Faecal incontinence is associated with an impaired rectosigmoid brake and improved by sacral neuromodulation

Background and aims: The rectosigmoid brake, characterized by retrograde cyclic motor patterns on high-resolution colonic manometry has been postulated as a contributor to the maintenance of bowel continence. Sacral neuromodulation (SNM) is an effective therapy for faecal incontinence, but its mechanism of action is unclear. This study aims to investigate the colonic motility patterns in the distal colon of patients with faecal incontinence, and how these are modulated by SNM. Methods: A high-resolution fibre-optic colonic manometry catheter, containing 36 sensors spaced at 1-cm intervals, was positioned in patients with faecal incontinence undergoing Stage 1 SNM. One hour of pre-meal and post-meal recordings were obtained followed by pre- and post-meal recordings with suprasensory SNM. A 700-kcal meal was given. Data were analysed to identify propagating contractions. Results: Fifteen patients with faecal incontinence were analysed. Patients had an abnormal meal response (fewer retrograde propagating contractions compared to controls; p=0.027) and failed to show a postmeal increase in propagating contractions (mean 17 +/- 6/h pre-meal vs 22 +/- 9/h post-meal, p = 0.438). Compared to baseline, SNM significantly increased the number of retrograde propagating contractions in the distal colon (8 +/- 3/h pre-meal vs 14 +/- 3/h pre-meal with SNM, p = 0.028). Consuming a meal did not further increase the number of propagating contractions beyond the baseline upregulating effect of SNM. Conclusion: The rectosigmoid brake was suppressed in this cohort of patients with faecal incontinence. SNM may exert a therapeutic effect by modulating this rectosigmoid brake.

Duodenal and proximal jejunal motility inhibition associated with bisacodyl induced colonic high amplitude propagating contractions

Bisacodyl is a stimulant laxative often used in manometric studies of pediatric constipation to determine if it can initiate propulsive high amplitude propagating contractions. While the effects of bisacodyl infusion on colonic motility are well described, the effects of the drug on other regions of the gut after colonic infusion are not known. The aim of the present study was to characterize the effects of bisacodyl on both colonic and small bowel motility. Methods. Twenty seven children (9.3 + 1.2 years) undergoing simultaneous high resolution antroduodenal and colonic manometry were included. Small bowel and colonic motor patterns were assessed prior to and after colonic infusion of bisacodyl. Patients were divided into 2 groups; responders and non-responders based on the presence of high amplitude propagating contractions (HAPC) after bisacodyl infusion. Results. Nineteen patients were responders. 188 post-bisacodyl HAPCs were identified with a mean count of 10.4 ± 5.5 (range, 3 -22), at a frequency of 0.6 ± 0.2/min and mean amplitude of 119.8 ± 23.6 mmHg.No motor patterns were induced in the small bowel. However, in the 19 responders the onset of HAPCs was associated with a significant decrease in small bowel contractile activity. In the non-responders there was no detectable change in small bowel motility after bisacodyl infusion. Conclusion. Bisacodyl induced HAPCs are associated with a significant reduction in small bowel motility probably mediated by extrinsic sympathetic reflex pathways. This inhibition is potentially related to rectal distension, caused by the HAPC anal propulsion of colonic content.

Spatiotemporal analysis of spontaneous myogenic contractions in the urinary bladder of the rabbit: timing and patterns reflect reported electrophysiology

The dynamics of propagating myogenic contractions in the wall of the resting ex vivo urinary bladder of the rabbit were characterized by spatiotemporal maps and related to cyclic variation in intravesical pressure (Pves). Patches of propagating contractions (PPCs) enlarged and involuted in near synchrony with peaks in Pves [mean 3.85 ± 0.3 cycles per minute (cpm)] and were preceded by regions of stretch. The maximum area of the bladder undergoing contraction (55.28 ± 2.65%) and the sizes of individual PPCs (42.61 ± 1.65 mm2) coincided with the peak in Pves. PPCs originated and propagated within temporary patch domains (TPDs) and comprised groups of nearly synchronous cyclic propagating individual contractions (PICs). The TPDs were located principally along the vertical axis of the anterior surface of the bladder. The sites of origin of PICs within PPCs were inconsistent, consecutive contractions often propagating in opposite directions along linear maps of strain rate. Similar patterns of movement occurred in areas of the anterior bladder wall that had been stripped of mucosa. Pves varied cyclically with area of contraction and with the indices of aggregation of PPCs, indicating that they grew by peripheral enlargement and collision without annihilation. The synchronization of PICs within PPCs was sometimes lost, uncoordinated PICs then occurring irregularly (between 4 and 20 cpm) having little effect on Pves. We postulate that the formation and involution of PPCs within a TPD resulted from cyclic variation in excitation that increased the incidence and distance over which component PICs propagated.