Anorectal incontinence and rectal prolapse: differential assessment of the innervation to puborectalis and external anal sphincter muscles.

The innervation of the puborectalis and external anal sphincter muscles was studied in 32 patients with idiopathic (neurogenic) faecal incontinence, 12 of whom also had complete rectal prolapse, using transcutaneous spinal stimulation, transrectal pudendal nerve stimulation, single fibre EMG, anorectal manometry, and measurement of perineal descent. Fourteen normal subjects served as controls. Significant increases in the spinal motor latencies from L1 to the puborectalis and external anal sphincter muscles were shown in all 32 incontinent patients (p less than 0.01). The single fibre (EMG) fibre density was increased in the puborectalis muscle in 60% and in the external anal sphincter in 75% of patients. An increased pudendal nerve terminal motor latency was found in 68% of patients; 69% had an abnormal degree of perineal descent and all had reduced anal canal contraction pressures. These data show that the different innervations of the puborectalis and external anal sphincter muscles are both damaged in patients with anorectal incontinence.     

Why do patients with faecal impaction have faecal incontinence.

To elucidate the phenomenon of faecal incontinence in impacted patients, manometric, radiological and other investigations were carried out in 55 elderly patients, who had impacted masses of faeces in the rectum and were incontinent of faeces and 36 elderly control subjects with no anorectal problems. Maximum basal pressure and the maximum squeeze pressure in impacted patients were not significantly different from elderly controls. Sphincter pressures were no different after disimpaction than they were with faecal masses in situ, suggesting that leakage and soiling were not caused by stretching of the anal ring or prolonged reflex inhibition of anal tone by the faecal mass. The anorectal angle was more obtuse in impacted patients than in elderly controls though there was no greater degree of perineal descent. Anal and perianal sensation was impaired in impacted patients compared with controls. Rectal sensation was also impaired in the impacted patients in that the volume in a rectal balloon that could be perceived by the subject and the volume that gave rise to a desire to defecate were much higher in impacted patients than in controls. The rectal volume required to cause anal relaxation was lower in impacted patients compared with controls though there was no reduction in the volume at which anal relaxation failed to recover its resting tone. Rectal distension elicited external sphincter contractions in 53% impacted patients compared with 80% of controls. In conclusion, faecal soiling in patients with faecal impaction is probably related to the combination of an obtuse anorectal angle and the low anal pressures, normally found in the elderly and to impaired anorectal sensation which prevents conscious contraction of the external sphincter when the internal sphincter is relaxed.     

The prevalence of anal sphincter defects in faecal incontinence: a prospective endosonic study.

Forty six patients (median age 61 years; 42 women) with faecal incontinence and 16 age and sex matched controls undergoing a restorative proctocolectomy were assessed by clinical examination, anorectal physiology, and anal endosonography. Forty patients (87%) with faecal incontinence had a sphincter defect demonstrated on anal endosonography (31 external and 21 internal anal sphincter defects). The commonest cause of faecal incontinence was obstetric trauma. This occurred in 35 women, 30 of whom exhibited a morphological defect in the anorectal sphincter complex. In 22 of these patients with a history of a perineal tear or episiotomy, 21 (95%) had a sphincter defect. Sphincter defects were commonly located at the level of the midanal canal.     

Critical reappraisal of anorectal function tests in patients with faecal incontinence who have failed conservative treatment

Objective

Anorectal function tests are often performed in patients with faecal incontinence who have failed conservative treatment. This study was aimed to establish the additive value of performing anorectal function tests in these patients in selecting them for surgery.

Patients and methods

Between 2003 and 2009, all referred patients with faecal incontinence were assessed by a questionnaire, anorectal manometry and anal endosonography. Patients with diarrhea, inflammatory bowel disease, pouches or rectal carcinoma were excluded.

Results

In total, 218 patients were evaluated. Of these, 107 (49%) patients had no sphincter defects, 71 (33%) had small defects and 40 (18%) had large defects. Anorectal manometry could not differentiate between patients with and without sphincter defects. Patients with sphincter defects were only found to have a significantly shorter sphincter length and reduced rectal capacity compared to patients without sphincter defects. Forty-three patients (20%) had a normal anal pressures ≥40?mmHg. Seventeen patients (8%) had also a dyssynergic pelvic floor both on clinical examination and anorectal manometry. Fifteen patients (7%) had a reduced rectal capacity between 65 and 100?ml. There was no difference in anal pressures or the presence of sphincter defects in these patients compared to patients with a rectal capacity >150?ml. There was no correlation between anorectal manometry, endosonography and faecal incontinence severity scores.

Conclusion

In patients with faecal incontinence who have failed conservative treatment, only anal endosonography can reveal sphincter defects. Anorectal manometry should be reserved for patients eligible for surgery to exclude those with suspected dyssynergic floor or reduced rectal capacity.     

Pelvic floor neuropathy: a comparative study of diabetes mellitus and idiopathic faecal incontinence.

Twenty one patients with diabetic peripheral neuropathy, 18 with idiopathic faecal incontinence and 11 normal controls were studied with techniques of mucosal electrosensitivity, rectal distension for the quantitative assessment of anorectal sensation, and manometric and electromyographic tests for the assessment of anorectal motor function. An asymptomatic sensorimotor deficit was found in the anal canal of patients with diabetic peripheral neuropathy. Mucosal electrosensitivity thresholds in the anal canal were significantly higher (p less than 0.01 v controls) and fibre density of the external anal sphincter significantly raised (p less than 0.0001 v controls). Anal manometry and pudendal nerve terminal motor latencies were similar to controls. In patients with idiopathic faecal incontinence the tests of sensory and motor function also showed a sensorimotor neuropathy; compared with controls, mucosal electrosensitivity thresholds were significantly higher (p less than 0.002), anal canal resting and maximum squeeze pressures were significantly lower (p less than 0.05 and p less than 0.002 respectively), and pudendal nerve terminal motor latencies and fibre density of the external anal sphincter were significantly raised (both p less than 0.05). Sensory thresholds to rectal distension were similar in all groups. Pelvic floor sensorimotor neuropathy in diabetic patients has several features in common with that of patients with idiopathic faecal incontinence but its functional significance remains uncertain.     

Relationship between symptoms and disordered continence mechanisms in women with idiopathic faecal incontinence

BACKGROUND AND AIMS: Anal sphincter weakness and rectal sensory disturbances contribute to faecal incontinence (FI). Our aims were to investigate the relationship between symptoms, risk factors, and disordered anorectal and pelvic floor functions in FI. METHODS: In 52 women with "idiopathic" FI and 21 age matched asymptomatic women, we assessed symptoms by standardised questionnaire, anal pressures by manometry, anal sphincter appearance by endoanal ultrasound and magnetic resonance imaging (MRI), pelvic floor motion by dynamic MRI, and rectal compliance and sensation by a barostat. RESULTS: The prevalence of anal sphincter injury (by imaging), reduced anal resting pressure (35% of FI), and reduced squeeze pressures (73% of FI) was higher in FI compared with controls. Puborectalis atrophy (by MRI) was associated (p<0.05) with FI and with impaired anorectal motion during pelvic floor contraction. Volume and pressure thresholds for the desire to defecate were lower, indicating rectal hypersensitivity, in FI. The rectal volume at maximum tolerated pressure (that is, rectal capacity) was reduced in 25% of FI; this volume was associated with the symptom of urge FI (p<0.01) and rectal hypersensitivity (p = 0.02). A combination of predictors (age, body mass index, symptoms, obstetric history, and anal sphincter appearance) explained a substantial proportion of the interindividual variation in anal squeeze pressure (45%) and rectal capacity (35%). CONCLUSIONS: Idiopathic FI in women is a multifactorial disorder resulting from one or more of the following: a disordered pelvic barrier (anal sphincters and puborectalis), or rectal capacity or sensation.     

Abnormal visceral autonomic innervation in neurogenic faecal incontinence.

Changes of denervation in the anal sphincter striated and smooth muscle in patients with neurogenic faecal incontinence are well established. This study aimed to determine if there is also a more proximal visceral autonomic abnormality. Thirty women with purely neurogenic faecal incontinence (prolonged pudendal nerve latencies and an intact sphincter ring) and 12 patients with neuropathic changes together with an anatomical disruption were studied. Two control groups consisted of 18 healthy volunteer women and 17 women with normal innervation but an anatomically disrupted sphincter. Rectal sensation was assessed using balloon distension and electrical mucosal stimulation, and anal sensation by electrical stimulation. Rectal compliance was studied to determine whether sensory changes were primary or caused by altered rectal wall viscoelastic properties. Anal canal pressure changes in response to both rectal distension and rectal electrical stimulation were measured to assess the intrinsic innervation of the internal anal sphincter. Patients with neurogenic incontinence alone had impaired rectal sensation to distension (53.1 v 31.5 ml, p < 0.05, neurogenic v controls) and to electrical stimulation (24.4 v 14.8 mA, p < 0.005). Patients with neurogenic incontinence and sphincter disruption also showed impaired sensation compared with healthy controls (55.8 ml v 31.5 ml, p < 0.05 and 22.9 mA v 14.8 mA, p < 0.05). Patients with only a disrupted sphincter had normal visceral sensation to both types of testing. Both rectal compliance and the response of the internal anal sphincter to rectal distension and electrical stimulation were normal in all patient groups. This study suggests that there is a visceral sensory abnormality in patients with neurogenic incontinence which is not caused by altered rectal compliance. As evaluated in this study the intrinsic innervation of the internal anal sphincter is not affected in this process.     

Relation between rectal sensation and anal function in normal subjects and patients with faecal incontinence.

The relation between sensory perception of rapid balloon distension of the rectum and the motor responses of the rectum and external and internal anal sphincters in 27 normal subjects and 16 patients with faecal incontinence who had impaired rectal sensation but normal sphincter pressures was studied. In both patients and normal subjects, the onset and duration of rectal sensation correlated closely with the external anal sphincter electrical activity (r = 0.8, p less than 0.0001) and with rectal contraction (r = 0.51, p less than 0.001), but not with internal sphincter relaxation. All normal subjects perceived a rectal sensation within one second of rapid inflation of a rectal balloon with volumes of 20 ml or less air. Six patients did not perceive any rectal sensation until 60 ml had been introduced, while in the remaining nine patients the sensation was delayed by at least two seconds. Internal sphincter relaxation occurred before the sensation was perceived in three of 27 normal subjects and 11 of 16 patients (p less than 0.001), and could be associated with anal leakage, which stopped as soon as sensation was perceived. The lowest rectal volumes required to induce anal relaxation, to cause sustained relaxation, or to elicit sensations of a desire to defecate or pain were similar in patients and normal subjects. In conclusion, these results show the close association between rectal sensation and external anal sphincter contraction, and show that faecal incontinence may occur as a result of delayed or absent external anal sphincter contraction when the internal anal sphincter is relaxed.     

Sphincter denervation in anorectal incontinence and rectal prolapse.

Biopsies of the external anal sphincter, puborectalis, and levator ani muscles have been examined in 24 women and one man with long-standing anorectal incontinence, 18 of whom also had rectal prolapse, and in two men with rectal prolapse alone. In 16 of the women anorectal incontinence was of unknown cause, but in eight there was a history of difficult labour. Similar biopsies were examined in six control subjects. In all the incontinent patients there was histological evidence of denervation, which was most prominent in the external anal sphincter muscle biopsies, and least prominent in the levator ani muscles. Myopathic features, which were thought to be secondary, were present in the more abnormal biopsies. There were severe histological abnormalities in small nerves supplying the external anal sphincter muscle in the three cases in which material was available for study. We suggest that idiopathic anorectal incontinence may be the result of denervation of the muscles of the anorectal sling, and of the anal sphincter mechanism. This could result from entrapment or stretch injury of the pudendal or perineal nerves occurring as a consequence of rectal descent induced during repeated defaecation straining, or from injuries to these nerves associated with childbirth.     

Anorectal function in incontinent patients with cerebrospinal disease

Anorectal manometry and the electrical activity of the external anal sphincter were measured in 20 patients with well-defined, incomplete spinal lesions who were referred because of fecal incontinence and in 30 normal subjects. Six patients had a high spinal lesion, 11 had a low spinal lesion, and 3 had mixed high and low spinal lesions. Patients with high spinal lesions had normal basal pressures but abnormally low squeeze pressures and impaired rectal sensation. Unlike normal subjects, there was no relationship between the depth of sphincter relaxation and the distention volumes. The external sphincter responses to rectal distention and increases in intraabdominal pressure were enhanced, and leakage of perfusion fluid was uncommon. Patients with low spinal lesions had abnormally low basal and squeeze pressures, blunted rectal sensation, and showed impaired external anal sphincter responses to rectal distention or increases in intraabdominal pressures. Most of these patients leaked the infused fluid during these maneuvers. Sphincter function in patients with mixed lesions was more severely impaired than in patients with low and high spinal lesions. Patients with mixed lesions showed abnormally low basal and squeeze pressures, impaired rectal sensation, and no external anal sphincter responses to either rectal distention or increases in intraabdominal pressure. Leakage occurred during these maneuvers in all patients with mixed lesions.     

Impaired internal anal sphincter in a subgroup of patients with idiopathic fecal incontinence

During multiport manometric recordings of the anorectum, 35 of 140 patients with idiopathic fecal incontinence had abnormally weak sphincters that did not relax during rectal distention, suggesting impaired function of the internal anal sphincter. This study documents this finding and compares anorectal function in these 35 patients with 25 matched normal subjects and the remaining 105 incontinent patients. Basal and squeeze pressures were significantly lower in the incontinent study group than in the other two groups. During rectal distention, 25 of 35 patients showed no anal relaxation at any volume, whereas 10 patients showed some relaxation after 60-ml distention because of the postinflation rebound in internal anal sphincter tone. The electrical responses of the external anal sphincter to rectal distention and to increases in intraabdominal pressure were greater in patients than in normal subjects, but the anal pressures were lower and anal leakage was common. Rectal sensations were not significantly different from normal subjects. These results indicate that 25% of patients with idiopathic fecal incontinence have markedly impaired function of the internal anal sphincter, but these patients also have extremely weak external sphincters.     

Impaired rectal sensation in idiopathic faecal incontinence

In 15 patients suffering from idiopathic faecal incontinence and in 15 matched controls, manometric studies of anorectal pressure and studies of the rectoanal reflex and rectal sensitivity were carried out. Patients with idiopathic faecal incontinence had normal resting pressure but reduced squeeze and stress pressures; the anal sphincter relaxed before a sensation of rectal distension occurred. The conclusion is that both reduced voluntary muscle contraction and impairment of rectal sensation are conducive to soiling in idiopathic faecal incontinence.     

Role of manometry, defecography and anal endosonography in the evaluation of colorectal disorders.

OBJECTIVE: altered motility or anatomy of the rectum, anus and perineal floor may lead to symptoms which are unresponsive to routine therapeutic approaches. These disturbances usually lead to constipation, fecal incontinence, or both. Different tests and techniques for evaluating anorectal and perineal disorders, developed in the last two decades, make a better understanding of these disorders possible. This study was designed to evaluate the diagnostic benefits of combining manometry, defecography and anal endosonography in the assessment of patients with anorectal disorders. METHODS: twenty-five children with constipation (with or without soiling), incontinence and/or prolapse underwent anal manometry, defecography and anal endosonography. Group A consisted of 9 children with fecal incontinence, group B consisted of 10 children with constipation with soiling, and group C comprised 6 children with constipation without soiling. RESULTS: in group A resting incontinence was associated with a hypotonic external sphincter in 4 out of 9 patients, 2 of whom had internal anal sphincter thinning. In group B resting incontinence was associated with a hypotonic external sphincter in 8 out of 10 patients, 6 of whom had internal anal sphincter thinning. In group C these associations were not seen in any of the patients. CONCLUSIONS: barium enema is not sufficient for an accurate diagnosis of anorectal disorders. No single test is capable of revealing the type of disease. Anal manometry, defecography and endosonography are complementary procedures in the assessment of this group of disorders. This new approach will improve our knowledge of the pathogenesis of these disorders in children. However, further studies are needed to obtain conclusive evidence.     

Rectal sensorimotor dysfunction in patients with urge faecal incontinence: evidence from prolonged manometric studies

BACKGROUND AND AIMS: Although external anal sphincter dysfunction is the major cause of urge faecal incontinence, approximately 50% of such patients have evidence of rectal hypersensitivity and report exaggerated stool frequency and urgency. The contribution of rectosigmoid contractile activity to the pathophysiology of this condition is unclear, and thus the relations between symptoms, rectal sensation, and rectosigmoid motor function were investigated. METHODS: Fifty two consecutive patients with urge faecal incontinence, referred to a tertiary surgical centre, and 24 volunteers, underwent comprehensive anorectal physiological investigation, including prolonged rectosigmoid manometry. Patients were classified on the basis of balloon distension thresholds into those with rectal hypersensitivity (n = 27) and those with normal rectal sensation (n = 25). Automated quantitative analysis of overall rectosigmoid contractile activities and, specifically, high amplitude contractions and rectal motor complex activity was performed. RESULTS: External anal sphincter dysfunction was similar in both patient groups. Overall, phasic activity and high amplitude contraction frequency were greater, and rectal motor complex variables significantly altered, in those with rectal hypersensitivity. Symptoms, more prevalent in the rectal hypersensitivity group, were also more often associated with rectosigmoid contractile events. For individuals, reduced compliance and increased rectal motor complex frequency were only observed in patients with rectal hypersensitivity. CONCLUSIONS: We have identified a subset of patients with urge faecal incontinence-namely, those with rectal hypersensitivity-who demonstrated increased symptoms, enhanced perception, reduced compliance, and exaggerated rectosigmoid motor activity. Comprehensive assessment of rectosigmoid sensorimotor function, in addition to evaluation of anal function, should be considered in the investigation of patients with urge faecal incontinence.     

Clinical, anorectal manometry and surface electromyography in the study of patients with fecal incontinence.

OBJECTIVE: to demonstrate the role of the clinical, anorectal manometry and surface electromyography in the assessment of patients with fecal incontinence. PATIENTS AND METHODS: ninety-three patients with fecal incontinence are retrospectively reviewed and the data obtained from the directed clinical history, physical examination of the anal region, digital rectal examination, anorectal manometry and surface electromyography are analyzed. A treatment was administered in accordance with the alterations encountered and the results evaluated at 3 and 12 months. RESULTS: fecal incontinence was predominant (91.4%) in women age 59.7+/-11. A background of obstetric risks (48.2%) was frequent in women. Also, 73.1% of the patients presented diarrhea. The anorectal manometry (ARM) demonstrated some alterations in 90.3% of the patients, whereas a hypotonic sphincter was the most common finding (85.7%). Rectal sensitivity or distensibility alterations were present in the rest of the patients. In 79.2% ofthe cases, hypotonic sphincter was associated with rectal sensitivity or distensibility alterations. In 65.2% of patients with hypotonic external anal sphincter, damage of the pudendal nerve was found and therefore biofeedback was indicated in 41.9% of them. CONCLUSIONS: the clinical study of the patients, together with the anorectal manometry and surface electromyography enables the identification of the cause of FI and its treatment. These studies demonstrate that in most cases the origin of the incontinence is due to multiple etiologies, however the treatment of some of the factors involved frequently improves the symptomatology.     

Anal endosonography for assessment of anal incontinence with a linear probe: relationships with clinical and manometric features

BACKGROUND AND AIMS: This study determined correlations of clinical and manometric features with those of anal endosonography (AES). PATIENTS AND METHODS: Between 1996 and 1999 we examined 58 patients suffering from anal incontinence (AI) by AES using a linear probe and anorectal manometry following a standardized protocol. RESULTS: Twelve of the 58 patients (21%) had a history of anal surgery. Of the 40 women who had under-gone at least one vaginal delivery 22 (55%) sustained an obstetric tear and 12 (30%) required forceps for delivery. A perineal descent was observed in 24 of 32 women with AI (75%) and urinary incontinence in 24 of 44 (54%). An anal sphincter defect was diagnosed in 45 of the 58 patients (77%). The internal anal sphincter defects occurring in 42 patients (72%) were significantly associated with a decrease in the resting anal pressure. The external anal sphincter defects occurring in 33 patients (57%) were significantly associated with a decrease in the voluntary anal contraction. CONCLUSION: Considering AES and manometric findings, a good correlation was observed between internal sphincter defect and the resting anal pressure and between external sphincter defects and the voluntary anal contraction. AI is usually associated with a global perineal insufficiency requiring special attention in terms of both training and medical management.     

Age and sex and anorectal manometry in incontinence

Although the prevalence of fecal incontinence is greater in women compared with men and in elderly subjects compared with younger subjects, data regarding the influence of age and sex on anorectal performance in continent and incontinent patients are conflicting. The authors, therefore, investigated age-and gender-related changes in anal resting and squeeze pressure as well as in sphincter relaxation after rectal balloon distention in 75 patients with fecal incontinence of different pathogenesis and in 99 continent patients by multichannel anorectal manometry. As a group, incontinent patients usually exhibit lower pressure profiles than do continent patients regardless of age and gender; however, both the resting pressure of the internal anal sphincter and the voluntary contractile pressure of the external anal sphincter are decreased with age, and both are lowered in women compared with men. Sphincter relaxation and perception of gastrointestinal events are not altered in incontinent patients, and they are not different between men and women or between elderly and younger patients. Supported by grant Er 142/1 from the Deutsche Forschungsgemeinschaft.     

Rectal compliance, capacity, and rectoanal sensation in fecal incontinence

OBJECTIVE: Assessments of the pathophysiology of fecal incontinence are skewed toward anal sphincter function; however, rectal compliance, rectoanal sensation and capacity may also be relevant. The aim of this study was to evaluate the usual and some novel diagnostic approaches in fecal incontinence. METHODS: In 22 unselected patients with fecal incontinence (21 F, 33-75 yr), we quantified: 1) symptoms, anorectal manometry, and anal ultrasound; 2) anal perception of temperature and light touch; 3) rectal sensitivity and compliance to distension; and 4) rectal reservoir function. Control values were obtained from two groups of 11 (seven F, 32-53 yr), and 32 (18 F, 19-44 yr) volunteers. RESULTS: Patients had urge (14), passive (four), or combined (four) fecal incontinence; symptoms were mild in three, moderate in nine, and severe in 10 patients. Most had low sphincteric pressures and ultrasonic abnormalities. Temperature perception was impaired (p < 0.05) in incontinent patients, to a greater extent in the proximal anal canal and in patients with passive, as opposed to urge, incontinence. Intraluminal pressures for sensations of rectal distension were lower in incontinent patients (p = 0.02). Artificial stools elicited sensations of rectal filling at lower volumes than did a barostat bag, and in patients with urge, as opposed to passive, incontinence. In patients and controls, the sensation of urgency was associated (r2 = 0.2, p < 0.01) with rectal compliance. CONCLUSIONS: We confirm that temperature sensation is impaired, and perception of rectal distension is not always reduced in fecal incontinence. Artificial stool tended to induce sensations at lower volumes than did balloon inflation. Altered sensory mechanisms may contribute to the pathophysiology of fecal incontinence.     

Anorectal sensory and motor function in neurogenic fecal incontinence. Comparison between multiple sclerosis and diabetes mellitus

We measured anorectal sensory and motor function in 11 patients with multiple sclerosis and fecal incontinence, 11 continent patients with multiple sclerosis, 10 diabetics with fecal incontinence, and 12 healthy control subjects. The threshold volume at which patients with multiple sclerosis and fecal incontinence experienced rectal sensation was higher than that in healthy controls (42.7 +/- 6.2 mL vs. 13.3 +/- 2.8 mL; P less than 0.01) and was similar to that in incontinent diabetics (36.5 +/- 5.7 mL). Patients with multiple sclerosis and incontinent diabetics also showed increased thresholds of phasic external sphincter contraction compared with controls (P less than 0.05). Diabetics with incontinence had reduced resting and maximal voluntary anal sphincter pressures compared with controls (P less than 0.05), whereas patients with multiple sclerosis and incontinence showed only decreased maximal voluntary anal sphincter pressures (P less than 0.01 vs. controls and diabetics). Incontinent patients with multiple sclerosis also required smaller volumes of rectal distention to inhibit internal sphincter tone compared with diabetics and controls (P less than 0.01). Decreased maximal voluntary squeeze pressures were less severe in continent patients with multiple sclerosis than in incontinent patients with multiple sclerosis. We conclude that impaired function of the external anal sphincter and decreased volumes of rectal distention to inhibit the internal anal sphincter or both may contribute to fecal incontinence in multiple sclerosis. In addition, increased thresholds of conscious rectal sensation in some incontinent patients with multiple sclerosis and diabetes mellitus may contribute to fecal incontinence by impairing the recognition of impending defecation.     

Role of anorectal sensation in preserving continence.

The role of anal sensation in preserving continence was studied in nine healthy volunteers. Objective assessment of sphincter function by manometry and rectal saline infusion was carried out during topical anaesthesia of the anal canal using 5% lignocaine gel and during lubrication with the same amount of inert gel. Anaesthesia successfully abolished anal sensation and reduced both the amplitude and duration of the voluntary squeeze. Basal pressure was unaffected, but the rectal volume required to produce a sustained internal sphincter relaxation was increased. Saline continence was not impaired. Indeed, two subjects, who were previously unable to retain the full 1500 ml of rectally infused saline, did so when the anal canal was anaesthetised. Our findings suggest that anal sensation is not a critical factor in preserving continence. This implies that the incontinence experienced after anorectal surgery or neuropathy cannot be explained by lack of anal sensation alone.