally or externally

  • Nervous system injuries

  • Intoxication from lead, mercury, phosphorus, or arsenic

  • Constipation also may be secondary to rhagades (anal fissures) and piles.

Genetic factors

In a retrospective study investigating the association between mitochondrial disorders and CIP in 80 patients, Amiot et al determined that 15 patients (19% of the study cohort) had mitochondrial defects, including mutations in the thymidine phosphorylase gene (5 patients), the DNA polymerase-gamma gene (5 patients), and tRNA(leu(UUR)) (2 patients); 3 of the patients had no identifiable genetic defects. [12] Extradigestive symptoms occurred in all 15 patients.

Unlike other CIP patients, patients in whom the condition was associated with a mitochondrial defect tend to require frequent and long-term parenteral nutrition. [12] Because of the frequent occurrence of digestive and neurologic complications, these patients also had a high incidence of premature death. The authors suggested that mitochondrial defects are an important cause of CIP and recommended that CIP patients be tested for such defects, particularly those with severe CIP who experience associated neurologic symptoms.



According to some epidemiologic reports, as many as 30 million Americans have intestinal motility disorders. Available data from the medical literature indicate that worldwide, 30-45% of all GI conditions are referable to intestinal motility disorders.

When intestinal motility disorders are idiopathic and not related to either malignancies or systemic diseases, morbidity is minimal and mortality from complications is low (1-1.5%); complications usually occur in patients with intestinal pseudo-obstruction.

Persons of any age group may be affected, depending on the specific intestinal motility disorder. For example, IBS occurs more frequently in people aged 20-40 years, whereas intestinal pseudo-obstruction may occur in either newborns or elderly patients. Most patients are female, with a female-to-male ratio of 2.8:1. Primary intestinal motility disorders are most common in white persons and are usually thought to be related to diet.



Primary intestinal motility disorders or disorders that are not secondary to malignancy or debilitating pathology have a good prognosis. According to many reports, the prognosis is excellent for patients with IBS and mild fecal incontinence.

The prognosis is worse for patients with intestinal pseudo-obstruction, which has a high mortality.