Defective Conduction of Anorectal Afferents Is a Very Prevalent Pathophysiological Factor Associated to Fecal Incontinence in Women

BACKGROUND/AIMS: Fecal incontinence (FI) is a prevalent condition among women. While biomechanical motor components have been thoroughly researched, anorectal sensory aspects are less known. We studied the pathophysiology of FI in community-dwelling women, specifically, the conduction through efferent/afferent neural pathways. METHODS: A cross-sectional study was conducted on 175 women with FI and 19 healthy volunteers. The functional/structural study included anorectal manometry/endoanal ultrasound. Neurophysiological studies including pudendal nerve terminal motor latency (PNTML) and sensory-evoked-potentials to anal/rectal stimulation (ASEP/RSEP) were conducted on all healthy volunteers and on 2 subgroups of 42 and 38 patients, respectively. RESULTS: The main conditions associated with FI were childbirth (79.00%) and coloproctological surgery (37.10%). Cleveland score was 11.39 ± 4.09. Anorectal manometry showed external anal sphincter and internal anal sphincter insufficiency in 82.85% and 44.00%, respectively. Sensitivity to rectal distension was impaired in 27.42%. Endoanal ultrasound showed tears in external anal sphincter (60.57%) and internal anal sphincter disruptions (34.80%). Abnormal anorectal sensory conduction was evidenced through ASEP and RSEP in 63.16% and 50.00% of patients, respectively, alongside reduced activation of brain cortex to anorectal stimulation. In contrast, PNTML was delayed in only 33.30%. Stools were loose/very loose in 56.70% of patients. CONCLUSIONS: Pathophysiology of FI in women is mainly associated with mechanical sphincter dysfunctions related to either muscle damage or, to a lesser extent, impaired efferent conduction at pudendal nerves. Impaired conduction through afferent anorectal pathways is also very prevalent in women with FI and may play an important role as a pathophysiological factor and as a potential therapeutic target.

Effect of Vaginal Delivery on Perineal Descent and Pudendal Nerve Terminal Motor Latency

PURPOSE: Significant associations between perineal descent (PD) and pudendal nerve terminal motor latency (PNTML) have previously been described in patients with fecal incontinence. This had led to the hypothesis that pelvic floor muscle and nerve injury initiated by childbirth might progress and cause fecal incontinence. Purpose: This study was undertaken to evaluate the association between vaginal delivery and PD, PNTML. Also, we evaluated the correlation between PD and PNTML. Methods: Sixty one women who visited the Dept. of Surgery from Aug. 1998 to May. 1999 were randomly selected. Women were excluded, who had chronic constipation,operation within 6 months before the investigation, anal trauma, diabetes mellitus, and neurologic disease. They had a mean year of 43 12.5 years (range: 23~70), a mean vaginal delivery 1.9 1.5 (range: 0~6). PD at rest and during push, and PNTML were measured. Results: PD during push (p=0.006) and the change of PD between at rest and during push (p=0.003) were significantly increased with increasing number of vaginal deliveries. Rt PNTML (p=0.08) and Lt PNTML (p=0.03) were significantly increased with increasing number of vaginal deliveries. There was correlation between Lt PNTML and change of PD (r=0.59, p=0.0). Conclusions: PD and Lt PNTML was increased with repeated vaginal deliveries. Our findings support the hypothesis that damage induced by vaginal delivery to pudendal nerve and pelvic floor will progress.

Functional Investigation with Use of Anorectal Physiology in the Patients with Fecal Incontinence

BACKGROUND: A large amount of attention in anorectal physiologic studies has been devoted to the diagnosis of fecal incontinence. The current study was designed firstly to assess the physiologic characteristics of fecal incontinence and secondly to analyze how the physiologic findings correlate with each other. METHODS: The physiologic findings of 47 patients (24 men and 23 women) were analyzed, retrospectively. Studies included anal manometry (n=38), anal electromyography/pudendal nerve terminal motor latency (PNTML) (n=30), and endoanal ultrasound (n=37). The degrees of continence were estimated by using continence grading scores (CGS) that ranged from 0 to 20 points based on the type and the frequency of incontinence. Control data were obtained from volunteers (n=23). RESULTS: The patients were categorized as having neurogenic (group I, n=25) or myogenic (group II, n=17) incontinence. Despite intensive investigations, unknown etiology was noted in 5 patients (10.4%). The CGS was not different between groups I and II. Pudendal neuropathy was found in 96% of group I and 37.5% of group II patients. Group I showed a higher value of PNTML than that of group II (2.96 1.0 msec vs. 2.07 0.48 msec, p=0.003). The CGS was proportional to the value of the PNTML in group I (r=0.476, p=0.01). However, no correlation was found between the mean PNTML and the CGS in group II. In the manometric parameters, there were no statistical differences between the values of the mean resting pressure (RP), the maximum RP, and the maximum voluntary contraction (MVC) between groups I and II. The MVC was inversely proportional to the CGS in group I (r= 0.616, p=0.02) and in group II (r= 0.664, p=0.02). No correlation was found between the PNTML and the manometric parameters. When we consider the presence of a defect or a scar as an abnormal anal ultrasound finding, such findings were more frequent in group II than in group I (group I, 20% vs. group II, 88%, p<0.001, Fisher's exact test). CONCLUSIONS: The value of the PNTML had relevance to the degree of symptoms in the patients with neurogenic incontinence. Specifically, the squeeze profiles of the manometric parameters were inversely related to the grade of incontinence. No correlation between the PNTML and the manometric parameters could be independently specified based on the etiology. Complementary examination by using the PNTML and anal ultrasound provided the only useful information to discriminate the etiology of incontinence.