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

Abstract

Background: The rectosigmoid brake, characterised 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 fibreoptic 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- 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 post meal increase in propagating contractions (mean 17 ± 6/h premeal 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 premeal vs. 14 ± 3/h premeal 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.

Keywords: faecal incontinence; implant; rectosigmoid brake; sacral nerve stimulation; sacral neuromodulation.

FIGURE 1

All (top) and cyclic motor pattern‐associated (bottom) retrograde propagating contractions in healthy controls, patients with faecal incontinence both before and after sacral neuromodulation. Plotting mean ± SE as per data reported in‐text.

FIGURE 2

Representative examples of pre‐ and post meal high resolution colonic manometry data in 10‐min epochs. (A) Significant increase in postprandial propagating contraction frequencies in healthy controls. (B) Decreased magnitude of colonic activity meal‐response with shorter distance of propagation and decreased activity in faecal incontinence patients compared to controls. (C) Increase in propagating contractions at baseline and postprandially with SNM in patients with faecal incontinence. SNM appears to increase frequency of propagating events but not to the level seen in the healthy control meal response. Despite variation in catheter used, only data distal to the splenic flexure were analysed in all cohorts.

FIGURE 3

Effect of stimulation on the cyclic motor pattern in patients with faecal incontinence stratified by meal and stimulation status. Plot depicts median (IQR) to visualise the range in the raw data; paired nonparametric Wilcoxon test between pre‐SNM and full‐SNM comparisons: Total p = 0.041, antegrade p = 0.264, retrograde p = 0.011. Mean and standard error are reported in the table below to compare to data within the text.

FIGURE 4

Anatomical registration of the event count distribution into a colonic geometry model, based on the estimated catheter insertion position. The colours represent the mean number of propagating events per hour. Propagating contractions were most active in the sigmoid colon. Total propagating contractions are depicted in blue and retrograde propagating contractions are depicted in red. FI, faecal incontinence; SNM, sacral neuromodulation.