Appropriate postprandial and interprandial motility propels chyme through the intestine at a rate suitable to facilitate the absorption of nutrients, prevent small bowel bacterial overgrowth, and promote the formation and evacuation of formed stool. Motility is mediated through the contractile activity, tone, and compliance of gastrointestinal smooth muscle. This is controlled by the enteric nervous system (ENS). Within the ENS, interstitial cells of Cajal function as pacemakers. Ascending and descending neuronal pathways promote coordinated muscle activity through excitatory and inhibitory motor neurons. ENS activity is modulated by extrinsic nerves as well as gastrointestinal hormones and peptides. Dysfunction of any of these components may cause dysmotility.

Primary myopathies and neuropathies, either familial or sporadic, may result in intestinal dysmotility. More commonly, systemic diseases may involve the digestive tract and cause dysmotility. However, gastrointestinal manifestations are rarely the presenting feature of these conditions. Secondary etiologies affecting the intestinal smooth muscle include collagen diseases (such as scleroderma, dermatomyositis, systemic lupus erythematosus, and mixed connective tissue disease) muscular dystrophy, and amyloidosis. Secondary neuropathies may occur as a consequence of diabetes mellitus, Chagas disease, Parkinson disease, neurofibromatosis, paraneoplastic visceral neuropathy or radiation. Diseases which are classically regarded as mucosal in origin, such as celiac disease or eosinophilic gastroenteritis, may also be associated with intestinal myopathies or neuropathies. Drugs acting directly or indirectly on cholinergic, opioid, calcium channel, dopamine, adrenergic, somatostatin or serotonin receptors can induce dysmotility. Abnormal secretion of endogenous gastrointestinal hormones (e.g., serotonin, vasoactive intestinal polypeptide) may result in rapid small intestinal or colonic transit due to abnormal intestinal motor and secretory function.

Regardless of the underlying causes, patients with dysmotility of the small intestine and colon may experience a wide range of clinical manifestations. Patients may be asymptomatic or, at the other end of the spectrum, may present with chronic intestinal pseudoobstruction. Between these two extremes, patients may have dyspeptic symptoms, including intermittent postprandial epigastric or periumbilical abdominal pain, bloating, nausea, vomiting, and diarrhea or constipation. Symptoms are often more pronounced in the postprandial period. Intestinal bacterial overgrowth occurs in severe cases of intestinal dysmotility and results in steatorrhea and sometimes diarrhea. Extraintestinal manifestations of the underlying disease may be detected in patients with secondary causes of small intestine and colonic dysmotility.

Small intestine dysmotility occurs less frequently than colonic dysmotility. However, evaluation of small bowel motility requires specialized equipment and is poorly tolerated by patients. Consequently, the true prevalence of small bowel dysmotility is unknown. In contrast, constipation affects 12–15% of the population and Hirschsprung disease, the prototypic congenital colonic dysmotility, affects 1 in 5000 births.

This chapter presents images relating to small bowel and colonic dysmotility.