1. Top of page
  2. Abstract
  3. Introduction
  5. Conclusions
  6. Acknowledgements
  7. References


To review the physiology of colonic motility and sensation in healthy humans and the pathophysiological changes associated with constipation and diarrhoea.


Medline Search from 1965 using the index terms: human, colonic motility, sensation, pharmacology, neurohormonal control, gastrointestinal transit, constipation, diarrhoea and combinations of these.


In health, the ascending and transverse regions of colon function as reservoirs to accommodate ileal chyme and the descending colon acts as a conduit; the neuromuscular functions and transmitters control colonic motility and sensation and play pivotal roles in disorders associated with constipation and/or diarrhoea. Disorders of proximal colonic transit contribute to symptoms in idiopathic constipation, diarrhoea-predominant irritable bowel syndrome and carcinoid diarrhoea. Colonic function in patients presenting with constipation is best assessed clinically by colonic transit time using radiopaque markers ingested orally. Measurements of colonic contractility are less useful clinically but they can help identify motor abnormalities including colonic inertia; in some patients with irritable bowel syndrome, abdominal pain, urgency and diarrhoea are temporally associated with high amplitude contractions, which originate in the proximal colon and traverse the distal conduit at very high propagation velocities. Visceral hypersensitivity contributes to the urgency and tenesmus in irritable bowel syndrome and inflammatory bowel disease. Colonic motility and sensation can be reduced by anticholinergic agents, somatostatin analogues and 5HT3 antagonists.


Physiological and pharmacological studies of the human colon have provided new insights into the pathophysiology of colonic disorders, and offer possibilities of novel therapeutic approaches for constipation or diarrhoea associated with colonic motor or sensory dysfunction.


  1. Top of page
  2. Abstract
  3. Introduction
  5. Conclusions
  6. Acknowledgements
  7. References

The human colon performs important functions including the absorption of water and electrolytes, the storage and transport of intraluminal contents aborally, and the salvage of some nutrients after bacterial metabolism of carbohydrate that is not absorbed in the small intestine. Alterations in motor and sensory functions of the human colon result in clinical syndromes such as irritable bowel syndrome, functional diarrhoea and chronic constipation, and contribute to symptoms in ulcerative colitis.

The factors controlling regional colonic motor and sensory functions and the actions of pharmacological agents used to modulate human colonic motility and sensation are reviewed to highlight their relevance in disorders characterized by constipation and diarrhoea. This update has focused on the colon and has excluded the anorectum or pelvic floor from detailed consideration. Understanding the pathophysiological principles operating in colonic disorders requires knowledge of colonic motor and sensory functions and their control in health as well as the methodology necessary to assess colonic function.

Colonic physiology

Neural control.

The colon, with other segments of the digestive tract, has intrinsic and extrinsic innervation.1 The intrinsic innervation of the colon, also called the enteric nervous system, comprises myenteric, submucosal and mucosal neuronal layers. Their function is modulated by interneurones through amine and peptide neurotransmitters, including acetylcholine, opioids, norepinephrine, serotonin, somatostatin, cholecystokinin, substance P, vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY) and others. The myenteric plexus regulates smooth muscle function and the submucosal plexus, mucosal ion transport and absorptive processes. In contrast to the upper gastrointestinal tract, there is no organized interdigestive, cyclical, migrating motor complex in the human colon, and the control of colonic motor function remains poorly understood.

The extrinsic innervation of the colon is part of the autonomic nervous system and modulates both motor and sensory functions. The parasympathetic nerve supply conveys both visceral sensory as well as predominantly excitatory pathways to the colon’s motor components. Parasympathetic fibres reach the proximal colon via the vagus nerves along the ileocolonic and middle colic branches of the superior mesenteric artery. The distal colon is supplied by sacral parasympathetic nerves (S2–4) via the pelvic plexus; these fibres traverse the colon as ascending intracolonic fibres as far as, and in some instances including, the proximal colon. The chief excitatory neurotransmitters controlling motor function are acetylcholine and the tachykinins, such as substance P.

The sympathetic nerve supply also conveys both visceral afferent and motor functions; it reaches the colon via the arterial arcades of the superior and inferior mesenteric vessels. Sympathetic input to the gut is generally excitatory to sphincters and inhibitory to non-sphincteric muscle. There is tonic sympathetic input to the gastrointestinal tract; this is at least partially mediated through alpha-2 adrenergic receptors2 located on the soma and axon of cholinergic myenteric neurones. Stimulation of the sympathetic postganglionic fibre hyperpolarizes the cholinergic neurones to relax the bowel muscle.3, 4 In humans, the alpha-2 agonist, clonidine, decreases colonic tone and increases its compliance, while the alpha-2 antagonist, yohimbine, decreases colonic compliance and transiently increases tone.5 In contrast, the alpha-1 agonist, phenylephrine, and the beta-2 agonist, ritrodine, do not appear to influence the tone of the colon.5 These data suggest that the alpha-2 adrenergic system is important in the control of colonic motor function.

Colonic storage and salvage.

The functions of the human colon include the absorption of water, electrolytes and nutrients and the storage and transport of intraluminal contents aborally. Segmentation into haustra compartmentalizes the colon, facilitating mixing, retention of residue and formation of solid stools. In health, the ascending and transverse regions of the colon function as reservoirs and the descending colon acts as a conduit.6 While this reservoir function has been characterized functionally, there is also evidence for an anatomical ‘sphincter’ characterized by a circumferential narrowing by a fold located at the caeco-ascending colon junction.7 The colon is extremely efficient at conserving sodium and water, a facility which is particularly important in sodium-depleted patients in whom the small intestine alone is unable to maintain sodium balance. The minor amount of colonic mucosal secretion that occurs in health is a passive rather than an active process. The metabolic processes of faecal flora in the right hemicolon, fuelled by the delivery of unabsorbed complex polysaccharides and bile acids results in the production of short-chain fatty acids and secondary bile acids which are available for colonic salvage by active reabsorptive processes.

Colonic sensation

The pathways and mechanisms involved in visceral sensation have been reviewed elsewhere.8, 9 The bowel has no specialized sensory end organs other than naked nerve endings within the wall and Pacinian corpuscles in the mesentery. Rapidly conducting A-delta myelinated fibres and slower conducting non-myelinated C fibres convey visceral sensation. Parasympathetic afferents, comprising the majority of nerve fibres in the vagus and pelvic nerves, convey non-conscious sensory information, e.g. to the solitary tract nucleus in the brainstem. Sympathetic afferents which convey painful stimuli travel to the spinal cord via the dorsal root ganglia. Conscious perception of gut events is mediated via a 3-neurone chain from the gut to the brain; the primary or spinal afferent has its cell body in the dorsal root ganglion and synapses with dorsal horn neurones in the spinal cord. The second neurone ascends in the spinothalamic or spinoreticular tracts towards the respective nuclei in the thalamus or reticular formation. The third neurone projects to the higher sensory centres such as the anterior cingulate cortex ( Figure 1).


Figure 1. Ascending sensory and descending modulating pathways involved in visceral sensation. Note the convergence of peripheral and central (descending) pathways on the dorsal horn neurones in the spinal cord (adapted from Camilleri et al., Gastroenterol Clin N Am 1. 996; 25: 247–58.

Download figure to PowerPoint

Visceral sensations and reflexes are modulated by several factors.9 First, a synapse between the spinal afferent and ganglion cells in the prevertebral ganglia which mediates entero-enteric reflex visceral responses10 that may alter the gut smooth muscle tone and increase or decrease the activation of nerve endings within the bowel wall or mesentery. Second, somatic afferents project on the same dorsal horn neurones in the spinal cord with which visceral afferents synapse; this common viscerosomatic projection results in referred pain (or somatic projection of the visceral stimulus) and may also control the ascending or central projection of visceral stimuli by changing the excitability of the dorsal horn neurone. There is wide overlap of projections of somatic and visceral afferents over many spinal laminae, and this may account for the poor localization of visceral sensations. The dorsal horn neurone functions as a ‘gate’ that controls central projections, and this may explain how physical methods such as transcutaneous electrical nerve stimulation or acupuncture can alter perception of visceral sensations. Third, descending noradrenergic and serotonergic pathways arising in the brainstem project to the dorsal horn neurones and modulate the latter’s responses to afferent input. Fourth, the reticular formation and thalamic projections to autonomic, satiety (hypothalamic) and emotional (limbic system) centres induce the changes in affect, appetite, pulse and blood pressure in response to visceral sensations.

Assessment of colonic motor function

Colonic transit.

Contrast fluoroscopy studies have confirmed that the colonic haustra represent static, segmenting contractions appearing as ring-like indentations which partially occlude the colon. During peristalsis, haustra rapidly disappear as concentric contraction waves spread aborally along the unsegmented colon; such mass movements can propel colonic contents from the right colon to the sigmoid colon and rectum in seconds.6, 11, 12 Stool frequency is a poor indicator of colonic transit time given the marked variability of whole gut transit in health. However, as expected, the form of the stool correlates with colonic transit time; the looser the stool, the faster the transit.13, 14

Radiopaque marker method. The most convenient method to assess colonic motor function includes the use of radiopaque markers ( Figure 2).15, 16 In one of the popular methods, for mathematic convenience, 24 markers are ingested at the same time of day on 3 successive days and abdominal radiography is undertaken on day 4 (and again on day 7 if all 72 markers were still present on day 4).16 In health, the average mouth-to-caecum transit time is ≈6 h17 and average regional transit times through the right colon, left colon and sigmoid colon each about 12 h.16 The normal mean colonic transit time is 36 h. Thus, on average, 36 markers are expelled from the colon by day 4 of the transit test; a whole gut transit time of 72 h or more is considered to be abnormally prolonged. Counting the total number of markers in the three segments can usefully distinguish patients with normal transit from those with slow transit constipation. Delayed transit of markers may result either from impaired colonic motility or from a disturbance in defecation, a process that requires a coordination of several functions including pelvic floor and external anal sphincter relaxation.18


Figure 2. Abdominal radiograph showing radiopaque markers in the ascending, descending and the rectosigmoid colonic segments to provide information about regional colonic transit rates. Disorders of pelvic floor function impairing the mechanics of defecation may delay transit through one or more regions; transit data must therefore be interpreted in conjunction with the clinical history and anorectal function test results. Reproduced from von der Ohe MR, Camilleri M. Measurement of small bowel and colonic transit: indications and methods. Mayo Clin Proc, 1992. ; 67: 1169–79.

Download figure to PowerPoint

Radioscintigraphic method.

A more detailed appraisal of regional colonic transit is provided by a non-invasive radio-scintigraphic technique which delivers radiolabelled solid particles to the colon in a pH-sensitive, methacrylate polymer-coated capsule (Figure 3).6 There is a pH gradient down the gastrointestinal tract;19 methacrylate dissolves in the alkaline pH that is unique to the distal small intestine. The terminal ileum delivers its content into the colon periodically as boluses;17 similarly, isotopically-labelled solid particles liberated from such a capsule are delivered to the colon. Sequential gamma camera images quantify the amount of radioactivity in each region as the isotope traverses the colon over time, and provide more detailed information regarding proximal colonic emptying than with radiopaque markers.

Colonic motility (contractility).

Colonic contractions may be simply summarized by short duration or phasic contractions and the background state of contractility or tone of the viscus. Research studies have used electromyography and/or manometry to assess phasic (short duration) colonic contractility. Until relatively recently, such studies have largely been confined to the sigmoid and rectum because of ease of access. Studies of colonic myoelectric activity have demonstrated two patterns: long spike bursts20 associated with high amplitude propagated contractions (HAPCs)21, 22 and short spike bursts20 that may or may not be associated with phasic contractions. HAPCs are sometimes associated with mass movements through the colon and they occur approximately five times per day, usually on awakening in the morning and postprandially.22

Using water-perfused, open-tipped manometry tubes or solid state transducers mounted on a teflon catheter, changes in intraluminal colonic pressure can detect strong contractions that occlude the bowel lumen, but not weak contractions,23 both of which are recorded when sensors are attached to the wall of the colon. Manometrically recorded activity has been widely used as a measure of significant colonic contractions.24 However, real time endoscopic observations of the prepared, human sigmoid colon during simultaneous manometric recordings in the fasting state, have shown that most manometric deflections coincide with relaxation rather than contraction, and that visible wall motion or contraction may produce no deflections on manometry.25 Interpretation of manometric recordings is therefore difficult and caution should be exercised before attempting to attribute manometric pressure profiles to colonic wall motion. Such studies of colonic contractility have not found wide application in the clinical arena.

Colonic tone.

Tone, defined as the state of relaxation or contraction of colonic smooth muscle, refers to the background contractility upon which phasic contractile activity (typically contractions lasting less than 15 s) is superimposed. In order to measure tone, an infinitely compliant polyethylene balloon26 is placed endoscopically, with the aid of fluoroscopy, into different regions of the colon. The balloon is linked to an electronically controlled barostat that maintains a constant intraballoon pressure. Changes in the pressure within the balloon induced by contraction or relaxation of colonic smooth muscle are sensed electronically, triggering the injection or withdrawal of air from the balloon to maintain a constant pressure within it. Thus, alterations in balloon volume reflect changes in colonic tone at the site of the balloon. The close apposition of the balloon with the bowel wall provides two significant advantages over the intraluminal devices. First, it provides a measure of relaxation of the colon, and second, it is more accurate than manometry in detecting significant phasic contractions in a large diameter viscus, especially when the diameter exceeds 5.6 cm.23 Because the rate of response to pressure changes is slower with the barostat than with manometry, it is best suited to measure slower, more sustained contractions, and to assess tone and compliance of the hollow viscera.

Insights into regional colonic function in health.

Using colonic radioscintigraphy, the ascending and transverse regions of the colon have been shown to function as reservoirs where isotope and residue are retained for prolonged periods of time (on average about 15 h in healthy individuals); the descending colon functions predominantly as a conduit in healthy subjects.6 The sigmoid colon and rectum act as a second reservoir until it is socially convenient to allow defecation to occur.6, 27 As will be discussed below, physiological studies show that diarrhoea or constipation may result from alteration in the reservoir function of the proximal colon, or the propulsive function of the left colon. Constipation may also result from disturbances of the rectal or sigmoid reservoir, typically as a result of dysfunction of the pelvic floor or the coordination of defecation.18

The rate of emptying of the proximal colon is influenced by the composition of chyme, for example the intraluminal concentration of fat28 and, to a lesser extent, short-chain fatty acids.29 Oral ingestion of a high-fat meal30 also accelerates proximal colonic emptying. Bowel preparation influences the contractile response of the colon and consequently regional colonic motility and transit profiles.31 Osmotic laxatives, which increase fluid loading to the colon, accelerate ascending colon transit.32 The rate of delivery of liquid to the proximal colon also influences its transit rate. For example, when directly injected after oroceacal intubation,12 marker empties more rapidly than after oral intake of the liquid marker.33, 34 Within the physiological range of rates of delivery of liquid to the ascending colon, fluids and solids have comparable transit.27, 35

Recent studies in humans have examined the physical properties of the wall (e.g. compliance and colonic tone) and sensory function of different regions of the colon. These properties are usually assessed by the subjective perception during distension of a balloon within the colon. Compliance refers to the volume response to an imposed increase in intraluminal pressure (ΔVP). Elastance is the reciprocal of compliance (ΔPV). These properties are assessed by inflating a polyethylene balloon within the colon to defined pressures, and measuring the corresponding volumes. Colonic compliance curves have a sigmoid shape which reflects an initial relaxation phase attributable to active muscle accommodation to the imposed pressure, followed by a linear phase attributable to the elasticity of the colonic wall constituents ( Figure 4). These physical properties vary in the different regions of the colon. Waldron et al. have shown in vivo that the descending colon is less compliant than the ascending colon, a finding attributable to the receptive accommodation which ‘cushions’ the initial pressure load.36Ex vivo, the ascending colon, but not the descending colon, becomes much more compliant than in vivo, an observation which is attributable to the loss of active muscle tone. Conversely, the elastance of the colon (i.e. the pressure increment during standardized volume distensions of 50 and 200 mL) is higher in the descending and sigmoid colon than the proximal regions of the colon.37


Figure 4. . Typical compliance (ΔVP) curve of human descending colon: note the two components, one of active accommodation at low pressure loads due to muscle relaxation, and the other, a more linear passive compliance that reflects the elastic properties of the colonic wall with higher pressure loads.

Download figure to PowerPoint

What are the mechanisms that control the contractile state of the human colon? Apart from the central or extrinsic neural control discussed above, there is evidence for local or peripheral modulation. For example, stretching smooth muscle cells alters their electrical conductance possibly by modulating mechanosensitive gated ion channels;38 peripheral reflexes relaying in the prevertebral ganglia10 are modulated by the level of contractility of the colon in response to mechanical stimulation. Local effects of some neurotransmitters, such as serotonin,39 and hormones, such as glucagon,40 are also different in the proximal and distal colon. These examples highlight the potential importance of the differences in colonic regions. The interactions between physical and neurohumoral factors in the control of colonic motility require further elucidation.

Colonic motility following meal ingestion: topography and pharmacological control

After meal ingestion, colonic phasic and tonic contractility increase for a period of ≈2 h ( Figure 5).41[42][43]–44 The initial phase of the response lasts about 10 min and is mediated at least partly by the vagus nerve since it can be closely simulated by mechanical distension of the stomach.45 The subsequent contractile response after meal ingestion requires caloric stimulation and is thought to be at least partly hormonally mediated, involving gastrin, opioids, serotonin and others.41[42]–43 The increase in tone postprandially is greater in the transverse and descending colon than in the smaller diameter sigmoid colon.44 In contrast, postprandial phasic (i.e. short duration) contractile activity is greater in the sigmoid than in the transverse colon ( Figure 5).44 Thus, the physical properties or diameter of the different colonic regions may influence their motor responses.


Figure 5. Comparison of phasic and tonic contractile response to meal ingestion in healthy humans. Tone response is expressed as the percentage reduction of the volume in a barostatically controlled balloon compared to the fasting period. Phasic contractility is summarized as an area under contractions, or activity index for each 10-min period. Note the greater tone response in the transverse colon and the greater phasic contractile response in the sigmoid colon (data reproduced from Ford et al. Gut 1995. ; 37: 264–69).

Download figure to PowerPoint

Meal ingestion can induce discomfort and a need to defecate in healthy people; a more prominent reflex may cause abdominal pain and/or urgency of defecation in up to a third of patients with irritable bowel syndrome.46 Understanding the mechanisms controlling the reflex colonic response to feeding could provide useful therapeutic options.

Recent studies of the pharmacological modulation of postprandial colonic tone have begun to decipher the neurohumoral codes that control colonic tone and motility. The muscarinic anticholinergic atropine has been shown to reduce tone in all regions of the colon.47 Cholecystokinin had previously been considered as a putative mediator of the postprandial response of the colon.42, 43 However, cholecystokinin in doses producing maximal pancreatic enzyme secretion does not stimulate colonic tone or phasic contractility in humans.48[49]–50

There are at least five subtypes of serotonin receptors and their potential role in modulating gastrointestinal motor and sensory function has been reviewed elsewhere.51, 52 Non-sphincteric gastrointestinal muscle appears to respond chiefly to 5HT3 and 5HT4 agents. The 5HT3 antagonist, ondansetron, inhibits the motor response of the colon to feeding in healthy individuals53, 54 and in patients with carcinoid diarrhoea.55 Other 5HT3 antagonists, such as alosetron, also inhibit colonic tone.56 The postprandial effects of the 5HT3 antagonist ondansetron may result from direct inhibition of colonic motility or from the inhibition of vagal afferents57 which are important in the afferent limb of the ‘reflex’ colonic response.

The somatostatin octapeptide analogue octreotide decreases the tonic response of the descending colon to the ingestion of a meal,58 but paradoxically increases phasic motility in the descending colon58 and rectum.59 The overall effect of relatively low doses of octreotide on colonic transit was not significant.58

Physiological and pharmacological perturbations of colonic sensation in humans

Colonic distension of an infinitely compliant polyethylene balloon results in an intensity-dependent perception of the stimulus.60 Perception of colonic distension can be altered by psychosensory modulation, such as by mental stress or relaxation,60 and by increasing the contraction of the gut smooth muscle by a meal61, 62 or a pharmacological agent, e.g. yohimibine,63 or by hyperventilation.64, 65 Conversely, the threshold for pain sensation is lower in the descending colon than in the more compliant ascending colon,36 suggesting that compliance and tone also modify colonic sensation.9 Visceral nerve endings are also sensitized by ischemia and inflammation.8

Several pharmacological agents alter colonic sensation. Alpha-2 adrenergic agents modulate the perception of pain during mechanical stimulation of the colon, probably via central effects.5 Octreotide alters colonic and rectal sensory function in health and irritable bowel syndrome.66[67][68]–69 Other agents that show promise in altering bowel sensation are the peripheral kappa-opioid agonist, fedotozine,70 and the 5HT3 antagonists such as alosetron71 and cilansetron.72 These pharmacological studies suggest that it may be possible in the future to modulate colonic functions with agents other than the classical antimuscarinic anticholinergic drugs.


  1. Top of page
  2. Abstract
  3. Introduction
  5. Conclusions
  6. Acknowledgements
  7. References


Constipation can result either from delayed transit or outlet obstruction to defecation ( Figure 6);18 other patients report severe constipation, but tests of colonic transit and defecatory function are normal. In idiopathic constipation, a subset of patients exhibit delayed emptying of the ascending and transverse colon with prolongation of colonic transit.73 Slow transit through the right colon was observed in 16 of 91 patients studied with chronic constipation.74 There is also evidence of delayed small bowel transit in some patients with idiopathic constipation,73 but whether this reflects a generalized gut dysmotility or reflex inhibition of small bowel motor function by the hypomotile or stagnant colon is unclear. Outlet obstruction to defecation may cause delayed colonic transit,75 which is usually corrected by biofeedback retraining of the disordered defecation.76 In some patients, constipation persists if colonic transit is still delayed despite the restoration of normal rectal expulsion; these patients may require laxatives or, rarely, subtotal colectomy with ileorectostomy.77 Patients with slow transit rather than normal transit refractory constipation have significantly greater psychological morbidity.78 The association of gastric or small bowel motor dysfunction may be of prognostic value since such patients with a generalized gut dysmotility have a lower rate of long-term success after colectomy than patients with selective colonic dysmotility.79


Figure 6. . Relative frequency of causes of intractable constipation in adult patients referred to the authors at Mayo Clinic. Note that 50% of patients have outlet obstruction to defecation (data reproduced from Surrenti et al. Am J Gastroenterol 1995; 90: 1471–75).

Download figure to PowerPoint

Earlier studies of the contractile activity of the rectum and sigmoid had suggested that functional diarrhoea was associated with absence of rectosigmoid contractions,80, 81 whereas spastic colon and constipation were associated with increased frequency of contractions.81, 82 More recent studies have assessed longer segments or the entire colon; the findings have been somewhat different and the differences are not easily reconciled. Patients with constipation83[84]–85 tend to have reduced colonic contractile activity and, particularly, a reduced number of high amplitude propagated contractions (HAPCs), the manometric correlates of mass movements in the colon.84 HAPCs are typically characterized by an amplitude of greater than 75 mmHg, propagation over a distance of at least 15 cm, and a propagation velocity of 0.15–2.2 cm/s.85 However, the paradoxical reduction of contractions in diarrhoea and increased contractions in constipation were not confirmed in recent studies.

Recent studies have explored the role of colonic tone and phasic contractility in subgroups of patients with constipation.86 These are summarized in Table 1. A few specific comments are pertinent. First, over 24 h, the number of proximal colonic HAPCs is diminished in patients with slow transit constipation.85 Second, the mechanism for the reduced motility of the left hemicolon in the group of patients with outlet obstruction to defecation is unclear. Reduced motility may result either from a viscero-visceral reflex inhibition, stimulated by the chronic distension of the rectum and mediated through extrinsic neural pathways,87, 88 or from a ‘combined’ disorder with associated colonic motor dysfunction.75 Third, megacolon is associated with decreased colonic tone; however, the phasic contractility of the dilated segment was normal;89 extrinsic denervation may cause acute pseudo-obstruction of the colon or Ogilvie’s syndrome,90 which is associated with autonomic imbalance, an impaired pelvic parasympathetic innervation, and a relative predominance of inhibitory sympathetic tone.91

Table 1.  . Colonic motility disorders Thumbnail image of

Patients with spinal cord injury also have delayed proximal and distal colonic transit attributable to the loss of the parasympathetic innervation.92 Fasting colonic tone is normal but the tonic response to feeding is reduced or absent, reflecting the effects of denervation.93 Phasic motility in the distal colon of spinal cord injury patients following feeding is variable,94, 95 and possibly reflects the level of cord injury, adaptation or partial recovery of function, and preservation of some reflex circuits.

Several medications used in the treatment of chronic diarrhoea or constipation have significant effects on proximal or right colon transit ( Table 2).33, 96[97][98][99][100][101][102][103][104][105][106][107]–108 There are no specific treatments for abnormal propulsion of residue through the left colon; left-sided colectomy has been advocated for some patients with intractable constipation109 or localized megacolon,110 but, in general, most colorectal surgeons would perform a subtotal colectomy with ileorectostomy because of the risk of persistence of constipation as a result of delayed transit in the unresected colonic segment.

Table 2.  . Pharmacological agents altering proximal colonic transit in humans Thumbnail image of


Accelerated transit through the proximal colon is demonstrable in a subset of patients with diarrhoea-predominant irritable bowel syndrome;111 proximal colonic transit in these patients may be slowed following therapy with the opioid receptor agonist, trimebutine.103 The marked acceleration (6 × normal) of proximal colonic transit in carcinoid diarrhoea is discussed below.112

Myoelectric and phasic pressure measurements of the left side of the colon in patients with diarrhoeal disorders and diverticular disease have been extensively studied.20, 80[81][82][83][84]–85, 113[114][115][116][117][118]–119 In patients with functional diarrhoea, reduced rectosigmoid myoelectric activity and contractility were reported,81, 82 but more recently some patients with functional diarrhoea had normal colonic tone120 and increased propagated contractions in the colon,113, 120 which often correspond to the postprandial abdominal pain and urgency to defecate in patients with irritable bowel syndrome.46 The clinical syndrome of diarrhoea-predominant irritable bowel syndrome may represent a spectrum of pathophysiological abnormalities which can be identified by careful investigation. Thus, some patients have excessively rapid emptying of the ascending and transverse colon that positively correlated with stool weight,111 others have urgency or increased frequency of defecation of several small volume or ‘pellety’ stools which may result from a ‘hypersensitive’ rectum.121, 122 Further studies are needed to systematically characterize motor and sensory functions in larger numbers of patients with irritable bowel syndrome. The 5HT3 antagonist, ondansetron, has been evaluated in diarrhoea-predominant irritable bowel syndrome and been shown to retard left colonic transit and improve stool consistency.108

Patients with diarrhoea associated with parasympathetic denervation and dysautonomia120 show a lack of contractions in the sigmoid and a markedly reduced tonic response of the descending region after ingestion of a meal. The role of colonic motility in patients with diabetic autonomic neuropathy and chronic diarrhoea is unclear.

In patients with diverticular disease of the colon, the increased colonic contractility suggested the hypothesis that the increase in intraluminal pressures in the sigmoid colon led to increased segmentation and the formation of diverticula;119 the predilection for diverticula in the sigmoid region may reflect the lower compliance of the sigmoid relative to the more proximal colon.44

Patients with ulcerative colitis exhibit urgency of defecation and increased stool frequency123, 124 but no evidence of rapid colonic transit.121, 122 There is increased sensitivity to rectal distention and reduced rectal compliance.123 Paradoxically, a retardation of proximal colonic transit rate124 and decreased colonic phasic contractility have been reported.125 There is no difference in total colonic transit compared to healthy subjects.122 Thus, the greatest contribution of neuromuscular dysfunction in ulcerative colitis appears to reflect alterations in sensation and compliance of the rectum.

Although carcinoid syndrome is a rare condition, much has been learned from in-depth studies of carcinoid patients about the roles of proximal colon capacitance, tone and transit ( Figure 7). Thus, in patients with carcinoid diarrhoea,112 the proximal colonic emptying rate is approximately six times that observed in healthy individuals. There is also accelerated small bowel transit112 and increased jejunal secretion126 resulting in the delivery of a large volume of small bowel content to the ascending colon due to rapid transit, reducing the time available for fluid and electrolyte absorption in the small bowel. The volume of the ascending colon in patients with carcinoid diarrhoea is about one-half that of healthy individuals.112 With an increased volume load delivered from the small intestine, this reduced capacitance of the ascending colon may contribute to the observed rapid emptying of content from the proximal colon. Carcinoid patients also have an exaggerated colonic tonic response to feeding as compared to healthy individuals.112 Ondansetron reduces the magnitude of this tonic response of the colon in patients with carcinoid diarrhoea55 and the new 5HT3 antagonist, alosetron, reduces the rate of emptying of the proximal colon.127 Such findings suggest that 5HT3 receptors mediate, at least in part, the motor dysfunction in carcinoid patients.


Figure 7. Colonic motor physiology in patients with carcinoid diarrhoea. Note the twofold acceleration in small bowel transit rate, sixfold acceleration of the emptying rate of the proximal colon, and reduced capacitance of the ascending colon as measured scintigraphically. Barostat measurement of descending colonic tone reveals hypertonicity of the colon in the postprandial period in carcinoid patients compared to controls. (Reproduced from von der Ohe M, Camilleri M, Kvols LK, Thomforde GM. Motor dysfunction of the small bowel and colon in patients with the carcinoid syndrome and diarrhoea. N Engl J Med 1993; 329: 107. 3–8.)

Download figure to PowerPoint

The results of motility studies in the left colon in functional diarrhoea and constipation are summarized in Table 1. These data suggest that the symptoms and transit disorder may be at least partly determined by alterations in tone, mixing contractions and the frequency of high amplitude propagated phasic contractions. However, little is known about the mechanisms controlling these contractile patterns.

Altered colonic sensation in human disease

Several functional gastrointestinal disorders are associated with visceral hyperalgesia.8 Stress increases perception of colonic mechanical stimuli in health ( Figure 8).60 Rectal hypersensitivity to distension in irritable bowel syndrome was first demonstrated by Ritchie128 and more recently was confirmed by several authors.129, 130 Lembo and co-workers130 also suggested that alteration in dorsal horn neurone function in the spinal cord was important in irritable bowel syndrome because of the widespread somatic projection (called receptive field stimulation) in those patients during rectal balloon distension. The putative mechanisms at play in hyperalgesia in functional gastrointestinal disorders are reviewed by Mayer & Gebhart.8


Figure 8. Effect of psychosensory modulation of sigmoid colonic sensation of a distension stimulus in healthy individuals. Relaxation reduces, and mental stress increases the sensation/perception of gas and pain in healthy individuals (data reproduced from Ford et al. Gastroenterology 1995; 109: 1772–8. 0). Data adjusted for somatic pain sensitivity and pre-treatment colonic sensory score.

Download figure to PowerPoint

Several approaches have been used to attempt to alter visceral sensory function pharmacologically in humans. Lidocaine applied topically to the rectum has been shown to inhibit rectal sensation of a distended balloon.130 Although it was hypothesized that this implied the presence of mucosal mechanoreceptors, it is conceivable that local absorption and spread of the local anaesthetic within the wall of the rectum may have also anaesthetized or desensitized the mechanoreceptors in the muscle layer. Octreotide inhibits the sensation of a rectal balloon distension in healthy subjects67, 69 and in patients with irritable bowel syndrome.66, 131 Based on these preliminary reports, it was suggested that octreotide might be useful to suppress symptoms in patients with irritable bowel syndrome. These interesting findings require confirmation and further study. In particular, it is possible that the effects of octreotide on colonic wall mechanoreceptors could be, at least in part, attributable to the reduction in colonic tone58 with this medication. More recently, the kappa-opioid agonist, fedotozine, was shown to reduce maximal and mean daily pain scores and abdominal bloating in patients with irritable bowel syndrome,132 and the 5HT3 antagonist, alosetron, reduced colonic compliance and tone which might influence sensation or pain perception in patients with irritable bowel syndrome.56

When should colonic motility or sensory tests be performed in clinical practice?

Although much has been learned about colonic sensorimotor function in disease states, the indications for clinical testing of these functions are relatively few. Certainly, the radiopaque marker transit test and tests evaluating the process of defecation have established their place in the evaluation of patients with constipation18 who do not respond to increased bulk or fibre in the diet or to an osmotic laxative such as milk of magnesia. The radiopaque marker transit test is not sensitive enough to detect accelerated transit and should not be used in people with diarrhoea in whom a therapeutic trial with an opioid agent is a more practical approach. Anorectal manometry is indicated in patients with diarrhoea who also experience incontinence.

Although it has been claimed that excessive rectal sensitivity is a biological marker of irritable bowel syndrome,122 the opinion of most workers in this field is that tests of rectal sensation are not yet indicated in the clinical diagnosis of the condition, particularly because the increased sensitivity may be restricted to patients with diarrhoea or urgency.121, 122 Intubated colonic motility studies are only rarely needed clinically because the marker transit tests15, 16, 133 are simple, cost-effective and non-invasive. Assessment of colonic contractility appears worthwhile in patients with slow transit constipation who are being considered for colectomy. In such patients, the preservation of the colon’s response to feeding,86 cholinergic agonists,134 or intraluminal bisacodyl100, 135 excludes inertia, and argues against pursuing a subtotal colectomy and in favour of conservative measures, including use of motility stimulating agents or pelvic floor retraining.


  1. Top of page
  2. Abstract
  3. Introduction
  5. Conclusions
  6. Acknowledgements
  7. References

Applied physiological techniques have facilitated a better understanding of the motor and sensory functions of the human colon in health and disease. These techniques, and the development of novel pharmacological agents, will facilitate further studies of colonic motor and sensory function and hopefully will ensure future improvements in the treatment of colonic disorders associated with constipation and/or diarrhoea.


  1. Top of page
  2. Abstract
  3. Introduction
  5. Conclusions
  6. Acknowledgements
  7. References

We thank Dr Sidney F. Phillips who has provided guidance and intellectual support over the past decade. We are also grateful for the technical support of George Thomforde, Duane Burton and Russell Hanson and the secretarial assistance of Cindy Stanislav. This work was supported in part by General Clinical Research Center grant RR00585 from the National Institutes of Health and by the Samsung Fund for Colonic Motility Research at Mayo Clinic.


  1. Top of page
  2. Abstract
  3. Introduction
  5. Conclusions
  6. Acknowledgements
  7. References
  • 1
    Christensen J. Gross and microscopic anatomy of the large intestine. In: Phillips SF, Pemberton JH, Shorter RG, eds. The Large Intestine: Physiology, Pathophysiology and Disease. New York: Raven Press, 1996: 13 35.
  • 2
    Gillis RA, Dias Souza J, Hicks KA, et al. Inhibitory control of proximal colonic motility by the sympathetic nervous system. Am J Physiol 1987; 253: G531 9.
  • 3
    Del Tacca M, Tadini P, Blandizzi C, Bernardini MC. Excitatory and inhibitory cholinergic effects of yohimbine on isolated guinea-pig small intestine. Pharmacol Res Comm 1988; 20: 673 84.
  • 4
    Hillsley K, Schemann M, Grundy D. Alpha-adrenoreceptor modulation of neurally evoked circular muscle responses of the guinea pig stomach. J Auton Nerv Syst 1992; 40: 5757 62.
  • 5
    Bharucha AE, Camilleri M, Zinsmeister AR, Hanson RB. Adrenergic modulation of human colonic motor and sensory function. Am J Physiol, 1997; 273: G997–1006.
  • 6
    Proano M, Camilleri M, Phillips SF, Brown ML, Thomforde GM. Transit of solids through the human colon: regional quantification in the unprepared bowel. Am J Physiol 1990; 258: G856 62.
  • 7
    Faussone Pellegrini MS, Manneschi LI, Manneschi L. The caecocolonic junction in humans has a sphincteric anatomy and function. Gut 1995; 37: 493 8.
  • 8
    Mayer EA & Gebhart GF. Basic and clinical aspects of visceral hyperalgesia. Gastroenterology 1994; 107: 271 93.
  • 9
    Camilleri M, Saslow SB, Bharucha AE. Gastrointestinal sensation: mechanisms and relation to functional gastrointestinal disorders. In: Camilleri M, ed. Gastroenterology Clinics of North America: Gastrointestinal Motility in Clinical Practice, Vol. 25. Philadelphia: WB Saunders, 1996: 247 58.
  • 10
    Parkman HP, Ma RC, Stapelfeldt WH, Szurszewski JH. Direct and indirect mechanosensory pathways from the colon to the inferior mesenteric ganglion. Am J Physiol 1993; 265: G499 505.
  • 11
    Ritchie JA. Colonic motor activity and bowel function. Part 1 Normal movement of the contents. Gut 1968; 9: 442 56.
  • 12
    Krevsky B, Malmud LS, D’ercole F, Maurer AH, Fisher RS. Colonic transit scintigraphy. A physiologic approach to the quantitative measurement of colonic transit in humans. Gastroenterology 1986; 91: 1102 12.
  • 13
    O’donnell LJ, Virjee J, Heaton KW. Detection of pseudodiarrhoea by simple clinical assessment of intestinal transit rate. Br Med J 1990; 300: 439 40.
  • 14
    Degen L & Phillips SF. How well does stool consistency reflect colonic transit? Gut 1996; 39: 109 13.
  • 15
    Arhan P, Devroede G, Jehannin B, et al. Segmental colonic transit time. Dis Colon Rect 1981; 24: 625 9.
  • 16
    Metcalf AM, Phillips SF, Zinsmeister AR, MacCarty RL, Beart RW, Wolff BG. Simplified assessment of segmental colonic transit. Gastroenterology 1987; 92: 40 7.
  • 17
    Camilleri M, Colemont LJ, Phillips SF , et al. Human gastric emptying and colonic filling of solids characterized by a new method. Am J Physiol 1989; 257: G284 90.
  • 18
    Camilleri M, Thompson WG, Fleshman JW, Pemberton JH. Clinical management of intractable constipation. Ann Intern Med 1994; 121: 520 8.
  • 19
    Fordtran JS & Locklear TW. Ionic constituents and osmolality of gastric and small intestinal fluids after eating. Am J Dig Dis 1966; 11: 503 21.
  • 20
    Frexinos J, Bueno L, Fioramonti J. Diurnal changes in myoelectric spiking activity of the human colon. Gastroenterology 1985; 88: 1104 10.
  • 21
    Schang JC, Hemond M, Hebert M, Pilote M. Myoelectrical activity and intraluminal flow in human sigmoid colon. Dig Dis Sci 1986; 31: 1331 7.
  • 22
    Narducci F, Bassotti G, Gaburri M, Morelli A. Twenty-four hour manometric recording of colonic motor activity in healthy man. Gut 1987; 28: 17 25.
  • 23
    Von Der Ohe M, Hanson RB, Camilleri M. Comparison of simultaneous recordings of human colonic contractions by manometry and a barostat. Neurogastroenterol Motil 1994; 6: 213 22.
  • 24
    Sarna SK, Latimer P, Campbell D, Whitehead WE. Electrical and contractile activities of the human rectosigmoid. Gut 1982; 23: 689 705.
  • 25
    Sakari Y, Hada R, Nakajima H, Munakata A. Difficulty in estimating localized bowel contraction by colonic manometry: a simultaneous recording of intraluminal pressure and calibre. Neurogastroenterol Motil 1996; 8: 247 53.
  • 26
    Steadman CJ, Phillips SF, Camilleri M, Haddad A, Hanson R. Variation of muscle tone in the human colon. Gastroenterology 1991; 101: 373 81.
  • 27
    Hammer J & Phillips SF. Fluid loading of the human colon: effects on segmental transit and stool composition. Gastroenterology 1993; 105: 988 98.
  • 28
    Spiller RC, Brown ML, Phillips SF. Decreased fluid tolerance, accelerated transit, and abnormal motility of the human colon induced by oleic acid. Gastroenterology 1986; 91: 100 7.
  • 29
    Kamath PS, Phillips SF, O’connor MK, Brown ML, Zinsmeister AR. Colonic capacitance and transit in man: modulation by luminal contents and drugs. Gut 1990; 31: 443 9.
  • 30
    Steed KP, Bohemen EK, Lamont GM, Evans DF, Wilson CG, Spiller RC. Proximal colonic response and gastrointestinal transit after high and low fat meals. Dig Dis Sci 1993; 38: 1793 800.
  • 31
    Lemann M, Flourie B, Picon L, Coffin B, Jian R, Rambaud JC. Motor activity recorded in the unprepared colon of healthy humans. Gut 1995; 37: 649 53.
  • 32
    Barrow L, Steed KP, Spiller RC, et al. Scintigraphic demonstration of lactulose-induced accelerated proximal colon transit. Gastroenterology 1992; 103: 1167 73.
  • 33
    Maurer AH & Krevsky B. Whole gut transit scintigraphy in the evaluation of small bowel and colon transit disorders. Semin Nucl Med 1995; 25: 326 38.
  • 34
    Maurer AH, Krevsky B, Knight LC, Brown K. Opioid and opioid-like drug effects on whole gut transit measured by scintigraphy. J Nucl Med 1996; 37: 818 22.
  • 35
    Proano M, Camilleri M, Phillips SF, Thomforde GM, Brown ML, Tucker RL. The unprepared human colon does not discriminate between solids and liquids. Am J Physiol 1991; 260: G13 16.
  • 36
    Waldron DJ, Gill RC, Bowes KL. Pressure response of human colon to intraluminal distension. Dig Dis Sci 1989; 34: 1163 7.
  • 37
    Frieri G, Ligas E, Ciccocioppo R, Onori L, Caprilli R. Human colonic compliance. Gastroenterology 1994; 106: A501(Abstract).
  • 38
    Burnstock G & Prosser CL. Responses of smooth muscles to quick stretch; relation of stretch to conductance. Am J Physiol 1960; 198: 921.
  • 39
    Fink S & Friedman G. The differential effect of drugs on the proximal and distal colon. Am J Med 1960; 28: 534 40.
  • 40
    Strom JA, Condon RE, Schulte WJ, Cowles V, Go VL. Glucagon, gastric inhibitory polypeptide and the gastrocolic response. Am J Surg 1982; 143: 155 9.
  • 41
    Snape WJ Jr, Wright SH, Battle WM, Cohen S. The gastrocolic response: evidence for a neural mechanism. Gastroenterology 1979; 77: 1235 40.
  • 42
    Snape WJ Jr, Matarazzo SA, Cohen S. Effect of eating and gastrointestinal hormones on human colonic myoelectrical and motor activity. Gastroenterology 1978; 75: 373 8.
  • 43
    Snape WJ Jr, Carlson GM, Cohen S. Human colonic myoelectric activity in response to prostigmin and the gastrointestinal hormones. Am J Dig Dis 1977; 22: 881 7.
  • 44
    Ford MJ, Camilleri M, Wiste JA, Hanson RB. Differences in colonic tone and phasic responses to a meal in the transverse and sigmoid human colon. Gut 1995; 37: 264 9.
  • 45
    Wiley J, Tatum D, Keinath R, Owyang C. Participation of gastric mechanoreceptors and intestinal chemoreceptors in the gastrocolonic response. Gastroenterology 1988; 94: 1144 9.
  • 46
    Chaudhary NA & Truelove SC. The irritable colon syndrome. A study of the clinical features, predisposing causes and prognosis in 130 cases. Q J Med 1962; 31: 307 22.
  • 47
    Steadman CJ, Phillips SF, Camilleri M, Talley NJ, Haddad A, Hanson R. Control of muscle tone in the human colon. Gut 1992; 33: 541 6.
  • 48
    O’brien MD, Camilleri M, Thomforde GM, Wiste JA, Hanson RB, Zinsmeister AR. Effect of cholecystokinin octapeptide and atropine on human colonic motility, tone and transit. Dig Dis Sci 1997; 42: 26 33.
  • 49
    Kellow JE, Miller LJ, Phillips SF, Haddad AC, Zinsmeister AR, Charboneau JW. Sensitivities of human jejunum, ileum, proximal colon, and gallbladder to cholecystokinin octapeptide. Am J Physiol 1987; 252: G345 56.
  • 50
    Mangel AW, Brazer SR, Smith JW, Fitz JG, Taylor IL. Inhibition of colonic motility by cholecystokinin. Ann Med 1992; 24: 341 2.
  • 51
    Camilleri M & Von Der Ohe MR. Drugs affecting serotonin receptors. Bailleres Clin Gastroenterol 1994; 8: 301 19.
  • 52
    Talley NJ. 5-hydroxytryptamine agonists and antagonists in the modulation of gastrointestinal motility and sensation: clinical implications. Aliment Pharmacol Ther 1992; 6: 273 89.
  • 53
    Von Der Ohe MR, Hanson RB, Camilleri M. Serotonergic mediation of postprandial colonic tonic and phasic responses in humans. Gut 1994; 35: 536 41.
  • 54
    Scolapio JS, Camilleri M, Von Der Ohe MR, Hanson RB. Ascending colon response to feeding: evidence for a 5-hydroxytryptamine-3 mechanism. Scand J Gastroenterol 1995; 30: 562 7.
  • 55
    Von Der Ohe MR, Camilleri M, Kvols LK. A 5HT3 antagonist corrects the postprandial colonic hypertonic response in carcinoid diarrhea. Gastroenterology 1994; 106: 1184 9.
  • 56
    Delvaux M, Louvel D, Mamet JP, Campos-Oriola R, Forster E, Frexinos J. Effect of alosetron on colonic sensitivity in patients with irritable bowel syndrome. Gastroenterology 1996; 110: A655(Abstract).
  • 57
    Cubeddu LX, Hoffmann IS, Fuenmayor NT, Finn AL. Efficacy of ondansetron (GR38032F) and the role of serotonin in cisplatin-induced nausea and vomiting. N Engl J Med 1990; 322: 810 16.
  • 58
    Von Der Ohe MR, Camilleri M, Thomforde GM, Klee GG. Differential regional effects of octreotide on human gastrointestinal motor function. Gut 1995; 36: 743 8.
  • 59
    Hasler WL, Soudah HC, Owyang C. A somatostatin analogue inhibits afferent pathways mediating perception of rectal distension. Gastroenterology 1993; 104: 1390 7.
  • 60
    Ford MJ, Camilleri M, Zinsmeister AR, Hanson RB. Psychosensory modulation of colonic sensation in the human transverse and sigmoid colon. Gastroenterology 1995; 109: 1772 80.
  • 61
    Musial F, Crowell MD, Kalveram KT, Enck P. Nutrient ingestion increases rectal sensitivity in humans. Physiol Behav 1994; 55: 953 6.
  • 62
    Erckenbrecht JF, Hemstege M, Ruhl A, Krause J. The sensory component of the gastrocolonic response revisited: postprandial colonic pain perception depends on meal composition. Gastroenterology 1994; 106: A494(Abstract).
  • 63
    Malcolm A, Phillips SF, Camilleri M, Burton DD, Hanson RB. Does rectal tone or compliance influence sensation? Dig Dis Sci 1996; 41: 1883.
  • 64
    Ford MJ, Camilleri M, Hanson RB, Wiste JA, Joyner MJ. Hyperventilation, central autonomic control, and colonic tone in humans. Gut 1995; 37: 499 504.
  • 65
    Bharucha AE, Camilleri M, Ford MJ, O’connor MK, Hanson RB, Thomforde GM. Hyperventilation alters colonic motor and sensory function: effects and mechanisms in humans. Gastroenterology 1996; 111: 368 77.
  • 66
    Hasler WL, Soudah HC, Owyang C. Somatostatin analog inhibits afferent response to rectal distension in diarrhea-predominant irritable bowel patients. J Pharm Exp Ther 1994; 268: 1206 11.
  • 67
    Plourde V, Lembo T, Shui Z, et al. Effects of the somatostatin analogue, octreotide, on rectal afferent nerves in humans. Am J Physiol 1993; 265: G742 51.
  • 68
    Mertz H, Walsh JH, Sytnik B, Mayer EA. The effect of octreotide on human gastric compliance and sensory perception. Neurogastroenterol Motil 1995; 7: 175 85.
  • 69
    Chey WD, Beydoun A, Roberts DJ, Hasler WL, Owyang C. Octreotide reduces perception of rectal electrical stimulation by spinal afferent pathway inhibition. Am J Physiol 1995; 269: G821 6.
  • 70
    Junien JL & Riviere P. Review article: the hypersensitive gut—peripheral kappa agonists as a new pharmacological approach. Aliment Pharmacol Ther 1995; 9: 117 26.
  • 71
    Maxton DG, Morris J, Whorwell PJ. Selective 5-hydroxytryptamine antagonism: a role in irritable bowel syndrome and functional dyspepsia. Aliment Pharmacol Ther 1996; 10: 595 9.
  • 72
    Sanger GJ. 5-hydroxytryptamine and functional bowel disorders. Neurogastroenterol Motil 1996; 8: 319 31.
  • 73
    Stivland T, Camilleri M, Vassallo M, et al. Scintigraphic measurement of regional gut transit in idiopathic constipation. Gastroenterology 1991; 101: 107 15.
  • 74
    Chaussade S, Khyari A, Roche H, et al. Determination of total and segmental colonic transit time in constipated patients. Results in 91 patients with a new simplified method. Dig Dis Sci 1989; 34: 1168 72.
  • 75
    Surrenti E, Rath DM, Pemberton JH, Camilleri M. Audit of constipation in a tertiary-referral gastroenterology practice. Am J Gastroenterol 1995; 90: 1471 5.
  • 76
    Enck P. Biofeedback training in disordered defecation. A critical review. Dig Dis Sci 1993; 38: 1953 60.
  • 77
    Nyam DC, Pemberton JH, Ilstrup DM, Rath DM. Long-term results of surgery for chronic constipation. Dis Colon Rectum 1997; 40: 273 9.
  • 78
    Wald A, Burgio K, Holeva K, Locher J. Psychological evaluation of patients with severe idiopathic constipation: which instrument to use. Am J Gastroenterol 1992; 87: 977 80.
  • 79
    Redmond JM, Smith GW, Barofsky I, Ratych RE, Goldsborough DC, Schuster MM. Physiological tests to predict long-term outcome of total abdominal colectomy for intractable constipation. Am J Gastroenterol 1995; 90: 748 53.
  • 80
    Connell AM & McKelvey ST. The influence of vagotomy on the colon. Gut 1970; 6: 37 9.
  • 81
    Connell AM. The motility of the pelvic colon; Part II. Paradoxical motility in diarrhoea and constipation. Gut 1962; 3: 342 8.
  • 82
    Bueno L, Fioramonti J, Ruckebusch Y, Frexinos J, Coulom P. Evaluation of colonic myoelectrical activity in health and functional disorders. Gut 1980; 21: 480 5.
  • 83
    Bazzocchi G, Ellis J, Villanueva-Meyer J, et al. Postprandial colonic transit and motor activity in chronic constipation. Gastroenterology 1990; 98: 686 93.
  • 84
    Bassotti G, Chiarioni G, Vantini I, et al. Anorectal manometric abnormalities and colonic propulsive impairment in patients with severe chronic idiopathic constipation. Dig Dis Sci 1994; 39: 1558 64.
  • 85
    Bassotti G, Crowell MD, Whitehead WE. Contractile activity of the human colon: lessons from 24 hour studies. Gut 1993; 34: 129 33.
  • 86
    O’brien MD, Camilleri M, Von Der Ohe MR, et al. Motility and tone of the left colon in constipation: a role in clinical practice? Am J Gastroenterol 1996; 91: 2532 8.
  • 87
    Weems WA & Szurszewski JH. Modulation of colonic motility by peripheral neural inputs to neurons of the inferior mesenteric ganglion. Gastroenterology 1977; 73: 273 8.
  • 88
    Kreulen DL & Szurszewski JH. Reflex pathways in the abdominal prevertebral ganglia: evidence for a colo-colonic inhibitory reflex. J Physiol 1979; 295: 21 32.
  • 89
    Von Der Ohe MR, Camilleri M, Carryer PW. A patient with localized megacolon and intractable constipation: evidence for impairment of colonic muscle tone. Am J Gastroenterol 1994; 89: 1867 70.
  • 90
    Ogilvie H. Large intestine colic due to sympathetic denervation: a new clinical syndrome. Br Med J 1948; 2: 671 3.
  • 91
    Vanek VW & Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie’s syndrome): an analysis of 400 cases. Dis Colon Rectum 1986; 29: 203 10.
  • 92
    Keshavarzian A, Barnes WE, Bruninga K, Nemchausky B, Mermall H, Bushnell D. Delayed colonic transit in spinal cord-injured patients measured by indium-111 Amberlite scintigraphy. Am J Gastroenterol 1995; 90: 1295 300.
  • 93
    Bruninga K & Camilleri M. Colonic motility and tone after spinal cord and cauda equina injury. Am J Gastroenterol 1997; 92: 891 4.
  • 94
    Connell AM, Frankel H, Guttmann L. The motility of the pelvic colon following complete lesions of the spinal cord. Paraplegia 1963; 1: 98 115.
  • 95
    Glick ME, Meshkinpour H, Haldeman S, Hoehler F, Downey N, Bradley WE. Colonic dysfunction in patients with thoracic spinal cord injury. Gastroenterology 1984; 86: 287 94.
  • 96
    Staniforth DH, Baird IM, Fowler J, Lister RE. The effects of dietary fibre on upper and lower gastro-intestinal transit times and faecal bulking. J Int Med Res 1991; 19: 228 33.
  • 97
    Pontes FA, Silva AT, Cruz AC. Colonic transit times and the effect of lactulose or lactitol in hospitalized patients. Eur J Gastroenterol Hepatol 1995; 7: 441 6.
  • 98
    Barrow L, Steed KP, Spiller RC, et al. Scintigraphic demonstration of lactulose-induced accelerated proximal colon transit. Gastroenterology 1992; 103: 1167 73.
  • 99
    Klauser AG, Muhldorfer BE, Voderholzer WA, Wenzel G, Muller-Lissner SA. Polyethylene glycol 4000 for slow transit constipation. Z fur Gastroenterologie 1995; 33: 5 8.
  • 100
    Preston DM & Lennard-Jones JE. Pelvic motility and response to intraluminal bisacodyl in slow transit constipation. Dig Dis Sci 1985; 30: 289 94.
  • 101
    Krevsky B, Malmud LS, Maurer AH, Somers MB, Siegel JA, Fisher RS. The effect of oral cisapride on colonic transit. Aliment Pharmacol Ther 1987; 1: 293 304.
  • 102
    Krevsky B, Maurer AH, Malmud LS, Fisher RS. Cisapride accelerates colonic transit in constipated patients with colonic inertia. Am J Gastroenterol 1989; 84: 882 7.
  • 103
    Schang JC, Devroede G, Pilote M. Effects of trimebutine on colonic function in patients with chronic idiopathic constipation: evidence for the need of a physiologic rather than clinical selection. Dis Colon Rectum 1993; 36: 330 6.
  • 104
    Schiller LR, Santa Ana CA, Morawski SG, Fordtran JS. Mechanism of the antidiarrheal effect of loperamide. Gastroenterology 1984; 86: 1475 80.
  • 105
    Awouters F, Megens A, Verlinden M, Schuurkes J, Niemegeers C, Janssen PAJ. Loperamide. Survey of studies on mechanism of its antidiarrhoeal activity. Dig Dis Sci 1993; 38: 977 95.
  • 106
    Krevsky B, Maurer AH, Niewiarowski T, Cohen S. Effect of verapamil on human intestinal transit. Dig Dis Sci 1992; 37: 919 24.
  • 107
    Talley NJ, Phillips SF, Haddad A, et al. GR 38032F (ondansetron), a selective 5HT3 receptor antagonist, slows colonic transit in healthy man. Dig Dis Sci 1990; 35: 477 80.
  • 108
    Steadman CJ, Talley NJ, Phillips SF, Zinsmeister AR. Selective 5-hydroxytryptamine type 3 receptor antagonism with ondansetron as treatment for diarrhea-predominant irritable bowel syndrome: a pilot study. Mayo Clin Proc 1992; 67: 732 8.
  • 109
    Kamm MA, Van Der Sijp JR, Hawley PR, Phillips RK, Lennard-Jones JE. Left hemicolectomy with rectal excision for severe idiopathic constipation. Int J Colorect Dis 1991; 6: 49 51.
  • 110
    Stabile G, Kamm MA, Phillips RK, Hawley PR, Lennard-Jones JE. Partial colectomy and coloanal anastomosis for idiopathic megarectum and megacolon. Dis Colon Rectum 1992; 35: 158 62.
  • 111
    Vassallo M, Camilleri M, Phillips SF, Brown ML, Chapman NJ, Thomforde GM. Transit through the proximal colon influences stool weight in the irritable bowel syndrome. Gastroenterology 1992; 102: 102 8.
  • 112
    Von Der Ohe M, Camilleri M, Kvols LK, Thomforde GM. Motor dysfunction of the small bowel and colon in patients with the carcinoid syndrome and diarrhea. N Engl J Med 1993; 329: 1073 8.
  • 113
    Bazzocchi G, Ellis J, Villanueva-Meyer J, et al. Effect of eating on colonic motility and transit in patients with functional diarrhea. Simultaneous scintigraphic and manometric evaluations. Gastroenterology 1991; 101: 1298 306.
  • 114
    Sarna SK, Latimer P, Campbell D, Waterfall WE. Electrical and contractile activities of the human rectosigmoid. Gut 1982; 23: 689 705.
  • 115
    Sakari Y, Hada R, Nakajima H, Munakata A. Difficulty in estimating localized bowel contraction by colonic manometry: a simultaneous recording of intraluminal pressure and calibre. Neurogastroenterol Motil 1996; 8: 247 53.
  • 116
    Eastwood MA, Smith AN, Brydon WG, Pritchard J. Colonic function in patients with diverticular disease. Lancet 1978; i: 1181 2.
  • 117
    Ritchie JA. Colonic motor activity and bowel function: Part 1. Normal movement of the contents Gut 1968; 9: 442 56.
  • 118
    Katshinski M, Lederer P, Ellermann A, Gansleben R, Lux G, Arnold R. Myoelectric and amanometric patterns of human rectosigmoid colon in irritable bowel syndrome and diverticulosis. Scand J Gastroenterol 1990; 25: 761 8.
  • 119
    Painter NS, Truelove SC, Ardran GM, Tuckey M. Segmentation and the localization of intraluminal pressures in the human colon with special reference to the pathogenesis of colonic diverticula. Gastroenterology 1965; 49: 169 77.
  • 120
    Choi M-G, Camilleri M, O’brien MD, Kammer PP, Hanson RB. A pilot study of motility and tone of the left colon in diarrhea due to functional disorders and dysautonomia. Am J Gastroenterol 1997; 92: 297 302.
  • 121
    Prior A, Maxton DG, Whorwell PJ. Anorectal manometry in irritable bowel syndrome: differences between diarrhoea- and constipation-predominant subjects. Gut 1990; 31: 458 62.
  • 122
    Mertz H, Naliboff B, Munakata J, Niazi N, Mayer EA. Altered rectal perception is a biological marker of patients with irritable bowel syndrome. Gastroenterology 1995; 109: 40 52.
  • 123
    Farthing MJG & Lennard-Jones JE. Sensibility of the rectum to distension and anorectal distension reflex in ulcerative colitis. Gut 1978; 19: 64 9.
  • 124
    Rao SSC, Read NW, Brown C, Bruce C, Holdsworth CD. Studies on the mechanism of bowel disturbance in ulcerative colitis. Gastroenterology 1987; 93: 934 40.
  • 125
    Reddy SN, Bazzocchi G, Chan S, et al. Colonic motility and transit in health and ulcerative colitis. Gastroenterology 1991; 101: 1289 97.
  • 126
    Donowitz M & Binder HJ. Jejunal fluid and electrolyte secretion in carcinoid syndrome. Am J Dig Dis 1975; 20: 1115 22.
  • 127
    Saslow SB, Scolapio JS, Camilleri M, et al. Medium-term effects of alosetron in patients with carcinoid diarrhea. Gut, in press.
  • 128
    Ritchie J. Pain from distension of the pelvic colon by inflating a balloon in the irritable colon sydnrome. Gut 1973; 14: 125 32.
  • 129
    Whitehead WE, Holtkotter B, Enck P, et al. Tolerance for rectosigmoid distension in irritable bowel syndrome. Gastroenterology 1990; 98: 1187 92.
  • 130
    Lembo T, Munakata J, Mertz H, et al. Evidence for the hypersensitivity of lumbar splanchnic afferents in irritable bowel syndrome. Gastroenterology 1994; 107: 1686 96.
  • 131
    Bradette M, Delvaux M, Staumont G, Fioramonti J, Bueno L, Frexinos J. Octreotide increases thresholds of colonic visceral perception in IBS patients without modifying muscle tone. Dig Dis Sci 1994; 39: 1171 8.
  • 132
    Dapoigny M, Abitbol JL, Fraitag B. Efficacy of peripheral kappa agonist fedotozine vs. placebo in treatment of irritable bowel syndrome. A multicenter dose–response study. Dig Dis Sci 1995; 40: 2244 9.
  • 133
    Camilleri M & Zinsmeister AR. Towards a relatively inexpensive, noninvasive, accurate test for colonic motility disorders. Gastroenterology 1992; 103: 36 42.
  • 134
    Bassotti G, Chiarioni G, Imbimbo BP, et al. Impaired colonic motor response to cholinergic stimulation in patients with severe chronic idiopathic (slow transit type) constipation. Dig Dis Sci 1993; 38: 1040 5.
  • 135
    Schang JC, Hemond M, Hebert M, Pilote M. Changes in colonic myoelectric spiking activity during stimulation by bisacodyl. Can J Physiol Pharmacol 1986; 64: 39 43.