A study of the surgical anatomy of the pudendal nerve (PN) was performed in 13 female and 7 male cadavers. The knowledge of the precise anatomy and anomalies of this important nerve would help in better localization of the nerve and its roots and branches for neurostimulation or for pudendal canal decompression in pudendal canal syndrome. Two routes were used in the dissection: gluteal and perineal. The PN was identified and its course was followed from its roots to its termination. The PN was composed of three roots derived from the 2nd, 3rd, and 4th anterior sacral rami (S 2,3,4). The roots received a contribution from S 1 in five cadavers and from S 5 in one. The three roots formed two cords. The first root continued as the upper cord while the second and third root fused together producing the lower cord. The PN was formed by union of the two cords a short distance proximal to the sacrospinous ligament, and then crossed the back of the ligament. In no specimen did the nerve cross the ischial spine. The inferior rectal nerve arose from the PN in the pudendal canal in 18 cadavers. In two cases it came out proximal to the canal; this would spare the two subjects the anorectal manifestations of the pudendal canal syndrome. As the PN crossed the back of the sacrospinous ligament, it gave origin to a branch that supplied the levator ani muscle. This branch was only found in male cadavers and we call it "accessory rectal nerve"; the levator ani muscle in such cadavers was doubly innervated on its perineal aspect.

Upon feeling the urge to urinate, the urinary bladder contracts, the urethral sphincters relax and urine flows through the urethra. These actions are mediated by the micturition reflex. We investigated the hypothesis that vesical contraction is maintained by positive feedback through continuous flow of urine through the urethra, and that the cessation of urine flow aborts detrusor contraction. Normal saline was infused into the urinary bladders of 17 healthy volunteers (age 35.2 years+/-4.2(SD); ten women and seven men) at a rate of 100 ml/min. On urge, which occurred at a mean volume of 408.6 ml+/-28.7 of saline, the subject micturated while the vesical and urethral pressures during voiding were being recorded; residual urine was measured. The test was repeated after anesthetizing the urethra with xylocaine gel or, on another occasion, after applying a bland gel. On micturition, the urine was evacuated as a continuous stream without straining; no residual fluid was collected. After urethral anesthetization, the fluid came out of the urethra in multiple intermittent spurts and only with excessive straining. There was a large amount of residual fluid (184.6 ml+/-28.4). The results of bland gel application showed no significant difference ( P>0.05) from those without gel. Detrusor contraction during micturition is suggested to be maintained by positive urethrovesical feedback elicited by the continued passage of urine through the urethra. This feedback seems to be effected through the urethrovesical reflex, which produces vesical contraction on stimulation of the urethral stretch receptors. Abortion of this reflex by urethral anesthetization resulted in failure of detrusor contraction and excessive straining was needed to achieve bladder evacuation in multiple spurts. The urethrovesical reflex is thus assumed to constitute a second micturition reflex responsible for the continuation of detrusor contraction and urination. The role of this reflex in the pathogenesis of micturition disorders needs to be studied.

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Colonic wall contains interstitial cells of Cajal. In view of studies demonstrating that Cajal cells generate electric waves which are presumably responsible for colonic motor activity, and that these waves are absent in total colonic inertia, we investigated the hypothesis that colonic Cajal cells might be disordered in patients with total colonic inertia. The study comprised 28 patients (age 41.6 +/- 8.2 SD years, 19 women, 9 men) with total colonic inertia in whom total colectomy was performed. Colonic specimens obtained from normal segments of the excised colon of 24 cancer patients acted as controls. Specimens were subjected to c-kit immunohistochemistry. Controls for antisera specificity consisted of tissue incubated with normal rabbit serum that had been substituted for the primary antiserum. C-kit-positive branched Cajal-like cells were detected in the musculature of the normal colonic segments. They were distinguishable from the C-kit-negative smooth muscle cells and the C-kit-positive but unbranched mast cells. No Cajal cells were detected in colon of total colonic inertia patients. The absence of Cajal cells in patients with total colonic inertia can be assumed to explain the absence of electric waves and motile activity previously reported in these patients. Further studies are needed to investigate the cause of Cajal-cell absence.

Esophageal acidification effected an increase of secreted saliva which clears the esophagus of the refluxed acid. Increased salivation on esophageal acidification is suggested to be a reflex and is mediated through the 'esophago-salivary' reflex. This reflex might be of diagnostic significance in the investigation of reflux esophagitis, a point that requires further study.

No abstract

Urethral distention is thought to cause vesical contraction through the stimulation of urethral stretch receptors. Vesical contraction at urethral distention postulates a reflex relationship that was abolished by individual anesthetization of the urethra and bladder. This relationship, which we call the urethrovesical reflex, appears to have a role in maintaining vesical contraction during voiding. Further studies are required to investigate the role of this reflex in voiding disorders.

The levator ani muscle (LAM) shares in the mechanism of defecation and urination as well as in visceral support. Levator dysfunction occurs in conditions of chronic straining or increased intra-abdominal pressure. Studies have shown that the gravid uterus, by virtue of its weight and associated increased intraabdominal pressure, might disturb the levator function. It is postulated that this effect is augmented with repeated pregnancies. The current study investigated the functional activity of the LAM in 50 multipara, 30 primipara and 20 nullipara (controls). The 50 multipara (age 46.4 years, 4-7 deliveries) were divided into group A (28 women with normal deliveries) and group B (22 women with a prolonged 2nd stage of labour). Of the 30 primipara (age 44.2 years) 18 had normal delivery (group A) and 12 prolonged 2nd stage of labour (group B). The mean age of the nullipara was 45.3+/-7.6. The LAM activity at rest and on contraction was recorded. The rectal and anal canal pressure response to LAM stimulation was also registered. In group A of the multipara, the LAM EMG activity at rest was similar to (P>0.05), and on contraction lower (P<0.05) than the LAM EMG of the controls (nullipara). Group B exhibited a lower activity at rest and on contraction (P<0.01, both). Primipara group A had a resting and contractile EMG activity similar to the controls, while group B showed diminished activity in both conditions (P<0.05, both) which was significantly higher (P<0.05, P<0.01, respectively) than that of group B multipara. The rectal pressure in the multipara and primipara did not differ from the nullipara (P>0.05, both). In groups A and B of multiparous women, the anal canal pressure at rest was significantly lower and on LAM contraction significantly higher than that of nullipara. Group A of the primipara showed no significant difference against the controls, while group B exhibited a decline at rest (P<0.05) and no difference on LAM contraction (P>0.05). In conclusion, levator dysfunction might occur in the parous women. It was more common in the multipara than the primipara and in particular those with a history of a prolonged 2nd stage of labour. Levator dysfunction may lead to constipation and faecal or urinary incontinence as a result of pudendal neuropathy and the development of pudendal canal syndrome.