The most distal part of the gastrointestinal tube is formed by the anal sphincter complex, and is responsible for maintaining fecal continence. This sphincter complex is embedded in the striated pelvic floor, where the puborectalis muscle joins the upper end of the external anal sphincter with a sling. The anal sphincter complex therefore consists of a smooth muscle component of the internal anal sphincter and a striated muscle component of the external anal sphincter and the puborectalis muscle. The internal anal sphincter is tonically contracted and generates 85% of the anal resting pressure, keeping the anal canal closed at rest. It is not under voluntary control, and is innervated by the enteric nervous system. Stimulation of mechanoreceptors in the rectal wall and the sigmoid activates intramural inhibitory neurons, leading to relaxation of the internal anal sphincter, called the anorectal inhibition reflex.7 This occurs after presentation of stool or gas to the anal canal. The external anal sphincter is innervated by the pudendal nerve and is under voluntary control. This muscle is to some degree contracted, but on demand it might be contracted or relaxed upon the decision to defecate or to have it postponed. The puborectalis muscle ends from the pubic bone, loops around the caudal part of the rectum at the junction with the anal canal and ends at the os pubis. This muscle is tonically contracted, maintains and forms the anorectal angle and keeps the rectum and anus closed during episodes of increased abdominal pressure. The pelvic floor and gluteus muscles can assist the anal sphincter complex in contraction. Sensation arising from the anorectal area is crucial for detecting the presence, volume and consistency of feces and gas in the rectum. Mucosal and intramuscular receptors are involved. These nerve endings detect the nature of the anal contents, discriminating between gas, liquids and solid feces. Intramural stretch and/or pressure receptors detect the degree of rectal filling and produce sensations of desire to defecate and urgency. Receptors located in the pelvic floor and/or the pelvis detect increases in intraabdominal pressure, causing changes in the anal sphincter complex, leading to expulsion of rectal contents. These receptors also activate compensatory reflexes to increase anal sphincter pressure and ensure fecal continence. Sensations arising from the anorectal area are transported by afferent neural pathways to the spine via ascending nerves in the spinal cord (the spinal thalamic tract). The information is transported to the thalamus. This sensory information is transferred to the limbic and somatosensory areas of the cerebellum, where sensations such as flatus and the desire to defecate will be perceived.8
Normal anorectal function depends on the complex interplay between the different anorectal and pelvic anatomic structures. The main task of the anorectum is to assure continuous fecal continence.
Defecation might be considered as a controlled episode of incontinence at a socially acceptable moment. Normal defecation is a complex mechanism depending on normal sensation and motility of the anorectal area, pelvic floor, sigmoid and descending colon, and also involving the abdominal and respiratory musculature. Psychological factors have a major impact on these pathways.
Fecal continence is produced by different mecha-nisms.9 First, the caudal end of the rectum is closed by the anal sphincter complex, creating an anal sphincter resting pressure of around 40 mmHg, to which the internal sphincter contributes 85%, and the external anal sphincter 15%. A reflex of the external anal sphincter increases this pressure when the intra-abdominal pressure increases acutely and counteracts imminent loss of feces. This is probably an important mechanism in normal daily life, since coughing, laughing, bending, sneezing, etc. instantly increase intra-abdominal pressure. This function of the anal sphincter for keeping the gate closed is supported by rectal motility, which is directed antegrade, to keep the rectum empty, transporting the feces back to the sigmoid and away from the anal canal. A third mechanism takes care of continence by a sensation in the cranial part of the anal sphincter. These receptors are located in the area of the skin close to the surface of the anus.
Transsection studies have shown that sensation is not lost, emphasizing the distal location of this sensation. Triggering of these receptors in the anal canal by feces or gas will result in the sensation of imminent loss, and gives the person the ability to prevent this loss of feces and gas by contracting the pelvic floor muscles. When defecation is not desired, the external sphincter complex and the pelvic floor muscles remain contracted until the rectal wall has adapted to the increased rectal volume; when the intrarectal pressure decreases, the sensation of urge will disappear. In addition, retrograde contraction of the caudal part of the rectum starts to occur, and transports the feces back into the sigmoid colon. The interplay of all these mechanisms starts when feces or gas enters the rectum, owing to increased propulsive activity of the colon after ingestion of a meal. Filling the rectal vault, these feces lead to an increase of intrarectal pressure and triggering of receptors located in the rectal wall. This induces the inhibition reflex, leading to a decrease of anal sphincter pressure (internal sphincter), which is more pronounced when rectal filling increases. Above a certain threshold in rectal pressure, the perception of urge occurs. At that time, due to a reflex triggered by this sensation of urge, the external anal sphincter complex contracts for a short time, preventing immediate loss of feces, thus creating time to consider whether the pelvic floor has to be contracted to stop imminent defecation or to permit the defecation process to continue. Defecation occurs when there is a difference in pressure in the rectum on the one hand (rectal contractions and straining), and the pelvic floor on the other hand (relaxation of the anal sphincter complex and pelvic floor, and flattening of the anorectal angle).10
Training is essential when a child tries to defecate without a sensation of urge (e.g. during toilet training). During the process of toilet training the child starts to obtain control of these complex mechanisms in the defecation process. The will of the child seems to be a crucial factor in this process. Aberrations in these complex interacting mechanisms might lead to clinical signs and symptoms of constipation and fecal incontinence. The patho-physiological mechanisms of these clinical entities are largely unknown. In the past decades, only little progress has been made in resolving these mechanisms.11
Colonic propagated contractions are tonic and phasic and propel the luminal contents to the distal colon and rectum. Non-propagated contractions move fecal material antegrade and retrograde and mix a shift of the fecal contents over short distances. High-amplitude propagated contractions (HAPCs) are a pattern of colonic motility originating in the proximal colon and proceeding to the distal sigmoid colon, and are associated with mass movements. They have an amplitude of at least 100mmHg, duration of <10s, and an unequivocal propagation of at least 30 cm. Children have more frequent HAPCs than adults, and HAPCs are more often associated with an urge to defecate or tenesmus in children than in adults. The number of HAPCs is increased after meals and upon awakening. The rectal motor complex is a cluster of contractions at a rate of 7-9/min found only in the rectum, and not related to feeding and awakening. They might have a role in keeping the rectum empty, especially at night, but their function is not yet well understood. The migrating motor complex (MMC) is the beginning of phase III motility. The MMC migrates slowly to the distal bowel, interrupted by feeding, and is probably necessary to prevent bacterial overgrowth during the interdigestive periods.
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