The perineal floor is composed of several striated muscles, attached on the branches of the pubis, ilio, and ischiatic bones, taking part together in the pelvic scaffold, named levator ani muscle. It covers a wide attachment line, from the pubic bone, along the arcus tendineous, to the ischial spine, and it is divided into three components according to its bone insertions: iliococcygeus, ischiococcygeus, and the pubococcygeus. Levator ani muscle contributes to continence, as its resting tone makes the lumen of pelvic organs a virtual space. Some fibers of the pubococcygeus component contribute to form the puborectalis muscle that is another important actor in controlling both defecation and continence, as its sling-shaped configuration around anorectal junction is responsible of the amplitude changes of the anorectal angle (ARA).

Although the puborectalis muscle itself seems to play a sphincter-like role, there is a well-defined sphincter apparatus, composed of the internal anal sphincter (IAS) and the external anal sphincter (EAS). IAS is formed by smooth muscle cells out of voluntary control, appearing as a 2–3 mm thick circular muscle layer of the rectum, extended for 2 cm below the dentate line and separated from the EAS by an intersphincteric plane. Its continuous electrical activity, recorded as slow- and ultraslow-pressure waves with low frequency at rest, is responsible for about 70 % of anal resting tone maintenance (Wankling et al. 1968; Kerremans 1969; Lestar et al. 1989); it is also involved in the rectoanal inhibitory reflex (RAIR) evoked by rectal distension (see below). EAS is a striated-fiber voluntary-controlled muscle; it is the distal part of the puborectalis muscle and, according to Shafik, consists of three components arranged around the anal canal as three U-shaped loops (Shafik 1975). Its contribution to the resting anal tone is reported to be around 20 % (Lestar et al. 1989); nevertheless, its main role is the increase of anal tone during voluntary squeeze and during transient increase of intra-abdominal pressure (Shafik 1975; Shafik 1987). Both pelvic floor and sphincter muscle activity are responsible to act as “triggers” or as “targets” of anal pressure changes, at rest and in squeezing. Finally, the hemorrhoid cushions seem to be able to give a modest contribution (5 %) in the resting anal tone, thus playing a role in the maintenance of fine continence (Lestar et al. 1989).

All neural network controls for every voluntary and involuntary activities work according to a “ranking order” from a simple reflex arch to the higher cortical brain control for more complex activities. Anorectal functions themselves are under this neural “step-by-step” control too. Until about 50 years ago, little was known about the role of the neural pathways and sensitive receptors involved in the control of defecation and continence (Dickinson 1978). Nowadays, it is known that two intrinsic enteric plexus-like nervous systems (Auerbach and Meissner) are located in the wall of the whole gastrointestinal tract and are in contact with smooth muscle cells, modulating their activity by releasing various neurotransmitters; as a matter of fact, they work as a semiautonomous system. Sympathetic and parasympathetic are the extrinsic neural pathways that modulate anorectal functions (sensitive and motor) with opposed roles (parasympathetic acetylcholine stimulates smooth cell muscle activity, adrenergic substances inhibit their contraction). While the sensory pathway for rectal distension is the parasympathetic system to S2, S3, S4 via pelvic plexus, the anal canal sensation pathway follows the pudendal nerve to the same spinal roots (Baeten and Kuijpers 2007). Of great importance, moreover, are the sensory pathways regarding the awareness of rectal filling and the urge to defecate that reach higher CNS control sites (superior frontal gyrus and anterior cingulated gyrus) and evoke the voluntary contraction of puborectalis and EAS as motor response to defer defecation (Porter 1962).

The most important reflex involved in anal continence is the rectoanal inhibitory reflex (RAIR) defined as “the transient decrease in resting anal pressure by ≥25 % basal pressure in response to rapid inflation of a rectal balloon with subsequent return to baseline” (Lowry et al. 2001). Inflating a balloon in the rectum simulates the increasing rectal filling with feces that progressively come from proximal gastrointestinal tract following the coordinated mass movements (rectosigmoid motility).

RAIR is controlled by a neural intrinsic reflex localized in the gut wall, independent of spinal cord involvement (Frenckner 1975), as it has been proven by its absence in Hirschsprung’s disease (Lund and Scholefield 1996) and by the pressure fall recorded even when autonomic nerve supply is blocked (Frenckner and Ihre 1976).