sphincter muscle [keywords]
- A Functional and Clinical Reinterpretation of Human Perineal Neuromuscular Anatomy. [JOURNAL ARTICLE]
- Clin Anat 2016 Aug 26.
Modern anatomical and surgical references illustrate perineal muscles all innervated by branches of the pudendal nerve but still organized into anatomically distinct urogenital and anal triangles with muscles inserting onto a central perineal body. However, this conflicts with the anatomy commonly encountered during dissection.We use dissections of 43 human cadavers to characterize the anatomical organization of the human perineum and compare our findings to standard references.We found bulbospongiosus and the superficial portion of the external anal sphincter (EAS) were continuous anatomically with a common innervation in 92.3% of specimens. The superficial transverse perineal muscle inserted anterior and lateral to the midline, interdigitating with bulbospongiosus. The three EAS subdivisions were anatomically discontinuous. Additionally, in 89.2% of our sample the inferior rectal nerve emerged as a branch of S3 and S4 distinct from the pudendal nerve and innervated only the subcutaneous EAS. Branches of the perineal nerve innervated bulbospongiosus and the superficial EAS and nerve to levator ani innervated the deep EAS.We empirically demonstrate important and clinically relevant differences with perineal anatomy commonly described in standard texts. First, independent innervation to the three portions of EAS suggests the potential for functional independence. Second, neuromuscular continuity between bulbospongiosus and superficial EAS suggests the possibility of shared or overlapping function of the urogenital and anal triangles. This article is protected by copyright. All rights reserved.
- In vitro effect of nicorandil on the carbachol-induced contraction of the lower esophageal sphincter of the rat. [JOURNAL ARTICLE]
- J Pharmacol Sci 2016 Jul 27.
The lower esophageal sphincter (LES) is a specialized region of the esophageal smooth muscle that allows the passage of a swallowed bolus into the stomach. Nitric oxide (NO) plays a major role in LES relaxation. Nicorandil possesses dual properties of a NO donor and an ATP-sensitive potassium channel (KATP channel) agonist, and is expected to reduce LES tone. This study investigated the mechanisms underlying the effects of nicorandil on the LES. Rat LES tissues were placed in an organ bath, and activities were recorded using an isometric force transducer. Carbachol-induced LES contraction was significantly inhibited by KATP channel agonists in a concentration-dependent manner; pinacidil > nicorandil ≈ diazoxide. Nicorandil-induced relaxation of the LES was prevented by pretreatment with glibenclamide, whereas N(G)-nitro-l-arginine methyl ester (l-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and iberiotoxin were ineffective at preventing nicorandil-induced LES relaxation. Furthermore, nicorandil did not affect high K(+)-induced LES contraction. Reverse-transcription polymerase chain reaction analysis and immunohistochemistry revealed expression of KCNJ8 (Kir6.1), KCNJ11 (Kir6.2), ABCC8 (SUR1) and ABCC9 (SUR2) subunits of the KATP channel in the rat lower esophagus. These findings indicate that nicorandil causes LES relaxation chiefly by activating the KATP channel, and that it may provide an additional pharmacological tool for the treatment of spastic esophageal motility disorders.
- [Incontinence - Etiology, diagnostics and Therapy]. [English Abstract, Journal Article]
- Dtsch Med Wochenschr 2016 Aug; 141(17):1251-60.
Fecal incontinence is defined by the unintentional loss of solid or liquid stool, and anal incontinence includes leakage of gas and / or fecal incontinence. Anal-fecal incontinence is not a diagnosis but a symptom. Many patients hide the problem from their families, friends, and even their doctors. Epidemiologic studies indicate a prevalence between 7-15 %, up to 30 % in hospitals and up to 70 % in longterm care settings. Anal-fecal incontinence causes a significant socio-economic burden. There is no widely accepted approach for classifying anal-fecal incontinence available. Anal-fecal continence is maintained by anatomical factors, rectoanal sensation, and rectal compliance. The diagnostic approach comprises muscle and nerve injuries by iatrogenic, obstetric or surgical trauma, descending pelvic floor or associated diseases. A basic diagnostic workup is sufficient to characterize the different manifestations of fecal incontinence in most of the cases. This includes patient history with a daily stool protocol and digital rectal investigation. Additional investigations may include anorectal manometry, anal sphincter EMG, conduction velocity of the pudendal nerve, needle EMG, barostat investigation, defecography and the dynamic MRI. Therapeutic interventions are focused on the individual symptoms and should be provided in close cooperation with gastroenterologists, surgeons, gynecologists, urologists, physiotherapeutics and psychologists (nutritional-training, food fibre content, pharmacological treatment of diarrhea/constipation, toilet training, pelvic floor gymnastic, anal sphincter training, biofeedback). Surgical therapy includes the STARR operation for rectoanal prolapse and sacral nerve stimulation for chronic constipation and anal-fecal incontinence. Surgery should not be applied unless the diagnostic work-up is complete and all conservative treatment options failed.
- Treatment of tailgut cysts by extended distal rectal segmental resection with rectoanal anastomosis. [JOURNAL ARTICLE]
- Surg Today 2016 Aug 22.
Complete surgical resection is the treatment of choice for tailgut cysts, because of their malignant potential and tendency to regrow if incompletely resected. We report our experience of treating patients with tailgut cysts, and discuss diagnostics, surgical approaches, and follow-up.We performed extended distal rectal segmental resection of the tailgut cyst, with rectoanal anastomosis. We report the clinical, radiological, pathological, and surgical findings, describe the procedures performed, and summarize follow-up data.Two patients underwent en-bloc resection of a tailgut cyst, the adjacent part of the levator muscle, and the distal rectal segment, followed by an end-to-end rectoanal anastomosis. There was no evidence of anastomotic leakage postoperatively. At the time of writing, our patients were relapse-free with no, or non-limiting, symptoms of anal incontinence, respectively.This surgical approach appears to have a low complication rate and good recovery outcomes. Moreover, as the sphincter is preserved, so is the postoperative anorectal function. This approach could result in a low recurrence rate.
- Regenerative Medicine Therapies for Stress Urinary Incontinence. [REVIEW, JOURNAL ARTICLE]
- J Urol 2016 Aug 17.
To summarize the current state of knowledge regarding cell therapy for stress urinary incontinence (SUI) and to introduce new approaches of using regenerative pharmacology as an adjunct or replacement for cell therapy.We reviewed the literature by searching PubMed®, Ovid, and Biological Abstracts. The years searched were from 1975 to December, 2015. The inclusion terms were separately, or in combination: "stress urinary incontinence, cell therapy, chemokine, vascularization, innervation, secretome, animal models". E-publication articles were not included. We did not exclude based on impact factor.Cell therapy is currently proposed to restore functional muscle cells and aid in closure of the sphincter in women with sphincter-associated incontinence. The clinical trials have included small numbers of patients and results vary depending on the patient cohorts, and the cells used. Results of preclinical studies also vary, but report a more favorable outcome. This difference is most likely explained by animal modeling not being directly translatable to the human condition. However, preclinical studies have identified an exciting new approach to regeneration of the urinary sphincter by using the components of cells (secretomes) or chemokines that home reparative cells to the sites of injury.Although cell therapy will continue to be explored, a regenerative pharmacologic approach to treatment of SUI holds the promise of bypassing the lengthy and expensive process of cell isolation and increase availability of treatment in many clinical settings. However, this approach will require careful preclinical modelling & attention to its health benefit/risk ratio.
- Botulinum Toxin Injection for Treatment of Chronic Anal Fissure: Is There Any Dose-Dependent Efficiency? A Meta-Analysis. [JOURNAL ARTICLE]
- World J Surg 2016 Aug 18.
Chronic anal fissure (CAF) is a linear split of the anoderm. The minimally invasive management of CAF such as botulinum toxin (BT) injection is recommended. However, the exact efficient dose of BT, number of injections per session and the injection sites are still debatable. The aim of this analysis was to assess the dose-dependent efficiency of botulinum toxin injection for CAF.PubMed and Web of Science databases were searched for terms: "anal fissure" AND "botulinum toxin." Studies published between October 1993 and May 2015 were included and had to meet the following criteria: (1) chronic anal fissure, (2) prospective character of the study, (3) used simple BT injection without any other interventions and (4) no previous treatment with BT.A total of 1577 patients from 34 prospective studies used either Botox or Dysport formulations were qualified for this meta-analysis. A total number of BT units per session ranged from 5 to 150 IU, whereas the efficiency across analyzed studies ranged from 33 to 96 %. Surprisingly, we did not observe a dose-dependent efficiency (Spearman's rank correlation coefficient, ρ = 0.060; p = 0.0708). Moreover, there were no BT dose-dependent postoperative complications or fecal incontinence and significant difference in healing rates compared BT injection into the anal sphincter muscles.BT injection has been an accepted method for the management of CAF. Surprisingly, there is no dose-dependent efficiency, and the postoperative incontinence rate is not related to the BT dosage regardless the type of formulation of botulinum neurotoxin used. Moreover, no difference in healing rate has been observed in regard to the site and number of injections per session.
- Dysfunctional Voiding In Pediatrics: A Review of Pathophysiology And Current Treatment Modalities. [JOURNAL ARTICLE]
- Curr Pediatr Rev 2016 Aug 16.
In Dysfunctional Voiding (DV), the patient contracts the external urethral sphincter or pelvic diaphragm (consisting of striated muscle) during voiding, contrary to normal physiological mechanism. In Flowmetry plus pelvic Electromyography (EMG), the perineal surface electrodes will show a persistent activity during voiding. The cause is believed to be the persistence of an immature bladder control. The overall prevalence of DV is estimated between 7 and 11% of girls of school age. Symptoms of DV comprises a range of symptoms, deriving from outlet obstruction, incomplete voiding and elevated Post Micturition Residual (PMR): from daytime urine leaks, nocturnal enuresis, Urinary Tract Infections (UTI), or Vesicoureteral reflux (VUR), to the final decompensation of upper urinary tract in extreme cases. The literature reflects a high prevalence of constipation among these patients: between 33 and 56% of dysfunctional voiders are constipated. Initially, therapy of functional voiding disorders such as DV, comprises a series of fundamental principles called Urotherapy or voiding re-education. Currently, Urinary animated Biofeedback (Bfb) is the treatment modality of choice. This therapy discloses patients their own physiological and muscular mechanisms. Most of studies on Bfb efficacy reflect an improvement/ cure rate of around 70-80%. Initial flowmetric improvement followed by symptom relief or clinical improvement as the Bfb sessions continue, is likely to occur. It has been observed that there are two variables associated with clinical success of Bfb in DV syndrome: the absence of PMR at the end of treatment and an adequate or even aggressive constipation management.
- Modulation of Upper Esophageal Sphincter (UES) Relaxation and Opening During Volume Swallowing. [JOURNAL ARTICLE]
- Dysphagia 2016 Aug 17.
UES opening occurs following cricopharyngeus deactivation and submental muscle contraction causing hyolaryngeal elevation and UES distraction. During impedance manometry, the inverse of impedance (admittance) can be used to measure bolus presence and infer UES opening. We hypothesized that the temporal relationship between UES relaxation, opening and hyolaryngeal elevation would change with increasing bolus volume. Simultaneous intramuscular cricopharyngeal (CP) electromyography (EMG), surface submental EMG (SM-EMG), and high-resolution impedance manometry were recorded in eight (aged 27 ± 7 years, 5 M) healthy volunteers, while swallowing 0.9 % saline boluses of 2, 5, 10, and 20 ml. Data were exported and analyzed via Matlab. Statistical analysis comprised repeated measures one-way ANOVA and Pearson correlation. A P value of <0.05 was considered significant. Duration of CP deactivation increased at 20 ml volume (P < 0.001). UES relaxation and opening increased with increasing bolus volume (P < 0.001); however, overall duration of SM activation did not change. As UES opening occurs progressively earlier with increasing volumes, peak SM-EMG activity occurs relatively later (P < 0.001) and shifts from occurring before to following peak UES distention. During healthy swallowing, there is sensory modulation of cricopharyngeal and submental muscle activity. Intrabolus pressures, transmitted from the tongue base and pharynx, play a progressively more important role in sphincter opening with increasing volume. The findings may explain why some healthy elderly and patients with oropharyngeal dysphagia have difficulty swallowing larger while tolerating smaller bolus volumes.
- [Sphincter Ochsner dyskinesia as a cause of superior mesenteric artery syndrome]. [English Abstract, Journal Article]
- Vestn Rentgenol Radiol 2016 Mar-Apr; 97(2):110-7.
to investigate the pathological physiology of superior mesenteric artery syndrome (SMAS).We selected 35 articles devoted to SMAS, which were published from 1990 to 2014, and performed radiometric analysis of X-rays, CT scans and MRI slices found in these articles. In pictures the narrowing in the third part of the duodenum was measured from the boundary of the expanded segment to the level of the superior mesenteric artery (SMA).Only in 6 (17%) of 35 cases the narrowing portion of duodenum was located directly between aorta and SMA, and its length was about 1 cm. In the remaining 29 cases, the beginning of the narrow segment was 2.5-4.6 cm (average 3.30 ± 0.15 cm) proximal to SMA, ie, most of the narrowed duodenum was out of aortomesenteric angle. Location and length of the narrowed segment of duodenum corresponded to the location and length (3.2 ± 0.15 cm) (P > 0.2) of the functional Ochsner sphincter.These data indicate that in most cases of SMAS the sphincter Oclisner dyskinesia causes the disease. It is likely that the disease is triggered by heavy stressful conditions that cause a sharp and sustained reduction in the pH of gastric secretions, which in turn leads to the spasms of the sphincter Ochsner. With time this condition progresses to hypertrophy of the contracted wall of the duodenum with subsequent replacement of the muscle fibers by connective tissue. This can lead to the rigidity of the wall.
- Increased anal basal pressure in chronic anal fissures may be caused by overreaction of the anal-external sphincter continence reflex. [Journal Article]
- Med Hypotheses 2016 Sep.:25-9.
Chronic anal fissure is a painful disorder caused by linear ulcers in the distal anal mucosa. Even though it counts as one of the most common benign anorectal disorders, its precise etiology and pathophysiology remains unclear. Current thinking is that anal fissures are caused by anal trauma and pain, which leads to internal anal sphincter hypertonia. Increased anal basal pressure leads to diminished anodermal blood flow and local ischemia, which delays healing and leads to chronic anal fissure. The current treatment of choice for chronic anal fissure is either lateral internal sphincterotomy or botulinum toxin injections. In contrast to current thinking, we hypothesize that the external, rather than the internal, anal sphincter is responsible for increased anal basal pressure in patients suffering from chronic anal fissure. We think that damage to the anal mucosa leads to hypersensitivity of the contact receptors of the anal-external sphincter continence reflex, resulting in overreaction of the reflex. Overreaction causes spasm of the external anal sphincter. This in turn leads to increased anal basal pressure, diminished anodermal blood flow, and ischemia. Ischemia, finally, prevents the anal fissure from healing. Our hypothesis is supported by two findings. The first concerned a chronic anal fissure patient with increased anal basal pressure (170mmHg) who had undergone lateral sphincterotomy. Directly after the operation, while the submucosal anesthetic was still active, basal anal pressure decreased to 80mmHg. Seven hours after the operation, when the anesthetic had completely worn off, basal anal pressure increased again to 125mmHg, even though the internal anal sphincter could no longer be responsible for the increase. Second, in contrast to previous studies, recent studies demonstrated that botulinum toxin influences external anal sphincter activity and, because it is a striated muscle relaxant, it seems reasonable to presume that it affects the striated external anal sphincter, rather than the smooth internal anal sphincter. If our hypothesis is proved correct, the treatment option of lateral internal sphincterotomy should be abandoned in patients suffering from chronic anal fissures, since it fails to eliminate the cause of high anal basal pressure. Additionally, lateral internal sphincterotomy may cause damage to the anal-external sphincter continence reflex, resulting in fecal incontinence. Instead, higher doses of botulinum toxin should be administered to those patients suffering from chronic anal fissure who appeared unresponsive to lower doses.