SEARCH

SEARCH BY CITATION

Keywords:

  • bisacodyl;
  • high-amplitude propagating contraction;
  • manometric recording;
  • slow transit constipation

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

Abstract  The aims of this study were to assess the prevalence of manometric colonic abnormalities and to evaluate the motor effect of intraluminal bisacodyl in a cohort of refractory constipated patients. Twenty-four hour colonic motility recordings were performed in 40 patients referred for a severe intractable chronic constipation. At the end of each recording session the motor effects of the endoluminal instillation of 10 mg bisacodyl were assessed. These patients were compared with 20 healthy subjects. The number of high-amplitude propagating contractions (HAPC) was significantly decreased in patients with slow transit constipation (12 ± 11.6 vs 1 ± 8.6, P < 0.001). Based on manometric patterns four groups of patients were isolated. Ten patients had no spontaneous HAPC, no food-induced colonic motor response and significantly lower colonic activity in transverse colon (374 ± 1220 vs 3249 ± 3458, P < 0.05). Five patients had significantly increased sigmoid segmental motility (20298 ± 6364 vs 88780 ± 3643, P < 0.001) and eight patients had significantly lower number of HAPC without other manometric abnormalities while 17 patients had normal colonic motility recordings. Endoluminal bisacodyl was able to induce HAPCs in all groups of patients. Patients with severe slow transit refractory constipation represented a heterogeneous group and endoluminal bisacodyl was able to promote a propagated motor activity in a majority of patients even in those suspected of having an inert colon.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

Some patients suffer from a severe constipation that is not improved by medical management and that impairs severely their quality of life, limiting their lifestyle. In these cases of severe chronic constipation, when clinical presentation and results of colonic transit time studies demonstrate a slow transit constipation without pelvic floor dysfunction, patients may be referred for surgical treatment.1,2 However the pathophysiology of this severe constipation has not been studied extensively. Colonic manometric studies performed have shown a decreased or absent colonic motor response to a meal and a lower incidence of high-amplitude propagated contractions (HAPC).3–6 But in these studies, only few patients were analysed and most of the time not compared with normal subjects. Moreover, the study of the effects of colonic local instillation of bisacodyl has been suggested by many teams as useful in the interpretation of colonic manometry, as this drug has proved to be able to induce HAPC in severe slow transit constipated patients.7–9 Manometric examination with bisacodyl provocative test is not routinely available in each centre and patients have to be referred to specialized tertiary centres to evaluate underlying pathophysiological disorder and to optimize management.

The aim of our study was to determine among a population of severely constipated patients referred to a tertiary centre for refractory slow transit constipation the prevalence of manometric abnormalities and to assess the effect of endoluminal colonic instillation of bisacodyl in these patients.

Patients

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

Forty consecutive patients, 34 women and six men, mean age 44 years (range: 19–68), were included in the study. Subjects were recruited between 1 January 1997 and 1 January 2001. All patients were referred to our unit to investigate a long-term (mean duration 20 years, range: 2–60) and severe intractable constipation; 16 of them have been suffering for constipated since early childhood.

All patients failed to respond to conventional high-fibre diet and to various medical treatments, including high doses of osmotic or saline laxatives and macrogol solutions. The failure of an oral therapeutic challenge using stimulant laxatives was required prior to the inclusion. Failure of treatment was defined by a number of stools remaining lower than three per week. An important faecal stasis on the abdominal plain film and a total colonic transit time longer than 100 h (median: 129, range: 100–144) with the Bouchoucha's technique10 was also used as an inclusion criteria. Subjects with an isolated delayed transit only in the rectal area were excluded.

Colonoscopy, blood chemistry and physical examination were performed in all patients to exclude the presence of constipation secondary to organic disease. In particular, diabetes mellitus and hypothyroidism were excluded in every patient. Pelvic floor clinical examination, anorectal manometry, rectal sensory testing and dynamic proctography were normal in all the 40 patients, excluding pelvic floor dysfunction as a possible cause of refractory constipation.11 None of the 40 patients were taking drugs acting on colonic motility, particularly calcium channel blockers and antidepressants that impair colonic motility.12

Seventeen patients (42.5%) had chronic intermittent abdominal pain and/or discomfort, although constipation was the predominant symptom. None of these 17 patients fulfilled ROME II criteria for irritable bowel syndrome.13

Healthy volunteers

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

A group of 20 healthy volunteers, 15 women and five men, mean age 37.5 years (range: 19–60) totally symptom-free was compared with the patient group. These patients had a normal bowel habit, defined as a stool frequency lower than three stools per day and higher than three stools per week. They had never been constipated in the past, had never complained from abdominal pain or bloating, had never received antidepressants or other drugs acting on the central nervous system and had not received any treatment in the month preceding the colonic motility recording. They had no history of previous gastrointestinal disorder or gastrointestinal surgery. Female subjects had a negative pregnancy test.

Recording system

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

 Open-tipped 12-lumen PVC mano- metric catheters with the recording ports spaced 10 cm apart (Marquat SA, Boissy-St Leger, France) were used. The lumen of the catheters was constantly perfused with air-free distilled water at 0.5 mL min−1 by a low compliance pneumohydraulic pump. At this perfusion rate, the system yielded a pressure rise to a distal occlusion of 200 mmHg s−1. Intraluminal pressures were recorded by external pressure transducers (Statham P23 ID, Oxnard, CA, USA) and pressure signals were digitized at a 5-Hz frequency channel to be stored on the hard disk of an IBM/PC computer.

Method

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

For several days, subjects underwent large bowel cleansing with several large tap water enemas and high doses of oral polyethylene glycol cleansing solution. They ate a low residue meal on the 5 days before the recording session and did not fast before being monitored. Patients were anaesthetized (propofol) and the probe was inserted into the colon by a colonoscope (Video CF 1301; Olympus Inc., Paris, France). A 12-catheter probe was attached to the colonoscope by a silk thread held by a biopsy forceps inside the operational channel of the endoscope and both were inserted into the colon. Once the probe was in place, the biopsy forceps was opened and the endoscope withdrawn leaving the catheter in place. The probe was inserted as far as possible into the transverse colon.14 The rigidity of the probe did not allow the probe to be clipped to the colonic wall to avoid migration as recently described.15

The probe was always inserted before 14.00 hours the first day. To eliminate any potential effect from enemas, air or anaesthesia, recording sessions always began at 08.00 am the following morning with an interval of at least 18 h between probe insertion and beginning of the recording. The position of the probe was checked by X-ray just before and after each recording session to be sure that the probe did not move distally during the measurement. The colonic site of each recording ports was determined according to the position of the probe on the X-ray control and allocated as rectosigmoid, descending and transverse colon for further analysis. Recordings were stopped on the third day at 12.00 am. Subjects remained supine in bed for the next 28 h of the recording session. They were not allowed to stand up. During recording sessions, patients were allowed to drink water ad libitum. The first day of recording, two 1000-Kcal standard meals (carbohydrates 40%, lipids 35%, proteins 25%) were given at 12.00 am and 07.00 pm. One 460-Kcal continental breakfast was served at 06.30 am (carbohydrates 46%, lipids 51%, proteins 3%) before the end of the recording.

Before the end of the recording sessions, bisacodyl (Dulcolax®; Boehringer Ingelheim, France), 10 mg dissolved in 10 mL water, was injected directly into the colonic lumen via the catheter located in the proximal or transverse colon. The colonic motor response to the drug was assessed during the 30-min period following the instillation of the laxative as colonic response to bisacodyl has been shown to begin, in average, 13 min after local administration in slow transit constipation.5,8

Data analysis

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

Firstly, recordings were visually analysed by two trained observers to determine the number of HAPC occurring either spontaneously (HAPCs) or after Bisacodyl. HAPCs were defined according to Bassotti et al.16 as contractions >50 mmHg, lasting at least 10 s and propagating over three or more recording sites. For each HAPC, the mean amplitude, duration and propagation velocity (based on the time between peristaltic wave peaks from adjacent transducers) were calculated. The number of spontaneous and bisacodyl-induced HAPC was recorded.

Secondly, the global area under the curve (AUC) was automatically calculated using previously validated software.17 AUC (mmHg min−1) values were calculated for each recording site and then averaged for each colonic location (transverse, descending and sigmoid segment).

Thirdly, the food-induced colonic motility response was assessed by comparing the AUC calculated at each colonic level before and after each meal. A 1-h preprandial period and a 2-h postprandial period were used to establish comparisons.

Statistical analysis

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

Nonparametric statistics were calculated using the Mann–Whitney U-test for unpaired data and the Wilcoxon rank sum test for paired data. Categorical data were analysed using a chi-square test. All tests were two-tailed. P < 0.05 was used as the criterion of statistical significance.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

A 24-h recording session was completed in all subjects. The correct position of the probe at the end of the recording session was checked in all patients except in two who ejected the probe the morning of the third day after a spontaneous HAPC before the instillation test.

When the whole group of constipated patients is considered, the number of spontaneous HAPC was significantly lower in constipated patients than in controls (1 ± 8.6 vs 12 ± 11.6, P < 0.001) while the number of bisacodyl-induced HAPC was not different between the two groups (5.5 ± 3.2 vs 5 ± 3.5, ns).

No difference was found between the global AUC calculated in the transverse, descending or sigmoid colon in patients with slow transit constipation and the global AUC measured in the same colonic segments in the control group. Food induced a colonic motor response in all the healthy subjects but in only 75% (30/40) of the constipated patients (P < 0.05).

Further analysis showed that the constipated group was heterogeneous and that four subgroups could be identified according to colonic motor results.

A first subgroup of 10 patients did not exhibit food-induced colonic motor response and spontaneous HAPC, while the mean number of HAPCs was 12 ± 11.6 in controls and 3 ± 9.3 in other constipated patients (P < 0.001). Six of them had bisacodyl-induced HAPC (3.3 ± 3.3) while bisacodyl induced 5.5 ± 3.2 HAPCs in controls and 6 ± 3.3 in other constipated patients, (P < 0.05). In this subgroup, segmental AUC value in transverse colon (374 ± 1220 mmHg min−1) was significantly lower when compared with healthy subjects (3249 ± 3458, P < 0.05) and to other constipated patients (3015 ± 3749, P < 0.05) while AUC in the descending and the sigmoid colon tended only to be lower than in controls or in the remaining 30 constipated patients. These patients without spontaneous HAPC and food-induced colonic motor response were 10 women, median age 39 (range: 19–68), with a median colonic transit time of 128 h (range: 100–144). In these women, the median duration of constipation was 23 years (range: 2–50). In eight of them, constipation appeared in early childhood. The only clinical or epidemiological characteristic significantly different between these 10 women and the other constipated patients was a more frequent onset of constipation in the early childhood (eight of 10 vs six of 30, P < 0.05).

Five other patients exhibited a significantly increased segmental colonic motility both in sigmoid (20298 ± 6364 mmHg min−1) and in descending colon (10081 ± 7138) compared with healthy controls (88780 ± 3643 and 5423 ± 4121 respectively, P < 0.001) and other constipated patients (6649 ± 5168 and 5213 ± 4978 respectively, P < 0.001) while segmental transverse colonic motility was not different. The number of both spontaneous and bisacodyl-induced HAPC in these patients was not significantly different than that of healthy subjects. They were three women and two men, median age 38 years (range: 22–41) with a median colonic transit time of 125 h (range: 100–144). All of them had chronic abdominal pain but none fulfilled Rome II criteria for the diagnosis of irritable bowel syndrome.

The only abnormal motor finding in eight patients was a low number of spontaneous HAPC (1 ± 1.06) when compared with healthy subjects (12 ± 11.6, P < 0.01) while both segmental activity in the different colonic areas and food-induced motor response were not different than that of healthy controls. They were seven women and one man, median age 45.5 years (range: 28–64), with a median colonic transit time of 144 h (range: 116–160).

The 17 remaining patients had both basal and postprandial normal colonic motility without any significant difference on each manometric parameters (number of spontaneous or induced HAPCs, colonic motor response to food and segmental colonic motility at each level) when compared with healthy controls. They were 14 women and three men, median age 51 years (range: 18–68), with a median colonic transit time of 130 h (range: 100–144).

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References

Patients with severe intractable constipation constitute a heterogeneous group presenting different levels of heterogeneity from pelvic floor dysfunction and outlet obstruction to slow transit constipation.18 The main result of our study is that the subgroup of patient suffering from slow transit constipation is also heterogeneous with several types of motor disturbances suitable to explain the delayed colonic transit time.

The aim of our study was to describe manometric abnormalities among a high selected group of constipated patients referred to our tertiary centre to assess their colonic motility activity. The main clinical issue is to define patients in whom surgery could be considered because of the failure of conservative treatment. However, as discouraging results of surgery for slow transit constipation has been described additional information is needed in patients who are considered candidates to undergo colectomy.19,20 A delayed and longer than 100-h colonic transit time with markers diffusely scattered throughout the colon cannot be considered as the best method to evaluate these patients.18,21,22 In a recent study, colonic transit time has shown a very low reproducibility in patients with colonic inertia confirming the lack of specificity of this method.23 In our study, 10 patients had severely impaired colonic manometric results with no spontaneous HAPC, no colonic motor response to eating and a decreased transverse colon segmental activity. In our laboratory, only these patients are considered as potential patients suffering from colonic inertia. However, intracolonic instillation of laxative substances, such as bisacodyl,24 sennosides25 or glycerol enema26 is known to produce powerful peristaltic waves via activation of the myenteric plexus. A topical infusion of bisacodyl in the colonic lumen has been proposed to assess intrinsic nerve function by promoting propagated waves (HAPC) associated with bowel movements.27 In two recent studies, it has been shown that endoluminal instillation in patients with severe slow transit type constipation was useful for testing residual colonic propulsive activity,7,8 suggesting that only patients who do not respond to bisacodyl instillation really have an inert colon. Our study supports this idea by demonstrating that 60% of patients with a possible ‘inert colon’ on the basis of basal and postprandial colonic motor activity remained able to exhibit colonic propulsive activity after bisacodyl instillation. It is interesting to note that all these patients failed to respond to oral stimulant laxatives. This could be explained by the fact that when bisacodyl is locally infused, the concentration into the lumen must be much higher than when it is orally used. We believe, similar to Schriver et al.,9 that the lack of response to bisacodyl could be one necessary additional criterion to define a true inert colon. It seems that only patients who do not respond to bisacodyl stimulation should be eligible for surgery. But this hypothesis requires to be tested by a prospective clinical trial.

In 17 patients, normal manometric recordings were obtained despite severe chronic constipation and an objectively very delayed colonic transit time without any distal explanation. In these patients, possible explanations for the slow transit could be abnormal variations of colonic tone, particularly during the postprandial period or abnormal rheological properties of the luminal content increasing viscosity. We cannot exclude that certain abnormal motor findings concerning, for instance, coordination of colonic pressure waves might have been detected by mathematical methods of analysis28,29 that are not routinely used in our centre. The normal motility in some cases of severe slow transit constipation could also explain why biofeedback techniques can be successful in the treatment of such patients.30

A subgroup of patients had increased segmental sigmoid motility while the remaining parts of the colon exhibited normal motor patterns. These patients complained of abdominal pain more frequently. Some authors have already hypothesized that an abnormal increase in this rhythmic pattern, particularly common at the recto-sigmoid junction, might be responsible for some cases of constipation, leading to functional obstruction31,32 while radionuclide studies have demonstrated that the sigmoid area could be a possible brake for the propulsion of colonic content.33,34 On the contrary, recent data obtained with ambulatory manometry suggest that both contractile frequency of rectal complex and the interval between complexes are increased leading to the conclusion that this localized increased motor activity is not responsible to flow obstruction.35 The demonstration of the clinical interest of sigmoidectomy to improve symptoms in this subgroup of patients is still lacking.

In conclusion, this study carried out in a large selected group of severe, intractable slow transit constipated patients confirmed the heterogeneity of such a group when colonic motility is considered. We think that manometric recordings including a provocative test, for instance with bisacodyl, is of major interest to select without any bias patients included in trials testing prospectively different surgical available options.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Healthy volunteers
  7. Manometric recordings
  8. Recording system
  9. Method
  10. Data analysis
  11. Statistical analysis
  12. Results
  13. Discussion
  14. References
  • 1
    Camilleri M, Thompson WG, Fleshman JW, Pemberton JH. Clinical management of intractable constipation. Ann Intern Med 1994; 121: 5208.
  • 2
    Devroede G. Constipation. In: SleisengerMH, FordtranJS, eds. Gastrointestinal Disease, Vol 1. Philadelphia: WB Saunders Company, 1993: 83787.
  • 3
    Ferrara A, Pemberton JH, Grotz RL, Hanson RB. Prolongated ambulatory recording of anorectal motility in patients with slow-transit constipation. Am J Surg 1994; 167: 739.
  • 4
    Bazzocchi G, Ellis J, Villanueva-Meyer J et al. Post prandial colonic transit and motor activity in chronic constipation. Gastroenterology 1990; 98: 68693.
  • 5
    Bassotti G, Gaburri M. Manometric investigation of high-amplitude propagated contractile activity of the human colon. Am J Physiol 1988; 255: G6604.
  • 6
    Bassoti G, Gaburri M, Imbimbo BP et al. Colonic mass movements in idiopathic chronic constipation. Gut 1988; 29: 11739.
  • 7
    Kamm MA, Van der sijp JR, Lennard-Jones JE. Observations on the characteristics of stimulated defecation in severe idiopathic constipation. Int J Colorectal Dis 1992; 7: 197201.
  • 8
    Bassotti G, Chiaroni G, Germani U, Battaglia E, Vantini I, Morelli A. Endoluminal instillation of bisacodyl in patients with severe (slow transit type) constipation is useful to test residual colonic propulsive activity. Digestion 1999; 60: 6973.
  • 9
    De Schryver AM, Samsom M, Smout AI. Effects of a meal and bisacodyl on colonic motility in healthy volunteers and patients with slow-transit constipation. Dig Dis Sci 2003; 48: 120612.
  • 10
    Bouchoucha M, Devroede G, Arhan P et al. What is the meaning of colorectal transit time measurement? Dis Colon Rectum 1992; 35: 77882.
  • 11
    Mertz H, Naliboff B, Mayer E. Physiology of refractory chronic constipation. Am J Gastroenterol 1999; 94: 60915.
    Direct Link:
  • 12
    Leroi AM, Lalaude O, Antonietti M et al. Prolongated stationary colonic motility recording in seven patients with severe constipation secondary to antidepressants. Neurogastroenterol Motil 2000; 12: 14954.
  • 13
    Thompson WG, Longstreth GF, Drossman DA, Heaton KW, Irvine P, Muller-Lissner SA. Functional bowel disorders and functional abdominal pain. Gut 1999; 45 (Suppl.): 11437.
  • 14
    Herve S, Leroi AM, Mathiex-Fortunet H et al. Effect of polyethylene glycol 4000 on 24-h manometric recordings of colonic motor activity. Eur J Gastroenterol Hepatol 2001; 13: 64754.
  • 15
    De Schryver AM, Samsom M, Akkermans LM, Smout AJ. Endoclips in prolongated colonic manometry. Gastrointest Endosc 2000; 52: 81920.
  • 16
    Bassotti G, Betti C, Erbella GS, Cavalletti ML, Pelli MA, Morelli A. Prolonged manometric investigation of the colon in research on chronic constipation. Ital J Gastroenterol 1991; 23 (Suppl. 1): 135.
  • 17
    Guedon C, Ducrotté P, Antoine JM, Denis P, Colin R, Lerebours E. Does chronic supplementation of the diet with dietary fibre extracted from pea or carrot affect colonic motility in man? Br J Nutr 1996; 76: 5161.
  • 18
    Faulk DL, Anuras S, Christensen J. Chronic intestinal pseudoobstruction. Gastroenterology 1978; 74: 92231.
  • 19
    Bernini A, Madoff RD, Lownry AC et al. Should patients with combined colonic inertia and non-relaxing pelvic floor undergo subtotal colectomy? Dis Colon Rectum 1998; 41: 13636.
  • 20
    Fan CW, Wang JY. Subtotal colectomy for colonic inertia. Int Surg 2000; 85: 30912.
  • 21
    Leon SH, Krishnamurthy S, Schuffer MD. Subtotal colectomy for severe idiopathic constipation. Dig Dis Sci 1987; 32: 124954.
  • 22
    Pikarsky AJ, Singh JJ, Weiss EG, Nogueras JJ, Wexner SD. Long-term follow-up of patients undergoing colectomy for colonic inertia. Dis Colon Rectum 2001; 44: 17983.
  • 23
    Nam YS, Pikarsky AJ, Wexner SD et al. Reproducibility of colonic transit study in patients with chronic constipation. Dis Colon Rectum 2001; 44: 8692.
  • 24
    Saunders DR, Sillery J, Rachmilewitz D, Rubin CE, Tytgat GN. Effect of bisacodyl on the structure and function of rodent and human intestine. Gastroenterology 1977; 72: 84956.
  • 25
    Frexinos J, Staumont G, Fioramonti J, Bueno L. Effects of sennosides on colonic myoelectrical activity in man. Dig Dis Sci 1989; 34: 2149.
  • 26
    Staumont G, Fioramonti J, Delvaux M. Glycerol induced colic is associated to a stimulation of colonic myoelectrical activity in man. Gastroenterology 1989; 96: A489.
  • 27
    Bassoti G, Betti C, Pelli MA, Morelli A. Extensive investigation on colonic motility with pharmacological testing is useful for selecting surgical options in patients with inertia colica. Am J Gastroenterol 1992; 87: 1437.
  • 28
    Bassotti G, Fratini M. Of tubes and men: studying manometrically the effects of laxatives on colonic motility. Eur J Gastroenterol Hepatol 2001; 13: 6313.
  • 29
    Michoux N, Lalaude O, Maheu B et al. Postprandial duodenojejunal motility in health and idiopathic severe gastroparesis: from conventional analysis to nonlinear dynamics analysis. Neurogastroenterol Motil 2000; 12: 7585.
  • 30
    Chiotakakou-Faliakou E, Kamm MA, Roy AJ, Storrie JB, Turner IC. Biofeedback provides long-term benefit for patients with intractable, slow and normal transit constipation. Gut 1998; 42: 51721.
  • 31
    Bassotti G, Germani U, Morelli A. Human colonic motility: physiological aspects. Int J Colorectal Dis 1995; 10: 17380.
  • 32
    Chowdhury AR, Dinoso VP, Lorber SH. Characterisation of a hyperactive segment at the rectosigmoid junction. Gastroenterology 1976; 71: 5848.
  • 33
    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: G85662.
  • 34
    Hammer J, Philips SF. Fluids loading of the human colon: effects on segmental transit and stool composition. Gastroenterology 1993; 105: 98898.
  • 35
    Hagger R, Kumar D, Benson M, Grundy A. Colonic motor activity in slow-transit idiopathic constipation as identified by 24-h pancolonic ambulatory manometry. Neurogastroenterol Motil 2003; 15: 51222.