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.
Interstitial cells of Cajal (ICC) are important players in the symphony of gut motility. They have a very significant physiological role orchestrating the normal peristaltic activity of the digestive system. They are the pacemaker cells in gastrointestinal (GI) muscles. Absence, reduction in number or altered integrity of the ICC network may have a dramatic effect on GI system motility. More understanding of ICC physiology will foster advances in physiology of gut motility which will help in a future breakthrough in the pharmacological interventions to restore normal motor function of GI tract. This mini review describes what is known about the physiologic function and role of ICCs in GI system motility and in a variety of GI system motility disorders.
When exposed to prolonged stress, rats develop gastric ulceration, enhanced colon motility with depletion of its mucin content and signs of physiological and behavioral arousal. In this model, we tested whether antidepressants (fluoxetine and bupropion), anxiolytics (diazepam and buspirone) or the novel nonpeptide corticotropin-releasing hormone (CRH) type-1 receptor (CRH-R1) antagonist, antalarmin, modify these responses. Fluoxetine, bupropion, diazepam and antalarmin all suppressed stress-induced gastric ulceration in male SpragueDawley rats exposed to four hours of plain immobilization. Antalarmin produced the most pronounced anti-ulcer effect and additionally suppressed the stress-induced colonic hypermotility, mucin depletion, autonomic hyperarousal and struggling behavior. Intraperitoneal CRH administration reproduced the intestinal but not the gastric responses to stress while vagotomy antagonized the stress-induced gastric ulceration but not the intestinal responses. We conclude that brain CRH-R1 and vagal pathways are essential for gastric ulceration to occur in response to stress and that peripheral CRH-R1 mediates colonic hypermotility and mucin depletion in this model. Nonpeptide CRH-R1 antagonists may therefore be prophylactic against stress ulcer in the critically ill and therapeutic for other pathogenetically related gastrointestinal disorders such as peptic ulcer disease and irritable bowel syndrome.
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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.