24.2.1

Pelvic Floor

The pelvic floor is a dome-shaped muscle structure that consists mainly of striated muscle with midline defects enclosing the bladder anteriorly, the uterus in women, and the rectum posteriorly. These defects are enclosed by connective tissue, which is located anterior to the urethra and both anterior and posterior to the rectum (perineal body and postanal plate, respectively). Together with the bladder and anorectum, the pelvic floor is responsible for storage and evacuation of urine and stool.

The muscle components of the pelvic diaphragm are the levator ani, coccygeus, and puborectalis muscles. The levator ani complex consists of the pubococcygeus and ileococcygeus muscles, which originate at the pubis bone, the arcus tendineus fascia pelvis, and the ischial spine and insert at the levels of the rectum, the levator plate, and the coccyx ( Fig. 24.1 ).

Pelvic view of the levator ani muscle demonstrating its four main components: puborectalis, pubococcygeus, iliococcygeus, and coccygeus. This assumes that the puborectalis muscle is part of the levator ani complex (see text).

(From Bharucha AE, Klingele CJ. Autonomic and somatic systems to the anorectum and pelvic floor. In: Dyck PJ, Thomas PK, editors. Peripheral neuropathy . 4th ed. Philadelphia: Elsevier Saunders; 2005. p. 279–98 with permission.)

There has been some controversy as to whether the puborectalis muscle is a component of the levator ani complex or of the external anal sphincter (EAS). Whereas developmental, innervation, and histological studies suggest that the puborectalis muscle is distinct from the other muscles of the levator ani, it is also true that the EAS and the puborectalis muscle have separate and distinct innervations, as do the levator ani and the EAS. In most animal species and probably humans, the levator ani and puborectalis are innervated by specific nerves emanating from the sacral cord, whereas the EAS is innervated by the pudendal nerve derived from S2,3 with possible contributions from S1 and S4. Recent studies also suggest that the activities of the puborectalis muscle and the EAS do not uniformly overlap, indicating important differences between them.

24.2.2

Rectum and Anal Canal

The rectum is a tubular structure, approximately 15–20 cm in length, extending from the rectosigmoid junction of the colon to the anal orifice. The rectum has a dual embryologic origin; the upper rectum is derived from the embryologic hindgut and is able to distend toward the peritoneal cavity whereas the lower rectum is derived from the cloaca and is surrounded by dense extraperitoneal connective tissue.

The anal canal is an anteroposterior slit. The literature describes a longer “surgical” anal canal (4.0–4.5 cm) and a shorter “anatomical” or “embryological” canal. The proximal 1 cm of the anal canal is lined by columnar epithelium; the middle 1.5 cm is lined by stratified (or modified columnar) epithelium; and the distal 1.5–2 cm is lined by stratified or squamous epithelium.

The anal canal is surrounded by the internal anal sphincter (IAS) and the EAS. The former is a thickened extension of the circular smooth muscle of the colon. In contrast to the rest of the gastrointestinal tract in which the interstitial cells of Cajal (ICCs) are located in networks along the submucosal and myenteric borders, the ICCs in the IAS are located along the periphery of the circular smooth muscle bundles.

The EAS consists of superficial, subcutaneous, and deep layers of striated muscle, the latter blending with the puborectalis. The EAS and IAS are separated by the longitudinal anal muscle, which runs vertically and consists of mixed smooth and striated elements. EAS fibers are oriented circumferentially, are small in size, and are separated by profuse connective tissue. There are few enteric ganglia in the rectum compared with the colon and very few in the anal canal. Recently, it has been recommended that the term “anal rhabdosphincter” be used by physiologists in place of the term “EAS,” although the latter is the commonly accepted term among clinicians. These muscles do not have attachments to skeletal structures and as with all true sphincters, contraction produces constriction of the lumen with little if any other movement.

24.2.3

Bladder

The urinary bladder is a hollow, tetrahedron-shaped, muscular organ that, when filled with urine, is spherical. The superior surface of the bladder is covered by the peritoneum whereas the posterior surface, or base of the bladder, lies on the ventral aspect of the rectum in the male and on the vagina in the female. The remaining bladder is surrounded by an intermediate stratum of retroperitoneal connective tissue. The bladder in the male is supported by the prostate and a condensation of intermediate stratum termed the puboprostatic ligaments. A similar condensation of endopelvic fascia, termed the pubovesical or pubourethral ligament, occurs in the female.

In most general descriptions of the gross anatomy of the bladder wall, three muscular layers are noted: outer longitudinal, middle circular, and inner longitudinal. It is probable that the arrangement most closely approaches a meshwork of musculature. A prominent detrusor band thickens toward the prostate as it progresses caudally where it divides and spreads around the neck of the bladder and base of the prostate. A further bundle of musculature that progresses from the anterior vesical neck posteriorly has been termed the bundle of Heiss. On the inner surface of the bladder is a mucosal layer composed primarily of transitional epithelium. Anatomically, the trigone is the triangle-shaped internal base of the bladder formed by ureteric muscles. In surgical practice, because the ureteral muscles are not particularly visible, the trigone is defined as a triangle formed by the ureteral orifices and the dorsal urethra. The muscular band that forms the base of the trigone is termed the inter-ureteric ridge. The ureteral orifices themselves appear slit-like as they enter into the bladder.

The bladder is innervated by the vesical plexus, which is part of the pelvic plexus located on the lateral aspects of the rectum. Sympathetic innervation is derived from T10 to L2 cord segments, whereas parasympathetic innervation is derived from S2 to S4 spinal cord segments, which reach the pelvic plexus via the pelvic splanchnic nerves. The detrusor is primarily supplied by parasympathetic nerves; the bladder neck receives sympathetic innervation in the male, in contrast to parasympathetic innervation in the female. The urethral sphincter is supplied by the pelvic splanchnic nerves. The sensory afferent fibers from the bladder accompany both the sympathetic and parasympathetic nerves to their respective spinal cord segments, as will be discussed later.

24.2.4

Urethra

24.3.1

Peripheral Innervation of Levator Ani Muscles (LAM)

In humans, the LAM is innervated by the levator ani nerve, which arises primarily from S3 to S5 and travels along the intrapelvic surface of the LAM ( Fig. 24.2 A). Although there have been differing opinions as to whether there is additional innervation from the pudendal nerve, there is universal agreement that there is no additional innervation in nonhuman species. This is consistent with the distinct embryological origins of LAM and the EAS and the compartmentalization of these muscles by connective tissue.

(A) Sagittal drawing of the medial surface of a female pelvic floor illustrating the course of the levator ani nerve (LAN) from its sacral roots across the surface of the coccygeus (Cm), iliococcygeus (ICm), puborectalis, (PRm), and pubococcygeus (PCm) muscles. S, sacrum; C, coccyx; I, ischial spine; U, urethra; V, vagina; R, rectum. (B) Drawing of posterior view of the hip illustrating the course of the pudendal nerve (PN) from its sacral roots across the surface of the superior gemellus (SG) and obturator internus muscle (OIm) through the pudendal canal (PC) and branching into the inferior rectal nerve (IRN) and perineal nerve (PeN). EAS, external anal sphincter; S, sciatic nerve.

(From Thor KB, DeGroat WC. Neural control of the female urethral and anal rhabdosphincters and pelvic floor muscles. Am J Physiol Regul Integr Comp Physiol 2010; 299 :416–38 as reproduced with permission from Barber MD, Bremer RE, Thor KB, Dolber PC, Kuehl TJ, Coates KW. Innervation of the female levator ani muscles. Am J Obstet Gynecol 2002; 187 :64–71.)

The location of the levator ani nerve on the intrapelvic surface of muscles has led to speculation that it is susceptible to damage during vaginal delivery and may contribute to the known correlation between parity and pelvic organ prolapse. In addition, the proximity of the levator ani nerve to the ischial spine may increase the risk of damage during various resuspension operations for pelvic organ prolapse. Lastly, asymmetrical responses to nerve stimulation have fostered the hypothesis that peripheral sensory and motor innervation of PFMs may show unilateral dominance. At present, this concept remains speculative.

24.3.2

Levator Ani Motor Neurons

Retrograde axonal tracer studies in animals show LAM motor neurons to be located in the sacral ventral horn of the longitudinal column and to exhibit a bimodal distribution of large (presumably α-motor) neurons and small (presumably γ -motor) neurons. As a result, and in contrast to rhabdosphincters, the LAM exhibits muscle-spindle evoked monosynaptic stretch reflexes.

LAM neuronal dendritic or axonal collateral processes project into two areas of the sacral spinal cord ( Fig. 24.3 B). One is the medial lamina VI area where afferent fibers from muscle spindles and Golgi tendon organs terminate ; the other is to Onuf’s nucleus, which contains rhabdosphincter motor neurons (see later in text). It is hypothesized that this apposition reflects a neuroanatomic milieu for the coordination of rhabdosphincter and PFMs during defecation and micturition.

(A) Distribution of afferent projections in the S1 section of the spinal cord from the EUS muscle of the cat, as labeled by anterograde transport of cholera toxin-B-HRP. Composite drawing showing labeled afferent nerves in 5 equal and sequential sections representing an axial distance of 280 mm. (B) Left : Distribution of EUS motor neuron dendrites in the S1 section of cat spinal cord as labeled by retrograde transport of cholera toxin-B-HRP. Right : Distribution of pseudo-rabies virus (PRV) infected interneurons in the S1 section of the spinal cord after injection of PRV into the EUS of the cat. It is likely that lateral interneurons provide an excitatory input (+) and medial interneurons in the dorsal commissure provide an inhibitory input (−) to sphincter motor neurons.

(Reproduced with permission from De Groat WC, Fraser MO, Yoshiyama M, Smerin S, Tai C, Chancellor MB, et al. Neural control of the urethra. Scan J Urol Nephrol Suppl 2001; 207 :35–43 [discussion 106-125].)

24.3.3

Levator Ani Afferent Innervation

Levator ani afferent fibers innervate muscle spindles and Golgi tendon organs and are far more prevalent in LAM than are motor neurons. Approximately 25% of primary afferent neurons are large myelinated neurons that do not contain the peptide transmitter calcitonin-gene-related peptide (CGRP), binding sites for isolectin-B4, or tyrosine receptor kinase A. About half of the small afferent neurons contain CGRP, isolectin-B4 binding sites, and tyrosine receptor kinase A. It has been speculated that the large myelinated neurons signal proprioceptive information and control reflex activity of the LAM and bladder reflex pathways during LAM contractile activity; in contrast, the small neurons transmit nociceptive signals. Trans -ganglionic studies in which cholera toxin B was injected into peripheral afferent terminals in the LAM have demonstrated terminals in medial lamina VI of the lumbosacral spinal cord where large myelinated proprioceptive fibers also terminate ( Fig. 24.3 A).

24.3.4

Levator Ani Reflex Activity

Except for a small number of animal studies, there is little information regarding reflex control of PFMs associated with visceral functions. A study in female rabbits demonstrated that the pubococcygeus muscle was active during bladder filling and quiet during micturition. In a study in male rats, the pubocaudalis muscle was active during bladder contractions. Similarly, it was shown that the EMG activity of the pubocaudalis muscle increased during a contraction associated with micturition in half of the rats and that the remaining animals had increased EMG activity after administration of α ₂ -adrenoreceptor agonists, which are known to increase motor neuron reflex activity.

24.3.5

Voluntary Activity of Pelvic Floor Muscles

PFMs are considered to be under voluntary control, that is, it is possible to voluntarily activate or inhibit the firing of their motor units. Using intra-cortical micro-stimulation techniques, Dubrovsky was able to demonstrate the presence of neuronal groups as they selectively activate both the EAS and LAM in the motor cortex of the cat. Nakagawa has provided histologic evidence for a direct cortical input to Onuf’s nucleus; the projection is bilateral, that is, the motor neurons also receive uncrossed corticospinal tracts. There have been some claims that in humans, the sphincter muscles can be voluntarily contracted but not relaxed at will. EMG studies have shown, however, that the activity of motor units in the urethral rhabdosphincter can be extinguished at both low and high bladder volumes even without initiating micturition. Nevertheless, the voluntary control of both sphincter and other perineal muscles and PFMs is not as straightforward as it is for limb muscles. It is well known that many otherwise neurologically healthy women cannot contract their PFMs on command, as has been demonstrated by kinesiologic EMG recordings. In contrast, most men appear to be able to contract their PFMs on command. These observed gender differences in the ability to contract PFMs between men and women may account for the observation that men appear to regularly “squeeze” the last drops of urine from the urethra, in contrast to women who perform their urogenital functions in ways that do not call for regular voluntary activation of PFMs.

Proprioceptive information is crucial for striated muscle motor control, both in the “learning” phase of a certain movement and for later execution of learned motor behaviors. Proprioceptive information is transmitted to the spinal cord by fast conducting, large diameter, myelinated afferent fibers and is influenced not only by the current state of the muscle, but also by the efferent discharge received by the muscle spindles from the nervous system via Y efferents.

To decipher the state of the muscle, the brain must take into account these efferent discharges and make comparisons between signals sent to the muscle spindles along _Y efferents and signals received from primary afferents. Essentially, the signals from the muscle spindles are compared with the motor command (the “corollary discharge” or “efferents copy”) sent to the intrafusal fibers of the muscle spindle by the central nervous system. These differences are employed to decide the state of the muscle. Experiments have been performed in limb muscles, but it also has been suggested that similar principles obtain in bladder neural control, that is, the brain would know which efferent discharges were caused by distension and which were caused by contractions because the latter would be initiated by the central nervous system. While this is generally true, the mechanism is quite “weakly developed” for PFMs. Also relevant to differences in neural control of PFMs compared with other muscles is that, in addition to proprioceptive afferent information and “corollary discharges” of efferent commands, there is more than just one sensory channel for information regarding limb movement, eye movement and, to some extent, bladder fullness and micturition. From these more “direct” experiences of limb and eye movement, the brain can build a complex “awareness” of such activity. Because of a lack of similar information, such awareness cannot be reliably acquired for PFMs, although they may contain the same somatic motor/proprioceptive afferent mechanisms as do other muscles.

24.4.1

Peripheral Innervation of Urethral and Anal Rhabdosphincters

The somatic motor fibers innervating the rhabdosphincters leave the spinal cord as ventral radices and fuse with dorsal radices to constitute the spinal nerve. The sacral roots travel within the spinal canal from levels T12/L1 as the cauda equina. After passing through the intravertebral foramen, the spinal nerve divides into a dorsal and a ventral ramus. The pudendal nerve is derived from the S2 to S4 ventral rami (also known as the sacral plexus), but there may be some contribution from S1. The pudendal nerve continues through the greater sciatic foramen and enters the ischiorectal fossa (Alcock’s canal) in a lateral direction through the lesser sciatic foramen. In the posterior part of Alcock’s canal, the pudendal nerve gives off the inferior rectal nerve (which innervates the EAS), then branches into the perineal nerve (which innervates the urethral sphincter) and the dorsal nerve of the penis/clitoris ( Fig. 24.2 B).

The branches of the perineal nerve are more superficial than the dorsal penile/clitoral nerve and generally travel on the upper surface of the perineal muscle to innervate the urethral sphincter bilaterally.

There appears to be significant variability of normal human neuroanatomy. For example, there is still controversy arising from anatomic studies of peripheral innervation of the pelvis which, as a rule, have been performed in few cases. Interestingly, anatomic studies apparently dissect specimens only unilaterally, so that intersubject variability is noticed but intrasubject variability (asymmetry) is not. Lastly, much less is known about the finer details of central pathways to pelvic floor rhabdosphincters in humans, as most studies have been done in experimental animals.

Urethral and anal rhabdosphincters as well as pudendal motor neurons contain neuronal nitric oxide synthase (nNOS), which is also found in a substantial subpopulation of muscle and nerve fibers. This enzyme is responsible for producing the neurotransmitter, nitric oxide (NO). nNOS is also concentrated at the neuromuscular junctions in humans. The role of NO in controlling the EAS and urethral sphincter and in neuromuscular transmission to these muscles is not established with certainty. In one experiment in an animal model, an NO donor decreased urethral pressures at the sphincter level but it is not clear whether the effect was on smooth or striated muscle.

24.4.2

Rhabdosphincter Motor Neurons ( Fig. 24.4 )

The motor neurons that innervate the striated muscle of the urethral and EASs and perineum originate from a localized column of cells in Onuf’s nucleus. Onuf’s nucleus in humans is found in the second and third sacral segments but occasionally extends into S1 and is located dorsolaterally in the outer horn. Within Onuf’s nucleus, there is some spatial separation between motor neurons concerned with the control of the urethral and the anal sphincters. Spinal motor neurons for the levator ani group of muscles are often considered part of Onuf’s nucleus. It appears, however, that the areas of the sacral gray matter that innervate the anal and urethral rhabdosphincters and the levator ani are adjacent to each other and show some overlap.

Efferent pathways of the lower urinary tract. (A) Innervation of the female lower urinary tract. Sympathetic fibers (shown in blue) originate in the T11-L2 segments in the spinal cord and run through the inferior mesenteric plexus (IMP) and the hypogastric nerve (HGN) or through the paravertebral chain to enter the pelvic nerves at the base of the bladder and the urethra. Parasympathetic preganglionic fibers (shown in green) arise from the S2 to S4 spinal segments and travel in sacral roots and pelvic nerves (PEL) to ganglia in the pelvic plexus (PP) and in the bladder wall. This is where the postganglionic nerves that supply parasympathetic innervation to the bladder arise. Somatic motor nerves (shown in yellow) that supply the striated muscles of the external urethral sphincter arise from S2 to S4 motor neurons and pass through the pudendal nerves. (B) Efferent pathways and neurotransmitter mechanisms that regulate the lower urinary tract. Parasympathetic postganglionic axons in the pelvic nerve release acetylcholine (ACh), which produces a bladder contraction by stimulating M3 muscarinic receptors in the bladder smooth muscle. Sympathetic postganglionic neurons release noradrenaline (NA), which activates β3 adrenergic receptors to relax bladder smooth muscle and activates α1 adrenergic receptors to contract urethral smooth muscle. Somatic axons in the pudendal nerve also release ACh, which produces a contraction of the external sphincter striated muscle by activating nicotinic cholinergic receptors. Parasympathetic postganglionic nerves also release ATP, which excites bladder smooth muscle, and nitric oxide, which relaxes urethral smooth muscle (not shown). L1, first lumbar root; S1, first sacral root; SHP, superior hypogastric plexus; SN, sciatic nerve; T9, ninth thoracic root (216).

(From Fowler CJ, Griffiths D, de Groat WC. The neural control of micturition. Nat Rev Neurosci 2008; 9 :453–66. Fig. 1—with permission.)

Rhabdosphincter motor neurons are uniform in size and are smaller than the other sacral α motor neurons. They are also characterized by bundles of dendrites from multiple neurons projecting along transverse and longitudinal axes. The neurons demonstrate high concentrations of amino acid-, neuropeptide-, norephinephrine-, serotonin-, and dopamine-containing terminals that represent the substrate for the distinctive neuropharmacologic responses of these neurons; these differ both from limb muscles and the bladder.

Studies in humans, cats, and monkeys demonstrate that the motor neurons of the urethral sphincter are located in the ventrolateral part of Onuf’s nucleus whereas those of the EAS are located in the dorsomedial part. This is in contrast to other species in which the motor neurons of the urethral and anal sphincters are located in separate nuclei.

As mentioned earlier, the motor neurons of the rhabdosphincters differ from those neurons that innervate skeletal muscles such as the PFMs. They are densely packed within Onuf’s nucleus with tightly bundled dendrites that lie rostrocaudally. The dendrites project into the lateral funiculus, dorsally to the sacral parasympathetic nucleus and dorsomedially toward the central canal. As this is similar to dendritic projections from the preganglionic neurons of the bladder, it suggests that both receive inputs from similar regions of the spinal cord.

In addition to their morphology, the motor neurons of the rhabdosphincters are physiologically different from the neurons of skeletal muscle. They do not have monosynaptic inputs, Renshaw cell inhibition, or crossed disynaptic inhibition. The properties of the passive membrane (high input resistance, low rheobase, short after-hyperpolarization, and nonlinear responses to depolarizing currents) are conducive to prolonged tonic activity, which is necessary for their functions.

24.4.3

Afferent Innervation of Urethral and Anal Rhabdosphincters

Because the function of the PFM is intimately connected to the function of the pelvic organs, all sensory information from the pelvic region is relevant to a discussion of the neural control of the PFM. The afferent pathways from the anogenital and pelvic regions are commonly divided into somatic and visceral afferents. The visceral afferents accompany both parasympathetic and sympathetic efferent fibers, whereas the somatic afferents accompany the pudendal nerves and other direct somatic branches of the sacral plexus. Proprioceptive afferents arise particularly from muscle spindles (which are scarce or absent in the EAS and urethral sphincter muscles). Monosynaptic reflexes that arise by stretching of muscle spindles are probably of little importance in pelvic floor sphincters. However, monosynaptic reflexes do play a major role in proprioception and are relevant for currently poorly understood perceptions from pelvic organs, particularly from the rectum. All afferent neurons have their cell bodies in spinal ganglia; those accompanying somatic and parasympathetic pathways are in the sacral segments (S1/S2–S4) and those accompanying sympathetic fibers are in T11-L2 dorsal root ganglia. The sensory neurons are bipolar, sending long processes to the periphery and central processes into the dorsal column of the spinal cord or to the brainstem.

Afferent pathways accompanying sympathetic nerves encompass sensory neurons residing in the T11-L2 dorsal root ganglia and terminate in the dorsal horn (lamina I V) of the spinal cord. High threshold sympathetic afferents transmit nociceptive (pain) information.

Afferent pathways accompanying somatic motor pathways include several groups of sensory fibers. Somatic afferents from the urethral sphincter, the distal vaginal mucosa, and the anogenital region travel in the pudendal nerves; they have cell bodies in S1/S2–S3/S4 dorsal root ganglia, and terminate in the sacral segments of the spinal cord. These are located in regions that overlap with those of afferents accompanying parasympathetic fibers in the pelvic nerve from the bladder.

Visceral afferent fibers of the pelvic and pudendal nerves enter the cord and travel rostrocaudally within Lissauer’s tract. Axon collaterals from Lissauer’s tract distribute transversely around the lateral and medial edges of the dorsal horn. These distributions (termed the lateral and medial collateral pathways of Lissauer’s tract, respectively) carry axons to deeper layers of the spinal cord. The terminals of pudendal nerve afferents are located ipsilaterally, but can also occur bilaterally with ipsilateral predominance. Muscle and cutaneous afferents in the pudendal nerve terminate in different regions of the cord. Projections of pudendal nerve afferents from the urethral sphincter muscle overlap with those of visceral afferents from the pelvic nerve.

Because the pudendal nerve innervates many visceral structures in addition to the skin and rhabdosphincters, it has been difficult to characterize the sensory innervation of the sphincters themselves. The paucity of large sensory neurons in the sacral dorsal root ganglia identified by tracer studies, the failure to identify muscle spindles or Golgi tendon organs in the rhabdosphincters, and the absence of large myelinated fibers in the pudendal nerves support the conclusion that large myelinated nerve fibers play no role in rhabdosphincter sensations.

24.4.4

Tonic Pelvic Floor Activity

Normal striated sphincter muscles, as demonstrated by kinesiologic EMG studies, exhibit some continuous motor unit activity at rest; such activity has been recorded continuously for up to 2 h and even during sleep. This physiologic spontaneous activity may be called tonic, and depends on prolonged activation of certain motor units (tonic motor units) rather than interchanging activation and inactivation of various motor units.

The number of motor unit activities recorded from the PFM depends on physiologic and technical factors. It usually increases with bladder filling, depending on the rate of filling. The amount of recorded activity also depends on technical factors such as the selectivity and positioning of the electrode ( Fig. 24.5 ). With concentric needle electrodes, activity from one to five motor units usually is recorded per detection site. Typically, small amplitude, “low threshold” motor unit potentials (MUPs) that fire rather regularly at lower frequencies constitute the “tonic activity” in the PFMs. In a study of 39 such motor units from the EAS in 17 subjects, discharge rates ranged from 2.5 to 9.4 Hz (mean 3.5 Hz). Any reflex voluntary activation is recorded first as an increase of the firing frequency of these motor units. Inhibition of firing occurs on both initiation or simulation of voiding. With stronger activation or an increase in abdominal pressure (and only for a limited period of time), new motor units are recruited and may be called “phasic” motor units. As a rule, phasic motor units have higher discharge rates and higher amplitude potentials. A small percentage of motor units with an “intermediate” activation pattern can also be recorded. In addition to differences in amplitude, the different types of MUPs may also differ in duration, as evidenced by EMG frequency analysis, and multi-MUP analysis. Others have also found a low firing rate of EAS motor neurons (3–5 Hz) which is far lower than seen in antigravity muscles such as the soleus, where discharge rates typically are 8–10 Hz in the standing position. This observation may be related to the important connections of the sphincter muscle with skin afferents, as the threshold to elicit a response with cutaneous electrical simulation is significantly lower in the EAS than in the LAM.

Examples of surface electromyography (EMG) detection from the anal sphincter muscle using different detection systems. (A) Schematic representation of the rectal probe (1) shown from the cable side. Multichannel EMG detection is obtained with a series of differential amplifiers (2). Conventional bipolar EMG recording is obtained by detecting a single signal as the difference between two opposite electrodes, (3) from which amplitude-based information can be extracted. (4) Effect of rotation of a bipolar probe by one-electrode step (22.5°) in the counterclockwise direction. (B) Sample epoch 100 ms in length of multichannel, single-differential, EMG signals detected from EAS during maximal contraction. (C) Sample epoch of conventional bipolar EMG signals calculated from opposite electrodes on the same signal shown in B in three different orientations: electrodes aligned to the left-right direction (BIP 0°, solid line), rotated by 22.5 degrees counterclockwise (BIP − 22.5°) and clockwise (BIP + 22.5°). In this case, a modest (− 22.5°) rotation of the probe in a counterclockwise direction would not produce a significant effect, whereas a rotation in the other direction would greatly affect both the amplitude (by approximately a twofold factor) and shape of the potentials.

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