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.     

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.     

Sonographic Characteristics of Rectal Sensations in Healthy Females

Purpose This study was designed to characterize rectal sensations by visualizing the internal and external anal sphincter and intra-anal transport of bolus during elicited rectal sensations. Methods The anal canal was visualized with real-time transperineal ultrasonography in 13 healthy female volunteers. Rectal sensations were elicited by injecting water into the rectum. The ultrasound images were recorded on a videotape and analyzed offline. Results The median time between an injection of water and the events studied was calculated in 105 rectal sensations. A relaxation in the internal anal sphincter (4 seconds after the injection of water), an antegrade transport of bolus (4 seconds) into the anal canal, and a contraction in the external anal sphincter (5 seconds) were observed before a sensation (6 seconds) was reported. The antegrade flow continued until the distal internal anal sphincter contracted (18 seconds) and the bolus moved in a retrograde transport direction (17 seconds) thereafter the sensation disappeared (18 seconds) and the external anal sphincter relaxed (22 seconds). A significant correlation in time between the end of the sensation, contraction in the internal anal sphincter, reversed flow of anal contents, and relaxation of the external anal sphincter was found (Pearson, P<0.01). Conclusions The results verified that the internal anal sphincter contributes to the perception of rectal sensations by a relaxation allowing intra-anal bolus to increase the pressure on the anoderm during rectal contraction. A new observation is presented on the time relation between contraction in the distal internal anal sphincter, reversed flow in the anal canal, and the end of rectal sensations. Presented at the meeting of the International Continence Society, Christchurch, New Zealand, November 27 to December 1, 2006. Supported by Hitachi Ultrasound, Supfstrasse 24, 6300 Zug Switzerland provided the sonography system. Reprints are not available.     

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.     

Hyperglycemia alters perception of rectal distention and blunts the rectoanal inhibitory reflex in healthy volunteers

Acute hyperglycemia has been shown to alter gastrointestinal motility. The effects of hyperglycemia on rectal afferent neural and anal sphincter function were studied. Perception of rectal balloon distention, pressure-volume relationships, volumes necessary to induce reflex internal anal sphincter relaxation, resting anal sphincter pressure, and maximal anal sphincter squeeze pressure were measured under basal, hyperglycemic clamp, and euglycemic, hyperinsulinemic clamp conditions in 9 healthy volunteers. Hyperglycemic clamping (258 ± 14 mg/dL) significantly blunted threshold perception and the urge to defecate in response to rectal distention without altering perception of maximally tolerated distention. In contrast, euglycemic, hyperinsulinemic clamping had no effect on perception of rectal distention. Rectal pressure-volume relationships after hyperglycemic clamping were unchanged compared with basal conditions. Hyperglycemic clamping caused a significant increase in the distention necessary to induce the rectoanal inhibitory reflex. This effect was not observed under euglycemic, hyperinsulinemic clamp conditions. Hyperglycemia did not significantly affect resting internal anal sphincter pressure or maximal external anal sphincter squeeze pressure. Acute hyperglycemia but not secondary hyperinsulinemia reduces sensation of rectal distention and blunts the onset of the rectoanal inhibitory reflex, suggesting effects both on visceral afferents projecting to the cortex and intrinsic afferents mediating local reflex activity.     

Rectal sensory perception in females with obstructed defecation

PURPOSE: Parasympathetic afferent nerves are thought to mediate rectal filling sensations. The role of sympathetic afferent nerves in the mediation of these sensations is unclear. Sympathetic nerves have been reported to mediate nonspecific sensations in the pelvis or lower abdomen in patients with blocked parasympathetic afferent supply. It has been reported that the parasympathetic afferent nerves are stimulated by both slow ramp (cumulative) and fast phasic (intermittent) distention of the rectum, whereas the sympathetic afferent nerves are only stimulated by fast phasic distention. Therefore, it might be useful to use the two distention protocols to differentiate between a parasympathetic and sympathetic afferent deficit. METHODS: Sixty control subjects (9 males; median age, 48 (range, 20–70) years) and 100 female patients (median age, 50 (range, 18–75) years) with obstructed defecation entered the study. Rectal sensory perception was assessed with an infinitely compliant polyethylene bag and a computer-controlled air-injection system. This bag was inserted into the rectum and inflated with air to selected pressure levels according to two different distention protocols (fast phasic and slow ramp). The distending pressures needed to evoke rectal filling sensations, first sensation of content in the rectum, and earliest urge to defecate were noted, as was the maximum tolerable volume. RESULTS: In all control subjects, rectal filling sensations could be evoked. Twenty-one patients (21 percent) experienced no sensation at all in the pressure range between 0 and 65 mmHg during either slow ramp or fast phasic distention. The pressure thresholds for first sensation, earliest urge to defecate, and maximum tolerable volume were significantly higher in patients with obstructed defecation (P<0.001). In each subject, the pressure thresholds for first sensation, earliest urge to defecate, and maximum tolerable volume were always the same, regardless of the type of distention. CONCLUSION: Rectal sensory perception is blunted or absent in the majority of patients with obstructed defecation. The observation that this abnormality can be detected by both distention protocols suggests that the parasympathetic afferent nerves are deficient. Because none of the patients experienced a nonspecific sensation in the pelvis or lower abdomen during fast phasic distention, it might be suggested that the sympathetic afferents are also deficient. This finding implies that it is not worthwhile to use different distention protocols in patients with obstructed defecation.     

Rectoanal reflex parameters in incontinence and constipation

PURPOSE: The transient relaxation of the internal anal sphincter in response to rectal distention is believed to play an important role in the continence mechanism. Most anorectal physiology laboratories merely report the rectoanal inhibitory reflex as being either present or absent. This study aimed to assess the parameters of the rectoanal inhibitory reflex in incontinent and constipated patients and healthy control subjects, in an attempt to analyze differences in internal anal sphincter function in these groups. We analyzed each response of the internal anal sphincter to rectal distention with progressively increasing volumes of air at a single site (proximal anal canal). METHODS: Fifty-five constipated and 99 incontinent patients and healthy control subjects underwent manometry. Various parameters of the rectoanal inhibitory reflex were analyzed, and percentage sphincter relaxation was calculated at each volume at which rectoanal inhibitory reflex occurred. RESULTS: There was no difference in the volume of rectal distention required to elicit sensation (P = 0.626) or the rectoanal inhibitory reflex (P = 0.371) in the three groups. There was a significant correlation between the volume required to elicit the rectoanal inhibitory reflex and that at which sensation was first felt only in the incontinent (P = 0.0001) group. Significantly greater sphincter relaxation was seen at each volume (P = 0.001) in the incontinent as compared with the constipated patients. With progressive rectoanal inhibitory reflex, consistently progressive increases in internal anal sphincter relaxation were found only in the incontinent group. This consistent relationship was not seen in the constipated patients or in healthy control subjects. CONCLUSIONS: Assessment of various parameters of the rectoanal inhibitory reflex yielded important information regarding the continence mechanism. Altered responses of the internal anal sphincter in anorectal disorders plays a role in the associated physiologic impairment. This may have significant clinical implications with regard to sphincter-saving resections.     

Electromyography of the internal anal sphincter performed under endosonographic guidance description of a new method

PURPOSE: The aim of our study was to investigate internal anal sphincter electromyographic signals. METHODS: Electromyography of the internal anal sphincter was performed with platinum wire electrodes in six healthy volunteers (three males and three females), inserted under endosonographic guidance. Platinum wire electrodes were also inserted into the external anal sphincter. Activity of both the internal and external anal sphincter in a 40-second period was measured. RESULTS: Internal anal sphincter median activity was 22.1 (range, 5.5–67.6) μ V. Slow-wave activity was 47 cycles/minute (range, 34–55 cycles/minute). After inflation of a rectal balloon with air until a constant relaxation of the anal canal was obtained, a decrease in internal anal sphincter activity to 15.9 (1.2–31.3) μV as well as a decrease in slow-wave activity to 34 cycles/minute (range, 27–40 cycles/minute) was found. The original internal anal sphincter EMG was resumed after deflation of the rectal balloon. External anal sphincter median activity was 31 (range, 0.77–18.6)μV. During inflation of the rectal balloon, a reflex increase in external sphincter EMG activity was found. With the rectal balloon fully inflated a part of this increase was still present, 11.0 (1.9–24.6)μV. In some of the subjects, this increased activity was superimposed on the internal anal sphincter recordings as well. During a voluntary squeeze it was not possible to identify internal anal sphincter activity due to activity of the external anal sphincter totally overriding the internal anal sphincter signal. CONCLUSION: Precise EMG recordings from the internal anal sphincter is possible with endosonographic guidance of the electrodes, except during voluntary squeezing of the external anal sphincter.     

Anorectal function in patients with complete supraconal spinal cord lesions.

Anorectal manometry and sphincter electromyography were performed in 23 patients with complete supraconal traumatic spinal injuries and 30 age and sex matched control subjects. Basal pressures in the spinal group were similar to those in normal subjects but conscious control of sphincter activity was abolished in all spinal patients. Discriminant rectal sensation was also abolished during rectal distension, but 40% of patients experienced a dull pelvic ache at maximum levels of distension. Phasic rectal contraction and anal relaxation were present but exaggerated and induced at lower distending volumes than in normal subjects. The configuration of the rectal pressure/volume relationship was linear in patients compared with a reversed 'S' shape in normal subjects. The external anal sphincter response to rectal distension was noticeably attenuated, reinforcing the view that this spinal reflex is heavily modulated by supraspinal centres under normal circumstances. The external anal sphincter response to increases in abdominal pressure was also attenuated, and the anal pressures were strongly correlated with the level of the lesion and the abdominal pressure the patient could generate. No spinal patient showed a decrease in external anal sphincter activity during straining 'as if to defecate.' The exaggerated anorectal smooth muscle responses to rectal distension and the attenuated external sphincter response explain why patients with complete supraconal spinal lesions experience uncontrollable reflex defecation, while the persistance of external and sphincter contraction and the absence of any external anal sphincter relaxation during straining 'as if to defecate' might explain the difficulty that these patients have in consciously expelling rectal contents.     

External anal sphincter function in spinal patients

Six patients with complete transection of the spinal cord and six healthy volunteers were examined by using anorectal manometry together with electromyographic (EMG) recording of the external anal sphincter composed of striated muscle. Anal pressure and EMG activity of the external anal sphincter were continuously recorded at rest and during gradual rectal distention (10, 20, 30, 40, and 50 ml) by means of an air-filled balloon eliciting a rectoanal inhibitory reflex (RAIR) at the upper part, and an inflation reflex (IR) at the lower part of the anal canal. All patients and controls had a RAIR for each rectal distention volume. A relationship between the duration of the RAIR and the rectal distention volume was present in controls only. In controls the IR was present for each rectal distention volume, whereas it was present in only one patient for a 40-ml volume. During the resting period, all controls showed continuous tonic EMG activity of the external anal sphincter, but after 30 minutes all the patients showed a decrease and ultimately in five cases a disappearance of the tonic EMG activity of the external anal sphincter. In spinal patients, the presence or absence of EMG activity of the external anal sphincter did not modify the anal canal pressure. These results indicate that: 1) the tonic EMG activity of the external anal sphincter seems to be under the control of supraspinal structures, because in spinal patients it disappears in the absence of sensitive inputs toward the spinal cord; 2) the absence of EMG activity at rest indicates that the external anal sphincter is not implicated in the RAIR disturbances observed in spinal patients; 3) the IR is not a spinal reflex but is under voluntary control, because it is not present in spinal humans; 4) in spinal humans the tonic EMG activity of the external anal sphincter does not play a role in the maintenance of the anal pressure at rest.     

Rectal hyperreactivity to distention in patients with irritable bowel syndrome: role of distention rate.

BACKGROUND AND AIMS: Rectal motor hyperreactivity to distention may be involved in the pathophysiological course of defecatory symptoms in patients with irritable bowel syndrome (IBS), but results of patient studies are conflicting, possibly because of differences in the applied distention rate. Because a fast rate of distention increases the rectal motor response in healthy subjects, it also may show hyperreactivity in patients with IBS. The aim of this study is to compare the effects of 2 distention rates on rectal motor responses and sensations in 16 patients with IBS and 12 healthy subjects. METHODS: Rectal distensibility and the frequency of rectal contractions and sensations were recorded during volume-controlled rectal distentions at 2 distention rates (10 and 100 mL/min). RESULTS: Recta of patients with IBS were significantly less distensible than those of healthy subjects during fast distention (P = 0.0006), but this difference was not statistically significant during slow distention (P = 0.07). The frequency of rectal contractions and sensations, the majority of which were sensations of gas and a desire to defecate, were significantly greater in patients with IBS during both slow and fast distentions (both P < 0.025). CONCLUSIONS: Recta of patients with IBS are hyperreactive to distention, and fast distention magnifies this abnormal motor response. A greater frequency of sensations during a fixed-time distention period may help to characterize the patients.     

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.     

Clinical and manometric features of the solitary rectal ulcer syndrome

We report 33 patients with the solitary rectal ulcer syndrome seen between 1975 and 1982. Twenty-four were women and the median age was 32 years. The principal symptoms were bleeding (89 per cent), chronic constipation (64 per cent), rectal pain (42 per cent), tenesmus (42 per cent), and mucous discharge (45 per cent). Twenty-eight patients gave a history of straining (85 per cent). A full-thickness rectal prolapse was present in six patients, an anterior rectal prolapse was observed in 11, and 12 patients had clinical evidence of perineal descent. Defecation was only possible by digital evacuation in six women, and three male patients were passive homosexuals. Manometric studies were performed on 16 patients; eight patients were unable to tolerate rectal distension with 200 cc of air and impaired rectal sensation was present in two. Rectal distention was associated with bursts of involuntary external sphincter activity in three patients, and the distention reflex was absent in six, despite normal ganglia on rectal biopsy. In only four patients was there electromyographic evidence of contraction of the puborectalis during attempted defecation. Fourteen patients were treated by rectopexy; healing of the ulcer occurred in five of six with a full-thickness prolapse compared with only two of eight without a complete prolapse. Work performed at the General Hospital, Birmingham, England.     

Effect of continuous rectal distention on anal resting pressure

PURPOSE: Intermittent distention of the rectum induces internal anal sphincter relaxation, but whether continuous rectal distention might affect the resting pressure of the anal canal and the frequency of internal anal sphincter relaxations has not yet been investigated. The aim of this study was to record anal pressure under resting conditions and at two levels of continuous rectal distention. METHODS: Anal pressure was recorded by means of water-perfused catheters under resting conditions and at two levels of rectal distention controlled by an electronic barostat in eight healthy subjects. RESULTS: Continuous rectal distention did not significantly change mean anal resting pressure, but it did significantly decrease the amplitude of ultraslow waves (from 29±9 mmHg under resting conditions to 23±6 and 21±3 mmHg during lesser and greater rectal distention;P=0.017 andP=0.012, respectively) and increase the frequency of internal anal sphincter relaxations (from 1.3±1.3/hour under resting conditions to 8.8±4.3/hour and 11.0±4.8/hour during lesser and greater distention;P=0.012 in both comparisons). CONCLUSIONS: The resting pressure of the anal canal is maintained during continuous rectal distention. The decreased amplitude of ultraslow waves and increased frequency of the internal anal sphincter relaxations induced by rectal distention reveal a complex functional relationship between the rectum and the anal canal.Supported by the Associazione Amici della Gastroenterologia del Padiglione Granelli and the CARIPLO Foundation.     

Utility of a combined test of anorectal manometry, electromyography, and sensation in determining the mechanism of ''idiopathic'' faecal incontinence.

Combined tests of anorectal manometry, sphincter electromyography and rectal sensation were carried out in 302 patients with faecal incontinence (235 women, 67 men). The results obtained were compared with 65 normal subjects (35 women, 30 men). A mechanism for incontinence was identified in all and the majority of patients had more than one abnormality. Two hundred and seventy eight patients (92%) had a weak external anal sphincter, 185 of these (67%, mostly women) also showed abnormal perineal descent, and 14 women showed clinical evidence of sphincter damage as a result of obstetric trauma. Ten per cent of patients with impaired external anal sphincter contraction showed associated evidence of spinal disease (impaired rectal sensation plus attenuated or enhanced reflex external anal sphincter activity). Unlike the other groups, the 'spinal' group contained equal numbers of men and women. Ninety seven patients (32%) had evidence of a weak internal anal sphincter. The external sphincter was also very weak and 92% of these patients also had perineal descent. Eighty two patients (27%) showed an unstable internal sphincter, characterised by prolonged 'spontaneous' anal relaxation under resting conditions and an abnormal reduction in anal pressure after conscious contraction of the sphincter or an increase in intraabdominal pressure. One hundred and forty two patients (47%) had a hypersensitive rectum associated with enhanced anorectal responses to rectal distension. All these patients had an abnormally weak external sphincter, suggesting that the hypersensitive or 'irritable' rectum should not be regarded as a cause of faecal incontinence unless accompanied by external sphincter weakness. Twenty four patients (8%) showed a normal basal and squeeze pressures and impaired rectal sensation; six showed giant rectal contractions during rectal distension. The results show that idiopathic faecal incontinence is not caused by a single abnormality, and it is suggested that combined anorectal manometry, electromyography, and sensory testing is a useful technique to identify the causes of faecal incontinence and provide a basis for appropriate treatment.     

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.     

Influence of loperamide on the internal anal sphincter in the opossum

The objective of this study was to examine the influence of the commonly used antidiarrheal agent loperamide on the internal anal sphincter of anesthetized opossums. Loperamide caused a rise in internal anal sphincter pressures, and a decrease in the rectal distention-induced internal anal sphincter relaxation. To define the mechanism of decrease in the rectal distention response of the internal anal sphincter, we examined the effects of sacral efferent nerve stimulation, local intramural stimulation, and ganglionic stimulant (which acts at the postganglionic inhibitory neuron). Loperamide caused a significant decrease in the internal anal sphincter relaxation caused by sacral nerve stimulation, but not in that caused by local intramural stimulation and nicotine. These effects of loperamide on the internal anal sphincter were antagonized by naloxone. These findings suggest that the therapeutic effects of loperamide on the internal anal sphincter as an antidiarrheal agent are due to a rise in the tone of the sphincter and the inhibition of its relaxation in response to rectal distention. Both of these actions are mediated by activation of opioid receptors. The inhibition of internal anal sphincter relaxation induced by rectal distention (which mimicks recto-anal reflex) is due to inhibition of release of neurotransmitter from the preganglionic sacral nerve fibers.     

Gradient of pressure and time between proximal anal canal and high-pressure zone during internal anal sphincter relaxation

PURPOSE: The normal response to rectal distention is a relaxation of the proximal anal canal (PAC). We hypothesized that this mechanism would require a gradient of pressure and time to preserve continence. METHODS: Sixteen volunteers (10 male), mean age, 41.5 (range, 24–60) years, were studied using an eight port axial catheter with a compliant balloon at its tip. Relaxation was induced by a small volume of rectal distention (15–30 ml of air) and was recorded until recovery of resting anal pressure (RAP). Duration of relaxation was measured until recovery of RAP. Amplitude of relaxation was determined between RAP before rectal distention (RAP-BR) and pressure at the point of maximum relaxation (RAP-PMR). Gradient of pressure was determined by comparing RAP-PMR in the high-pressure zone (HPZ) and PAC. Contraction in the distal anal canal was interpreted as external anal sphincter contraction (EASC) and was compared with RAP-PMR in the HPZ. RESULTS: Relaxation was significantly greater in PAC than in HPZ (50vs. 36 percent;P=0.001). RAP-PMR was significantly higher in HPZ than in PAC (30.7vs. 12.6 mmHg;P= 0.001). EASC was observed in six patients and did not show significant difference with RAP-PMR in HPZ (39.7vs. 36.3 mmHg; not significant). Relaxation began at the same time in all levels but lasted significantly longer in PAC compared with HPZ (13.5vs. 9.4 sec;P=0.003). CONCLUSION: Anal relaxation induced by small volume rectal distention involves a gradient in the pressure and time of relaxation between PAC and the HPZ.Dr. Goes is supported at the University of Southern California by grants from the Fundacao de Amparo a Pesquisa do Estado de Sao Paulo-FAPESP, Brazil.Read at the meeting of The American Society of Colon and Rectal Surgeons Investigation/Surgical Research Forum, Montreal, Quebec, Canada, May 7 to 12, 1995.     

Coloanal motor coordination in association with high-amplitude colonic contractions after pharmacological stimulation

OBJECTIVE: The rectoanal inhibitory reflex facilitates defecation by relaxation of the internal anal sphincter during rectal distention by gas or stool. Defecation is sometimes preceded by high-amplitude propagated contractions (HAPCs). Our objective was to seek evidence for motor coordination between human colonic and anal sphincter functions. METHODS: As part of a study of alpha2 modulation of colonic and anal motor functions in 32 healthy volunteers, we studied the relationship between high HAPCs and anal sphincter pressure with colonic manometry, barostat, and a Dent sleeve in the anal canal. RESULTS: Twenty-two HAPCs were observed; in 19/22 HAPCs there was optimal positioning of the Dent sleeve to assess the anal sphincter. Eighteen of 19 HAPCs occurred postprandially; 14 HAPCs occurred after administration of yohimbine, three after clonidine, and one before any drug administration. Seven followed experimental balloon distention. Anal sphincter relaxation occurred (14 +/- 4 s) before the recorded onset of HAPC in the descending colon and 88 +/- 7 s before the arrival of the HAPC in the rectum. After or during the HAPCs, anal sphincter pressure decreased by 40 +/- 4% and increased by 56 +/- 8% in the postrelaxation phase. CONCLUSIONS: The close temporal association between anal sphincter relaxation and onset of HAPC in the descending colon suggests a coloanal reflex that may facilitate defecation during mass movements independently of the rectoanal inhibitory reflex.     

Relation Between Anal Electrosensitivity and Rectal Filling Sensation and the Influence of Age

PURPOSE The aim of this study was to assess the effect of age and sex on the rectal filling sensation and anal electrosensitivity and to explore the relation between anal electrosensitivity and the parameters of the rectal filling sensation.METHODS Anal mucosal electrosensitivity and anorectal manometry, including the rectal filling sensation test were performed in 19 control subjects; 10 were younger than 60 years and 9 were older than that. Altogether, there were 11 men and 8 women. RESULTS Anal electrosensitivity did not differ between the two age groups. Women had a significantly lower electrosensitivity 4 and 5 cm from the anal verge than men, as well as a significantly shorter anal high-pressure zone. The rectal filling sensation did not differ between sexes. In the older age group, the rectal volumes required to induce filling sensations were smaller than those observed in the younger age group, but rectal pressures were comparable; as a consequence, rectal compliance was lower in older subjects. Anal electrosensitivity at different anal levels did not correlate with the rectal volume or pressure parameters of successive rectal filling sensations. The pressure recorded in the proximal anal canal at the consecutive rectal filling sensations strongly correlated with the rectal balloon pressure needed to elicit them.CONCLUSIONS The zones of high anal electrosensitivity and high pressure seem to coincide. The fact that both are shorter in females did not influence the parameters of the rectal filling sensation. Lower rectal volumes but comparable rectal pressures were needed to induce the rectal filling sensation in the older age group. Rectal sensation did not correlate with anal electrosensitivity, probably because the receptors are not stimulated by the type of anal stimulation used or because different receptors are involved. Hence, the rectal filling sensation test cannot be replaced by the simpler anal electrosensitivity test.