Ismail Ahmed

Percutaneous Peripheral Neuromodulation in the Treatment of Fecal Incontinence

Background/Aims: To assess the results of peripheral neuromodulation for the treatment of fecal incontinence (FI) resulting from uninhibited rectal contraction (URC) or uninhibited anal sphincter relaxation (UASR). Methods: The work comprised 32 patients (age 38.2 ± 6.7 years; 22 women) with FI in whom conventional therapy had failed before enrollment in the study. Twenty-six had URC and 6 UASR. Peripheral neurostimulation was effected by posterior tibial nerve stimulation using a Stoller Afferent Nerve Stimulator (UroSurge, Coralville, lowa, USA). The needle was introduced into the skin cephalad to the medial malleolus. Stimulation (parameters: 0.5–10 mA, 200 µs, 20 Hz) was performed every other day for 4 weeks. Functional assessment was done by a questionnaire (incontinence score: 0–20) and physiologic studies. Results: Group 1: 17 patients (13 URC, 4 UASR) had FI improvement, recording a mean score of 1.7 of 20. Group 2: 10 patients (8 URC, 2 UASR) had fair improvement (score 8.6). Group 3: 5 patients had poor results (score 14.8). Rectometric recording showed improvement in groups 1 and 2. Recurrence of symptoms occurred in 8 patients; 6 improved after retreatment. Conclusions: A percutaneous access to the S3 spinal region was achieved through the posterior tibial nerve. Improvement of FI was achieved in 78.2%. The technique is simple, easy, without complications and cost-effective. It can be done as an outpatient procedure or by the patient at home. The results need to be reproduced on a large number of patients.

Diverticular Disease: Electrophysiologic Study and a New Concept of Pathogenesis

The cause of diverticular disease (DD) is not exactly known, although colonic motor disorder has been proposed as a factor in the pathogenesis of the condition. We investigated the hypothesis that disordered colonic electrical activity is responsible for the colonic motor dysfunction and the development of DD. The electromyographic (EMG) activity and pressure of the sigmoid colon (SC) were recorded in 36 patients [16 early cases, 20 advanced cases; age (mean ± SD) 53.3 ± 5.6 years; 19 women, 17 men] and 22 healthy volunteers. The percutaneous route was used for recording the SC EMG. The healthy volunteers exhibited SC slow waves with a regular rhythm and the same frequency, amplitude, and conduction velocity from the three electrodes in the same subject. The SC basal pressure (7.9 cm H2O) was interrupted by bouts of high pressure (26.8 cm H2O). The early-DD cases showed slow waves with an irregular rhythm and significantly higher variables (p < 0.05) than the volunteers. Action potentials followed randomly or were superimposed on the slow waves. The SC basal pressure was significantly higher than that of the volunteers (21.4 cm H2O, p < 0.01). Bouts of pressure (58.6 cm H2O) coupled with action potentials were recorded. No waves were recorded from 15 of 20 of the advanced-DD patients. In 5 patients, slow waves with an irregular rhythm and lower variables (p < 0.05) than those of the volunteers were recorded. The basal SC pressure was significantly above normal. Three electrical activity patterns could be identified in DD patients: “tachyrhythmic” in the early-DD patients and “bradyrhythmic” or “silent” in the late-DD patients. These dysrhythmias may result from a disordered colonic pacemaker. The similarity between early DD and the irritable bowel syndrome suggests that DD is an advanced stage of the irritable bowel syndrome; studies are required to investigate this hypothesis further.

Parasympathetic Extrinsic Reflex: Role in Defecation Mechanism

The rectum has an intrinsic nervous mechanism represented by the enteric nervous plexus (ENP) and an extrinsic one mediated by the parasympathetic nerves. Rectal distension evokes the rectoanal inhibitory reflex, which acts through the ENP and is considered the main mechanism responsible for defecation. However, the role of the parasympathetic innervation compared to the role of the intrinsic mechanism of the defecation act has so far not been sufficiently addressed in the literature. The current study investigated this point. Twelve dogs were anesthetized. The anal and rectal pressures were recorded during rectal balloon distension with normal saline in 10 ml increments until the balloon was expelled to the exterior. The test was repeated after ENP block with α (phentolamine) and β (propranolol) adrenoceptor blocking agents and then after rectal denervation by bilateral pelvic ganglionectomy. The rectal balloon was expelled to the exterior at rectal balloon distension with 30 to 40 ml. After separate administration of phentolamine and propranolol, it was dispelled at a distending volume of 50 to 60 ml, and after rectal denervation at a volume of 80 to 90 ml. The results were reproducible. The balloon expulsion test suggests that the intrinsic defecation reflex is weaker than the extrinsic one for inducing defecation, although the two reflexes appear to be complementary. The difference between them in inducing defecation might be significant to our understanding the defecation act in the neurogenic rectum, a point that needs further study.RésuméLe rectum possède un mécanisme nerveux intrinsèque représenté par le plexus nerveux entérique (PNE) et un mécanisme nerveux extrinsèque, représenté par les nerfs parasympathiques. La distension rectale provoque un réflexe rectoanal inhibiteur, agissant par l’intermédiaire du PNE qui est considéré comme le mécanisme principal de la défécation. Cependant, le rôle de l’innervation parasympathique, comparé au mécanisme intrinsèque, peu étudié dans la littérature, fait l’objet de cette étude. Chez 12 chiens anesthésiés, on a enregistré les pressions anale et rectale lors d’une distension progressive du rectum par apports de 10 mL dé sérum physiologique par un ballonnet jusqu’à l’expulsion du dit ballonnet. Ce test a été répété après infiltration du PNE par des anti-adrénocepteurs alpha (phentolamine) et bêta (propranolol), et puis, après dénervation par ganglionectomie pelvienne bilatérale. Le ballonnet rectal a été expulsé après une distension de 30–40 ml. Cet effet a été annulé après administration séparée de phentolamine et de propranolol, pour un volume de distension de 50–60 ml, et après dénervation rectale, pour un volume de 80–90 ml. Ces résultats ont été reproductibles. Le test d’expulsion du ballonnet suggère que le réflexe de défécation intrinsèque est plus faible que le réflexe extrinsèque. Cependant, les deux réflexes apparaissent comme complémentaires. La différence, cependant, dans l’induction de la défécation, pourrait être importante dans la compréhension du mécanisme de la défécation du rectum neurogénique, un point qui nécessite plus d’études.ResumenEl recto posee un mecanismo nervioso intrínseco representado por el piejo nervioso entérico (PNE) y uno extrínseco mediado por los nervios parasimpáticos. La distensión rectal provoca un efecto recto anal inhibitorio, el cual actúa a través de PNE y es considerado como el principal mecanismo responsable de la defecación. Sin embargo, aún no se ha estudiado suficientemente el papel de la inervación parasimpática en comparación con el del mecanismo intrínseco en el acto de la defecación. El presente artículo se refiere a este punto. Doce perros fueron anestesiados para registrar las presiones anales y rectales durante una maniobra de distensión rectal por medio de un balón inyectado con solución salina en incrementos de 10 mi hasta su expulsión al exterior. La prueba fue repetida luego del bloqueo del PNE con agentes de adrenoreceptores alpha (fentolamina) y beta (propranolol) y luego de la denervación mediante ganglionectormía pélvica bilateral. El balón rectal fue expelido cuando la distensión llegó a 30–40 mS. Luego de la administración, por separado, de fentolamina y de propranolol, fue expelido al alcanzar un volumen de 50–60 ml y luego de la denervación al alcanzar un volumen de 80–90 mi. Los resultados fueron reproducibles. La prueba de expulsión del balón sugiere que el reflejo intrínseco de defecación es más débil que el extrínseco en cuanto a inducir la defecación, aunque los dos reflejos parecen ser complementarios. La diferencia en cuanto inducir defecación puede ser significante en la comprensión del acto de defecación en el recto neurogénico, pero esto es algo que requiere estudio adicional.

On the pathogenesis of rectocele: the concept of the rectovaginal pressure gradient

Coughing or straining evokes reflex bulbocavernosus (BCM) and puborectalis (PRM) muscle contraction, which apparently transforms the vagina into a closed high-pressure cavity [13]. This elevated vaginal pressure counteracts the increased intra-abdominal pressure and the tendency of the uterus to prolapse, and also supports the rectovaginal septum against the high straining-induced intrarectal pressure and possible consequent rectocele (posterior vaginal prolapse) formation. We investigated the hypothesis that a weak BCM and PRM share in the genesis of rectocele by changing the rectovaginal pressure gradient. Twenty-three women with rectocele (mean age 43.2±6.6 years) and 12 healthy women volunteers (mean age 41.6±6.2 years) were studied. The response of the intrarectal (intra-abdominal) and intravaginal pressure, as well as the EMG activity of the BCM and PRM to straining or coughing, was recorded. In the healthy volunteers the rectal and vaginal pressures showed a significant increase on coughing or straining, with no significant difference between the rectal or vaginal pressures. Also, the BCM and PRM EMG activity exhibited a significant increase. Rectocele patients showed a significantly low resting vaginal pressure. The increase in rectal and vaginal pressure, as well as of the EMG activity of the BCM and PRM on straining or coughing, was significantly lower and the latency of the EMG response was significantly longer than those of the healthy volunteers. A difference in the rectovaginal pressure gradient showing a significant increase in the rectal against the vaginal pressure, particularly on coughing or straining, is suggested to be the basic factor in the genesis of rectocele. This pressure difference appears to be caused by diminished BCM and PRM contractile activity. A disrupted rectovaginal septum is not a prerequisite for rectocele formation, as the septum appears normal in obstructed defecation despite the common occurrence of rectocele. A histopathologic study of the septum in rectocele seems necessary.

Role of positive anorectal feedback in rectal evacuation: the concept of a second defecation reflex: the anorectal reflex.

Abstract Background/Objective: The present study investigated the hypothesis that rectal contraction is maintained by positive anorectal feedback elicited by continuous passage of stools through the rectal neck (anal canal), and that cessation of stool passage aborts rectal contraction. Methods: Anal and rectal pressures were measured in 18 healthy volunteers (mean age = 38.6 years; 10 men, 8 women) during evacuation of saline infused into the rectum. Residual fluid volume was calculated. The test was repeated after separate application of lidocaine or bland gel to the rectal neck. Results: On evacuation, fluid emanated from the rectal neck in continuous flow with no, or mild, straining. No residual saline was collected from 16 of 18 participants. After anal anesthetization, evacuation occurred in gushes induced with excessive straining; residual fluid was huge. Repetition of the test 2 hours after anesthetization produced the same results as before anesthetization. Bland gel applied to the rectal neck yielded results similar to those before gel application. Conclusion: Rectal contraction at defecation is suggested to be maintained by positive anorectal feedback evoked by continuous passage of stool through the rectal neck. This feedback appears to be affected through an anorectal excitatory reflex (ARR), which produces rectal contraction upon stimulation of anal stretch receptors. Abortion of this reflex by anal anesthetization seems to result in failure of the rectum to contract and in excessive straining to achieve rectal evacuation. ARR thus is suggested to be a second defecation reflex necessary to continue defecation, whereas the rectoanal inhibitory reflex is the primary reflex. The role of the ARR in pathogenesis of constipation and its utility in spinal cord injury need to be investigated.

The identification of specialized pacemaking cells in the anal sphincters

Background and aimsInterstitial cells of Cajal (ICC) are claimed to generate the electrical activity in the colon and stomach. As the external (EAS) and internal (IAS) anal sphincters exhibit resting electrical activity, we hypothesized the presence of ICC in these sphincters. This hypothesis was investigated in the current study.Patients/MethodsSpecimens from the EAS and IAS were taken from normal areas of the anorectum which had been surgically excised by abdominoperineal operation for rectal cancer of 28 patients (16 men, 12 women, mean age 42.2±4.8 years). The specimens were subjected to c-kit immunohistochemistry. Controls for the specificity of the antisera consisted of tissue incubation with normal rabbit serum substituted for the primary antiserum.Results/FindingsFusiform, c-kit positive, ICC-like cells were detected in the anal sphincters; they had dendritic processes. They were clearly distinguishable from the non-branching, c-kit negative smooth and striated muscle cells of the anal sphincters. The specimens contained also c-kit positive mast cells, but they had a rounded body with no dendritic processes. Immunoreactivity was absent in negative controls in which the primary antibody was omitted.Interpretation/ConclusionWe have identified, for the first time, cells in EAS and IAS with morphological and immunological phenotypes similar to ICCs of the gut. These cells appear to be responsible for initiating the slow waves recorded from the anal sphincters and for controlling their activity. A deficiency or absence of these cells may affect the anal motile activity. Studies are needed to explore the role of these cells in anal motility disorders.

Electric activity of the colon in irritable bowel syndrome: The ‘tachyarrhythmic’ electric pattern

Background and Aim:  The etiology of irritable bowel syndrome is unknown. It presents with crampy abdominal pain associated with alternating constipation and diarrhea but with no anatomic abnormality on diagnostic testing. Because the condition is related to motility disturbance, the hypothesis that a disorder of the colonic electromyographic activity is responsible for the colonic motile disorders in irritable bowel syndrome, was investigated.

Study of the role of the second defecation reflex: anorectal excitatory reflex in the pathogenesis of constipation.

BACKGROUND Previous studies have shown that anal distension caused rectal contraction, an action mediated through the anorectal excitatory reflex. Anal anesthetization aborted rectal contraction and rectal evacuation was induced by excessive straining. We investigated the hypothesis that inhibition or absence of the anorectal excitatory reflex could lead to constipation. METHODS We studied 18 patients (mean age +/- SD: 40.6 +/- 5.8 years, 14 women) with rectal inertia, 14 (41.7 +/- 6.6 years, 12 women) with puborectalis paradoxical syndrome, and 10 healthy volunteers (37.9 +/- 4.8 years, 8 women). The rectum was filled with normal saline until urge and then evacuated; residual fluid was calculated. The anal and rectal pressure response to anal balloon distension in increments of 2 mL of saline was recorded by a two-channel microtip catheter. RESULTS In the healthy volunteers, saline was evacuated as a continuous stream without straining except occasionally at the start of evacuation; no residual fluid was encountered. Anal balloon distension effected notable rectal pressure increase. In rectal inertia patients, evacuation occurred in small fluid gushes produced with excessive straining; residual fluid of large volume was collected. Anal balloon distension up to 10 mL produced no notable rectal pressure changes. The patients with PPS failed to evacuate more than a few mL of fluid despite excessive straining; the volume of residual fluid was considerable. Anal balloon distension caused a notable rectal pressure rise. The results were reproducible. CONCLUSIONS These results suggest that the defecation reflexes (rectoanal and anorectal) are absent in rectal inertia patients and this presumably denotes a neurogenic disorder. The anorectal reflex is active in puborectalis paradoxical syndrome, but the rectoanal reflex is not, indicating a possible myogenic defect in the puborectalis muscle.

Effect of colonic distention on ileal motor activity with evidence of coloileal reflex

Chyme delivery from the ileum to the colon is controlled by various neurologic and hormonal factors, many of which remain to be identified. In this report we investigated the effect of colonic distention on ileal motility with the aim of identifying the mechanism of chyme delivery from the ileum to the colon. The right colon of 16 healthy volunteers (12 men and 4 women; mean age 36 ± 9 years standard deviation) was distended by a balloon that was filled with saline solution in increments of 20 ml. The pressure response of the terminal ileum to the colonic distention was recorded by a saline-perfused tube. The test was repeated in nine subjects after the colonic segment around the balloon was anesthetized by xylocaine injection into the colonic wall. Twenty and 40 ml colonic distention produced no significant ileal pressure response. Colonic distention with 60 ml produced an increase in colonic pressure (P < 0.05), as measured by intraballoon pressure, and a decrease in ileal pressure (P < 0.05); a similar response was achieved with 80 ml distention. At 100 ml colonic distention, the balloon was dispelled to the transverse colon. Distention up to 100 ml of the anesthetized colonic segment produced no significant colonic or ileal pressure response. The flow of chyme from the small to the large gut appears to be controlled by a reflex mechanism that we call the ‘coloileal reflex.’ Whenever the right colon is distended with a substantial volume of chyme that increases the intraluminal pressure, it is suggested that ileal relaxation occurs, which delays the emptying of chyme from the ileum.Chyme delivery from the ileum to the colon is controlled by various neurologic and hormonal factors, many of which remain to be identified. In this report we investigated the effect of colonic distention on ileal motility with the aim of identifying the mechanism of chyme delivery from the ileum to the colon. The right colon of 16 healthy volunteers (12 men and 4 women; mean age 36 ± 9 years standard deviation) was distended by a balloon that was filled with saline solution in increments of 20 ml. The pressure response of the terminal ileum to the colonic distention was recorded by a saline-perfused tube. The test was repeated in nine subjects after the colonic segment around the balloon was anesthetized by xylocaine injection into the colonic wall. Twenty and 40 ml colonic distention produced no significant ileal pressure response. Colonic distention with 60 ml produced an increase in colonic pressure (P < 0.05), as measured by intraballoon pressure, and a decrease in ileal pressure (P < 0.05); a similar response was achieved with 80 ml distention. At 100 ml colonic distention, the balloon was dispelled to the transverse colon. Distention up to 100 ml of the anesthetized colonic segment produced no significant colonic or ileal pressure response. The flow of chyme from the small to the large gut appears to be controlled by a reflex mechanism that we call the ‘coloileal reflex.’ Whenever the right colon is distended with a substantial volume of chyme that increases the intraluminal pressure, it is suggested that ileal relaxation occurs, which delays the emptying of chyme from the ileum.

Do vesical and voided urine have identical compositions

Objective: In view of the concept that the urothelium is a functioning epithelium, we investigated the hypothesis that the composition of urine is modified as it passes through the urethra from the urinary bladder to the exterior. Material and Methods: The study was performed in 22 healthy volunteers (13 males, 9 females; mean age 44.6 ± 6.2 years). Vesical and voided urine were collected separately; pH was determined using a pH electrode, osmolality by means of micro‐osmometry and electrolytes (Na, K) using flame photometry. Results: Voided urine showed significant increases in pH, osmolality and Na and K concentrations compared to urine contained in the bladder (p < 0.05 for each). Gender and age differences were not significant. Conclusions: Vesical urine undergoes changes in some of its components during its passage through the urethra. These findings presumably indicate that the urethral urothelium is a functioning epithelium and also that voided and vesical urine are not identical. The study raises the question to what extent is the analysis of voided urine representative of that of vesical urine?