Colonic pacing in the control of colonic and rectal motile activity.
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INTRODUCTION: Sacral nerve modulation has been demonstrated to be a new efficacious treatment for fecal incontinence. The effectiveness of the procedure is preliminarily tested by means of a peripheral nerve evaluation. Integrity of the sacral neural pathway is generally believed to be a necessary condition for a good response, but no data are available to confirm whether electrophysiologic anal tests are predictive of the clinical outcome of the peripheral nerve evaluation. METHODS: Eighty-two incontinent patients underwent the peripheral nerve evaluation after full evaluation of the anorectal physiology. Univariate analysis was performed, and the positive predictive value, sensitivity, and specificity were calculated for each of the tests. RESULTS: Forty-six patients had successful results to the peripheral nerve evaluation and were subjected to permanent implant of a sacral electrostimulator. Anal sphincter electromyography had been performed in 60 patients, whereas pudendal nerve terminal motor latency had been assessed in 68 and evoked sacral potentials in 29 patients. Anal electromyography was statistically related to the outcome of the peripheral nerve evaluation ( P = 0.0004) with a positive predictive value of 81 percent, a sensitivity of 44 percent, and a specificity of 81 percent. Pudendal nerve terminal motor latency on the right side did not correlate with the outcome, but left pudendal nerve terminal motor latency was weakly correlated ( P = 0.02), although both tests had a low positive predicting value and sensitivity vs. good specificity. Evoked sacral potentials did not correlate with the outcome and had a low positive predictive value, sensitivity, and specificity. CONCLUSIONS: Simple anal sphincter electromyography can predict the outcome of the peripheral nerve evaluation with good positive predictive value and specificity in patients with fecal incontinence. Other, more expensive, electrophysiologic anal tests do not add further prognostic information.
Fecal incontinence is a common condition that causes major impairment of social life. Sacral nerve stimulation is a promising treatment in idiopathic fecal incontinence when conventional treatments have failed. However, new indications for sacral nerve stimulation are emerging. The present case shows that sacral nerve stimulation for treatment of fecal incontinence may be justified in other diseases in which fecal incontinence is a major problem.
PURPOSE: The effect of sacral nerve stimulation was studied in 45 patients with fecal incontinence. METHODS: All patients were initially tested in general anesthesia. Sacral nerves 2, 3, and 4 were tested on both sides. If a perineal/perianal muscular response to sacral nerve stimulation could be obtained, electrodes were implanted for a three-week test-stimulation period. If sacral nerve stimulation resulted in at least a 50 percent reduction in incontinence episodes during the test period, a system for permanent sacral nerve stimulation was implanted. RESULTS: When tested in general anesthesia, 43 of 45 patients had a muscular response to sacral nerve stimulation and had electrodes implanted for the three-week test period. Percutaneous electrodes were used in 34 patients, and 23 of these had at least a 50 percent reduction in incontinence episodes, whereas the electrodes dislocated in 7 patients and 4 had a poor response. Permanent electrodes with percutaneous extension electrodes were used primarily in 9 patients and after dislocation of percutaneous electrodes in an additional 6 patients; 14 of these had a good result. In the last patient, no clinical response to stimulation with the permanent electrode could be obtained. A permanent stimulation system was implanted in 37 patients. After a median of six (range, 0-36) months follow-up, five patients had the system explanted: three because the clinical response faded out, and two because of infection. Incontinence score (Wexner, 0-20) for the 37 patients with a permanent system for sacral nerve stimulation was reduced from median 16 (range, 9-20) before sacral nerve stimulation to median 6 (range, 0-20) at latest follow-up ( P < 0.0001). There was no differences in effect of sacral nerve stimulation in patients with idiopathic incontinence (n = 19) compared with spinal etiology (n = 8) or obstetric cause of incontinence (n = 5). Sacral nerve stimulation did not influence anal pressures or rectal volume tolerability. CONCLUSIONS: Sacral nerve stimulation in fecal incontinence shows promising results. Patients with idiopathic, spinal etiology, or persisting incontinence after sphincter repair may benefit from this minimally invasive treatment.
PURPOSE: Fecal incontinence is a psychologically devastating and socially incapacitating condition. Conventional treatment is likely to improve continence in many patients; however, there remains a group with persisting symptoms who are not amenable for a simple surgical repair. We evaluated the effect of sacral neuromodulation in patients with structurally intact sphincters after failure of conventional treatment. METHODS: Patients aged 18 to 75 years were evaluated. Incontinence was defined as involuntary loss of stool at least once per week, which was objectified by completion of a three-week bowel-habits diary during ambulatory electrode stimulation at the S3 or S4 foramen. Patients were qualified for permanent stimulation when showing a reduction of at least 50 percent in incontinence episodes or days. RESULTS: Seventy-five patients (66 females; mean age, 52 (range, 26-75) years) were treated. Three patients had partial spinal cord injury, two patients a previous low-anterior resection, and nine patients had a previous sphincter repair. Evaluation after trial screening showed that 62 patients (83 percent) had improved continence. Median incontinence episodes per week decreased from 7.5 to 0.67 (P < 0.01), median incontinence days per week from 4 to 0.5 (P < 0.01). The symptomatic response stayed unchanged after implantation of a permanent electrode and pacemaker in 50 patients. After a median follow-up of 12 months, this effect could be sustained in 48 patients. Anal manometry during stimulation showed no increase of sphincter pressures. CONCLUSIONS: Sacral neuromodulation is a feasible treatment option for fecal incontinence in patients with structurally intact sphincters.
OBJECTIVE: The aim of this study was to present an overview of sacral nerve stimulation in the treatment of fecal incontinence. We describe the evolution in technique, patient selection, and indications, and review results and complications. METHODS: All articles on sacral nerve stimulation for fecal incontinence that were recovered on MEDLINE search were reviewed. With multiple articles from an institution, the most recent reports with the longest follow-up and largest cohort of patients were selected, unless information from earlier reports was relevant. RESULTS: The technique of sacral stimulation is well established, carries little risk, and continues to be refined (e.g., a less invasive approach has been proposed). Patient selection is based on a two-stage diagnostic test stimulation (acute and subchronic), for which the predictive value is high. On this basis, permanent sacral nerve stimulation has proved effective in both single-center and multicenter trials in patients with a functional deficit but limited morphologic lesions or no morphologic lesions. The clinical benefit derives from multiple symptomatic improvements contributing to better bowel control and from substantially improved quality of life. The underlying mechanism of action remains undefined, but both somatic and autonomic function appears affected. CONCLUSION: Sacral nerve stimulation offers a safe treatment mode in a patient population in whom conservative treatment has failed and traditional surgical approaches would have limited success. The high predictive value of the diagnostic approach offers a unique therapeutic advantage.
PURPOSE: Fecal incontinence may occur in patients who have undergone anterior resection for rectal cancer without presenting sphincter lesions. Chemoradiation may contribute to disrupting continence mechanisms. Treatment is controversial. Assessment of fecal incontinence in patients who agreed to integrate treatment for rectal cancer and treatment with sacral neuromodulation are reported. METHODS: Fecal incontinence following preoperative chemoradiation and anterior resection for rectal cancer was evaluated in four patients. A good response was observed during the percutaneous sacral nerve evaluation test, and so permanent implant of sacral neuromodulation system was performed. Reevaluation was performed at least two months after implant. RESULTS: After device implantation, the mean fecal incontinence scores decreased, and the mean number of incontinence episodes dropped from 12.0 to 2.5 per week (P < 0.05). Permanent implant resulted in a significant improvement in fecal continence in three patients, and incontinence was slightly reduced in the fourth. Manometric parameters agreed with clinical results: maximum and mean resting tone and the squeeze pressure were normal in three patients and reduced in one. In these same three patients, neorectal sensation parameters increased when the preoperative value was normal or below normal and decreased when the preoperative value was higher than normal, whereas in one patient in whom extremely low values were recorded all of the parameters decreased significantly. CONCLUSIONS: Fecal incontinence following anterior resection and neoadjuvant therapy should be carefully evaluated. If a suspected neurogenic pathogenesis is confirmed, sacral neuromodulation may be proposed. If the test results are positive, permanent implant is advisable. Failure of this approach does not exclude the use of other, more aggressive treatment.
PURPOSE: A proportion of patients have fecal incontinence secondary to a full-thickness rectal prolapse that fails to resolve following prolapse repair. This multicenter, prospective study assessed the use of sacral nerve stimulation for this indication. METHODS: Patients had to have more than or equal to four days with fecal incontinence per 21-day period more than one year after surgery. They had to have failed conservative treatment and have an intact external anal sphincter. RESULTS: Four female patients aged 42, 54, 68, and 65 years met the inclusion criteria. Three of the four patients had had more than one operation for recurrent full-thickness rectal prolapse before sacral nerve stimulation, one of whom had undergone a further operation for recurrence following stimulation. One patient had undergone one operation for prolapse repair. The preoperative duration of symptoms was ten, eight, three, and nine years, respectively. Although patients had an intact external anal sphincter, one patient had a fragmented internal anal sphincter. The frequency of fecal incontinent episodes changed from 11, 24.7, 5, and 8 per week at baseline to 0, 1.5, 5.5, and 1 per week at latest follow-up. Ability to defer defecation was also improved in two of three patients who had this documented. Fecal incontinence-specific quality of life assessment showed an improvement in all four domains. CONCLUSION: Sacral nerve stimulation should be considered for patients with ongoing fecal incontinence following full-thickness rectal prolapse repair if they prove resistant to conservative treatment.
PURPOSE: Sacral neuromodulation is a novel treatment for selected urinary and bowel dysfunctions. A new method is described for electrode implantation, the "minimally invasive sacral neuromodulation implant technique." METHODS: After the percutaneous nerve evaluation test, a small longitudinal incision (3 cm) is made, and a catheter cannula segment is inserted through the sacral foramen beside an insulated needle. The electrode is introduced into the catheter cannula, which is then removed and fixed to the sacrum by means of small anchors. The proximal part of the lead is tunneled into the subcutaneous tissue, reaching the pocket made to accommodate the neurostimulator. RESULTS: This procedure was performed in ten patients (5 male; mean age, 50.4 years). In four patients a single electrode was implanted, and in six patients two electrodes were implanted. The minimally invasive technique was significantly faster, saving a mean time of 20 minutes for each electrode. The incision made directly on the sacral foramen was significantly reduced (3 vs. 12 cm), avoiding the wide, blunt dissection of subcutaneous fat tissue. Application of the catheter cannula allowed the electrode to be introduced easily and correctly. The electrode anchors never failed: no cases of lead displacement or suboptimal position of the electrode occurred. A unilateral, sterile subcutaneous seroma occurred in one of the ten patients. CONCLUSIONS: The minimally invasive sacral neuromodulation implant technique seems to be a safe procedure-making sacral neuromodulation implant easier, faster, and safer, in as much as complications could be potentially reduced.
PURPOSE: Hyperbaric oxygen therapy has several physiologic effects on damaged nerves in animal models, which lead to an improvement in neurologic function. Idiopathic fecal incontinence secondary to pudendal neuropathy is usually treated with biofeedback, which shows improvement in only 50 percent of patients. METHODS: Thirteen patients (12 females, age range, 40-75 years) with chronic pudendal neuropathy and fecal incontinence were identified. They received 30 treatments of hyperbaric oxygen during a period of 6 weeks. Each treatment was at 2.4 atmospheres breathing pure oxygen for 90 minutes. Pudendal latencies were performed sequentially throughout the treatment and one and six months after it had finished. Questionnaires were used to assess improvements in symptoms and quality of life (Wexner fecal incontinence quality of life score). RESULTS: All patients completed the treatment without major complications. There was a consistent improvement of the latencies (on the left 2.36 msec initially, reduced to 2.08 msec at 6-month follow-up and on the right 2.23 msec, on the left reduced to 2.07 msec at 6 months). These improvements were significant (Wilcoxon's two-tailed, asymptomatic significance, comparing pretreatment to 6-month follow-up, left 0.005, right 0.003). Incontinence sores also improved (12.08 initially to 11.64 at the end of treatment, 10.55 at 1-month follow-up, and 10.45 at 6-month follow-up). Using the same test, the improvement in incontinence scores also was significant when comparing pre-end (0.05) and pre-one month (0.011) but not pre-six month (0.054). CONCLUSIONS: Hyperbaric oxygen therapy has improved pudendal nerve function and continence in this group of patients. The cause for this improvement in latencies is unclear at present but may be because of a direct effect on the nerve or an improvement in blood flow to the nerve through angiogenesis. However, these results are good enough to schedule further trials.
PURPOSE: This study was designed to determine whether patients with fecal incontinence and endoanal ultrasound evidence of anal sphincter disruption may be successfully treated by sacral nerve stimulation. METHODS: Five consecutive females with incontinence to solids and endoanal ultrasound evidence of anal sphincter disruption were treated by a two-week trial of sacral nerve stimulation. If successful, patients then proceeded to permanent sacral nerve stimulation implantation. RESULTS: Five patients, aged 34 to 56 years, were treated by temporary sacral nerve stimulation. Four had symptoms starting after childbirth. Two had previously had an anterior sphincter repair. After a two-week trial, three females reported full continence and an improvement in all aspects of their Rockwood fecal incontinence quality of life scores. These three females underwent permanent sacral nerve stimulation implantation. The remaining two patients reported no improvement and underwent dynamic graciloplasty or end colostomy respectively. CONCLUSIONS: Sacral nerve stimulation may successfully restore bowel continence in some patients with endoanal ultrasound evidence of a defect in their external anal sphincter.
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PURPOSE: Few studies have demonstrated the feasibility of cross innervating a skeletal muscle neosphincter with the pudendal nerve in an animal model. This study was designed to evaluate in humans the technical feasibility of anastomosing the nerve of the gracilis muscle and the pudendal nerve when the gracilis muscle is transposed around the anus. METHODS: Anatomic assessment was made in 30 cases. The gracilis muscle and its principal neurovascular pedicle were dissected and the nerve to the gracilis divided at its origin. The gracilis muscle, accompanied by its nerve, was then transposed around the anus. The pudendal nerve was dissected in its extrapelvic portion and divided at its termination. Gracilis reinnervation was considered feasible when the proximal end of the nerve to the gracilis muscle and the distal end of the pudendal nerve were able to be placed into tension-free contact. RESULTS: The mean lengths of the nerve to the gracilis and the pudendal nerve were 126.5 +/- 20.6 mm and 57.5 +/- 16.3 mm. Anastomosing the nerve of the gracilis muscle and the pudendal nerve was possible in 28 cases. There was a total mean surplus nerve length of 25.1 +/- 20.9 mm. In 26 cases, the distal end of the pudendal nerve (mean, 3.3 +/- 1.1 mm) was similar or larger than the end of the nerve to the gracilis (mean, 3 +/- 0.8 mm). CONCLUSIONS: Anal sphincter reconstruction using transposed gracilis muscle with pudendal nerve anastomosis is anatomically achievable in cadavers, and supports the potential applications of this technique for perineal reconstruction in clinical practice.
PURPOSE: Pudendal nerve terminal motor latency testing has been used to test for pudendal neuropathy, but its value remains controversial. We sought to clarify the relationship of pudendal nerve terminal motor latency to sphincter pressure and level of continence in a cohort of patients with intact anal sphincters and normal pelvic floor anatomy. METHODS: We reviewed 1,404 consecutive patients who were evaluated at our pelvic floor laboratory for fecal incontinence. From this group, 83 patients had intact anal sphincters on ultrasound and did not have internal or external rectal prolapse during defecography. These patients were evaluated by pudendal nerve terminal motor latency testing, a standardized questionnaire, and anorectal manometry, which measured resting and squeeze anal pressures. Incontinence scores were calculated by using the American Medical Systems Fecal Incontinence Score. Values were compared by using the Fisher's exact test and Wilcoxon's rank-sum test; and significance was assigned at the P < 0.05 level. RESULTS: 1) Using a 2.2-ms threshold, 28 percent of patients had prolonged pudendal nerve terminal motor latency unilaterally and 12 percent bilaterally. 2) At a 2.4-ms threshold, 18 percent of patients had prolonged pudendal nerve terminal motor latency unilaterally and 8 percent bilaterally. 3) Bilaterally prolonged pudendal nerve terminal motor latency was significantly associated with decreased maximum mean resting pressure and increased Fecal Incontinence Score, but not decreased maximum mean squeeze pressure, at both 2.2-ms and 2.4-ms thresholds. 4) Unilaterally prolonged pudendal nerve terminal motor latency was not associated with maximum mean resting pressure, maximum mean squeeze pressure, or fecal incontinence score at either threshold. CONCLUSIONS: The majority of incontinent patients with intact sphincters have normal pudendal nerve terminal motor latency. Bilaterally but not unilaterally prolonged pudendal nerve terminal motor latency is associated with poorer function and physiology in the incontinent patient with an intact sphincter.
PURPOSE: Sacral nerve stimulation has proven to be a promising treatment for fecal incontinence when conventional treatment modalities have failed. There have been several hypotheses concerning the mode of action of sacral nerve stimulation, but the mechanism is still unclear. This study was designed to evaluate the results of rectal volume tolerability, rectal pressure-volume curves, and anal pressures before and six months after permanent sacral nerve stimulation and to investigate the mode of action of sacral nerve stimulation. METHODS: Twenty-nine patients with incontinence (male/female ratio = 6/23; median age, 58 (range, 29-79) years) underwent implantation of a permanent sacral electrode and neurostimulator after a positive percutaneous nerve evaluation test. Wexner incontinence score, rectal distention with thresholds for "first sensation," "desire to defecate," and "maximal tolerable volume," rectal pressure-volume curves, anal resting pressure, and maximum squeeze pressure were evaluated at baseline and at six months follow-up. RESULTS: Median Wexner incontinence score decreased from 16 (range, 6-20) to 4 (range, 0-12; P < 0. 0001). Median "first sensation" increased from 43 (range, 16-230) ml to 62 (range, 4-186) ml (P = 0.1), median "desire to defecate" from 70 (range, 30-443) ml to 98 (range, 30-327) ml (P = 0.011), and median "maximal tolerable volume" from 130 (range, 68-667) ml to 166 (range, 74-578) ml (P = 0.031). Rectal pressure-volume curves showed a significant increase in rectal capacity (P < 0.0001). The anal resting pressure increased significantly from 31 (range, 0-109) cm H(2)O to 38 (range, 0-111) cm H(2)O (P = 0.045). No significant increase in maximum squeeze pressure was observed. CONCLUSIONS: For patients with fecal incontinence successfully treated with sacral nerve stimulation, there was a significant increase in rectal volume tolerability and rectal capacity. A significant increase in anal resting pressure, but not in maximum squeeze pressure, was found. We suggest that sacral nerve stimulation causes neuromodulation at spinal level.
1. Brief interruption of spinal cord blood flow resulting from transient abdominal aortic occlusion may lead to degeneration of specific spinal cord neurons and to irreversible loss of neurological function. The alteration of nitric oxide/nitric oxide synthase (NO/NOS) pool occurring after ischemic insult may play a protective or destructive role in neuronal survival of affected spinal cord segments. 2. In the present study, the spatiotemporal changes of NOS following transient ischemia were evaluated by investigating neuronal NOS immunoreactivity (nNOS-IR), reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, and calcium-dependent NOS (cNOS) conversion of [(3)H] l-arginine to [(3)H] l-citrulline. 3. The greatest levels of these enzymes and activities were detected in the dorsal horn, which appeared to be most resistant to ischemia. In that area, the first significant increase in NADPHd staining and cNOS catalytic activity was found immediately after a 15-min ischemic insult. 4. Increases in the ventral horn were observed later (i.e., after a 24-h reperfusion period). While the most intense increase in nNOS-IR was detected in surviving motoneurons of animals with a shorter ischemic insult (13 min), the greatest increase of cNOS catalytic activity and NADPHd staining of the endothelial cells was found after stronger insult (15 min). 5. Given that the highest levels of nNOS, NADPHd, and cNOS were found in the ischemia-resistant dorsal horn, and nNOS-IR in surviving motoneurons, it is possible that NO production may play a neuroprotective role in ischemic/reperfusion injury.
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In 1981, Tanagho and Schmidt introduced chronic electrical stimulation of the sacral spinal nerves using a permanently implanted sacral foramen electrode and a battery-powered pulse generator for treatment of different kinds of lower urinary tract dysfunction, refractory to conservative treatment. At our department, chronic unilateral electrical stimulation of the S3 sacral spinal nerve has been used for treatment of vesicourethral dysfunction in 55 patients with a mean postoperative follow-up of 44.3 months. Lasting symptomatic improvement of more than 50% was achieved in 16 of 21 patients with motor urge incontinence (76.2%) and in 22 of the 28 patients with urinary retention (78.6%). In our opinion, chronic sacral neuromodulation offers a sustained therapeutic effect to treatment responders that is not achieved by temporary neuromodulation techniques. Chronic neuromodulation should be considered predominantly in patients with urinary retention and in patients with motor urge incontinence who refuse temporary techniques or who require too much effort to achieve a sustained clinical effect.