Fig. 1.1
The female bony pelvis
The ischial spine, at the midst of the brim of the ischiatic foramen, is the anchorage of several connective and muscular tissues. Some authors describe the spine and the related ligament complex as a star. The sacrospinous ligament, the coccygeal muscle, the posterior portion of the arcus tendineus fasciae pelvis, and the arcus tendineus levator ani leaving the spine stand like beams around it. The sacrospinous ligament extends from the ischial spines to the lateral margins of the sacrum and coccyx anteriorly to the sacrotuberous ligament. During the dissection it can be seen as a separate structure, just behind the ischiococcigeus muscle, or as a complex with the muscle, superficial or deep. The greater and lesser sciatic foramina are above and below the ligament (Fig. 1.2).
Fig. 1.2
The female bony pelvis with the sacro-spinous and the sacro-tuberous ligaments ant the greater and lesser sciatic foramen (Grant (1962) An atlas of anatomy)
1.3 The Muscular Pelvic Floor
1.3.1 Pelvic Diaphragm
The pelvic diaphragm is a thin and wide muscular structure that forms the inferior limit of the abdominopelvic cavity. It is formed of a tunnel-shaped muscle that extends with its fascia from the symphysis pubis to the coccyx and laterally from one wall of the pelvis to the other. The levator ani and coccygeus muscles that are attached to the internal surface of the minor pelvis form the muscular floor of the pelvis.
They originate from the pubic bone at the level of pectinate line and from the obturator internus fascia and are connected to the coccyx.
The levator ani muscle (LAM) is composed of two major muscles: the pubococcygeus and iliococcygeus muscles from medial to lateral. The medial portion of the LA is the bulky pubococcygeus muscle that takes origin from the middle of inferior pubic rami, the pubic symphysis and anterior portion of its arcus tendineus. The arcus tendineus of the LA is indeed a dense structure made of connective tissue, running from the pubic ramus to the ischial spine along the surface of the obturator internus muscle. The muscle passes behind the rectum in an almost horizontal direction. The inner aspect forms the margin of the urogenital hiatus, which is crossed by the urethra, vagina, and anorectum.
The medial portions of the pubococcygeus has been divided in various subparts to reflect the attachments of the muscle to the urethra, vagina, anus, and rectum [1]. These portions are often called by some investigators as the pubourethralis, pubovaginalis, puboanalis, and puborectalis muscles or, all together, as the pubovisceralis muscle, because of their attachment to the pelvic viscera [2].
The pubovisceralis definition was originally championed by Lawson and currently supported by a lot of writings of Delancey [3, 4]. While this term is well accepted in the urogynecological literature, it is rarely mentioned in the anatomical or gastroenterology textbooks.
Lawson felt that the portions of the pubovisceralis muscle are inserted into the urethra, vagina, anal canal and perineal body and he assigned respectively the names pubouretheralis, pubovaginalis, puboperinealis, and puboanalis muscles to those portions.
The urethral portion of the muscle forms part of the periurethral musculature; parallely the vaginal and anorectal parts insert into the vaginal walls, perineal body, and external anal sphincter (EAS) [5].
Posteriorly the puborectalis portion passes behind the rectal canal and is fused with the muscle of the opposite site to form a sling behind the rectum itself.
Other parts of the pubococcygeus run more posteriorly taking attachment to the coccyx.
The lateral part of the levator ani is rather thin and is called iliococcygeus; it takes origin from the arcus tendineus of the levator ani and reaches the ischial spine and the last two segments of the coccyx. The fibers from the two sides also fuse to form a raphe denominated as the anococcygeal ligament. This median raphe linking the anus and the coccyx is known as the levator plate and is the structure on which the pelvic organs rest. It is formed by the connection of the two iliococcygeus and the posterior fibers of the pubococcygeus. During the standing position, the plate is almost horizontal and supports the pelvic viscera situated just above, that is the rectum and the upper two thirds of vagina. Every event leading to a weakness of the levator ani affects this plate and may cause the levator plate to sag. As a consequence of that, the urogenital hiatus opens and predisposes to pelvic organ prolapse. Women affected by genital prolapse have been shown to have an enlarged urogenital hiatus [6, 7].
The coccygeus muscle that runs from the ischial spine to the coccyx and to the lower portion of the sacrum forms the posterior part of the pelvic diaphragm. It is situated on the anterior surface of the sacrospinous ligament (Fig. 1.3). Using 3D MRI imaging of the pelvic diaphragm, we can clearly verify its peripheral attachments and illustrate the urogenital hiatus [8].
Fig. 1.3
The levator ani and its components
As regards the type of these striated muscle, it has been shown that the majority of the fibers are of the slow-twitch type: they can maintain a constant tone (type I) [9] while an increased presence of fast-twitch (type II) fibers is present in the periurethral and perianal areas. This concept confirms that the normal levator ani maintains its tone in the upright position to support the pelvic viscera. Furthermore, a voluntary contraction of the puborectalis during squeezing may increase the tone to balance an increased intra-abdominal pressure.
The urogenital diaphragm, also called the triangular ligament, is a strong, muscular membrane that lies in the area between the symphysis pubis and ischial tuberosities being therefore situated in the triangular anterior portion of the pelvic outlet.
The analysis of the urethral structure has led recently to abandon the term “external urethral sphincter” because the urethral rhabdosphincter is not really external to the urethra, but more properly it surrounds the middle of the urethra. The term “urethral rhabdosphincter” has been therefore recommended.
In contrast to the levator ani muscles, the rhabdosphincter and perineal muscles embryologically develop from the cloaca, with a 2-week delay in striated muscular differentiation compared with the LA and other skeletal muscles [10].
We remember that they are completely separated from the LA by connective tissue [11].
Thus, the striated muscles associated with the viscera are quite distinct from the striated skeletal muscle of the pelvic floor.
1.3.2 Anal Sphincters
The prolongation of the circular muscle layer of the rectum, expanding caudally into the anal canal, becomes the internal anal sphincter (IAS), as reported by Varuna Raizada and Ravinder K. Mittal. In a parallel fashion, the longitudinal muscles of the rectum extend into the anal canal and end up as thin septa that penetrate into the puborectalis and external anal sphincter (EAS) muscles [12]. The autonomic nerves, sympathetic (spinal) nerves and parasympathetic (pelvic) nerves supply the IAS [13].
Sympathetic fibers originate from the lower thoracic ganglia and form the superior hypogastric plexus. Parasympathetic fibers originate from the 2nd, 3rd and 4th sacral nerves and form the inferior hypogastric plexus, which gives rise, from up to down to the superior middle and inferior rectal nerves: they innervate the rectum and the anal canal. These nerves synapse with the myenteric plexus of anal canal and the rectum. The majority of muscular tone of the IAS is myogenic, i.e., due to the properties of the smooth muscle itself. Angiotensin 2 and prostaglandin F2α play modulatory roles. Sympathetic nerves mediate IAS contraction through the stimulation of α and relaxation through β1, β2, and β3 adrenergic receptors.
Recent studies show that low affinity β3 receptors are predominant in the IAS. Anal sphincter relaxation is obtained by stimulation of parasympathetic pelvic nerves through nitric oxide containing neurons that are situated in the myenteric plexus. A more limited role is played by other potential inhibitory neurotransmitters like VIP (vasointestinal peptide) and by CO (carbon monoxide). Acetylcholine and substance P are the neuromediators for excitatory motoneurons located in the myenteric plexus of IAS.
The anatomy of external anal sphincter (EAS) has been largely investigated; it is formed by three parts: subcutaneous, superficial and deep ones. However, several investigators have found that the EAS is constituted only by the subcutaneous and superficial muscle bundles [14, 15].
The first is located caudal to the IAS, while the superficial one surrounds the distal part of the IAS. The deep portion is very thin and is often confused with the puborectalis muscle. 3D US and RMN studies have confirmed this anatomical point of view. EAS is attached to the perineal body and to the transverse perineal muscle anteriorly and to the anococcygeal region posteriorly. We must underline that the EAS is not completely circular in all its sections: the posterior part is indeed shorter in the inferior aspect. This should not be misconstrued as a muscle defect in the axial US and MR images of the lower anal canal.
The muscolaris propria of the rectum contains low threshold slowly adapting mechanoreceptors: they are involved in the detection of mechanical deformation of the myenteric ganglia and of the tension of the longitudinal rectal muscle. Mechanical deformations of the anal canal stimulate numerous free and organized nerve endings like Meissner, Krause and Golgi-Mazzoni corpuscles. They are exclusively sensitive and respond to light touch, pain and temperature. Afferent unmyelinated C and larger A fibers are responsible for neural transmission from the rectum and the anal canal to the spinal cord [16].
1.3.3 Urethra
Female urethra presents an outer layer that is formed by the striated muscular structure of the urogenital sphincter: it can be found in the middle three fifths of its length. In its upper two thirds, the sphincter-like fibers are disposed in a circular fashion. In the distal part, the fibers leave the urethra and surround the vaginal wall forming the urethrovaginal sphincter; other parts of the same muscle extend along the inferior pubic rami above the perineal membrane being indicated as the urethral compressor. This muscle is composed mainly by fibers of the slow-twitch type that are especially suited for maintaining a constant tone. When needed, a voluntary muscle activation of this striated muscle can increase the constrictive action on the urethra.
The urethral mucosa extends from the bladder (that presents a transitional epithelium) to the external meatus: its epithelium is primarily a nonkeratinizing squamous one. Among its characteristics we must underline that it is hormonally sensitive undergoing important changes with stimulation. This submucosal tissue is hormonally sensitive too and contains a rich vascular plexus. Groups of a specialized type of arteriovenous anastomoses have been found in it: they are thought to provide a watertight closure of the mucosa, also thanks to an increase in blood flow contemporary to an increase in abdominal vessel pressure. The considerable quantity of connective tissue that is interspersed within the muscle and submucosa contains collagen and elastin fibers: its function is that of a passive addiction to urethral closure. A series of glands, mostly predominant in the middle and lower third of the urethra, are found in the submucosal space, mainly along its vaginal surface. Therefore we can conclude that the admixture of the smooth and striated muscle, connective tissue, mucosa, and submucosa accounts for the urethral functional sphincter. This sphincter needs obviously an intact neural control to provide the watertight closure of the urethral lumen, the compression of the wall around the lumen, and to create a sophisticated means for compensating abdominal pressure changes.
1.3.4 Pelvic Floor Imaging
The anatomy and the functions of pelvic floor muscles has been recently deeply investigated with MRI and 3D US, so that novel insights have been reached and diffused. After that, muscles themselves have been analyzed during contraction and defecation with ultrafast CT scanning [17]. These studies demonstrated that the changes of pelvic floor hiatus are in relationship with puborectalis activity, being smaller during contraction and larger during defecation (Figs. 1.4 and 1.5). The changes in the pelvic floor hiatus size are predominantly related to the puborectalis muscle and they reflect the constrictor function of pelvic floor. On the contrary the other muscles, i.e., pubococcygeus, ischiococcygeus, and ileococcygeus muscles, are mainly responsible for pelvic floor and levator plate ascent and descent. The anorectal angle becomes acute and moves cephalad during pelvic floor contraction, while opposite changes occur during relaxation and defecation. Diffusion tension imaging (DTI) with fiber tractography has recently been used to analyze normal pelvic floor anatomy in a three-dimensional fashion (Fig. 1.6) [18].
Fig. 1.4
Seated CT defecography, axial images of puborectalis at rest (a), squeeze (b), and defecation (c). Note that the pelvic floor hiatus becomes smaller during squeeze and larger during defecation (Adapted from Li D, Guo M. Morphology of the levator ani muscle. Dis Colon Rectum. Nov 2007;50(11):1831−1839, with permission)
Fig. 1.5
Magnetic Resonance images (MRI) in the mid-sagittal and coronal planes: these images were obtained at rest (solid) and squeeze (dotted) and the images were overlapped to show the movements of various structures during squeeze. LP levator plate, AV anal verge, ARA ano-rectal angle
Fig. 1.6
Fiber tractography demonstrates the complex, multidirectional organization of the different pubovisceral (PV) muscle components in a 28-year-old female subject in both oblique-anterior (a) and anterior-posterior view (b). At the bottom of the pelvic floor transverse orientation of the fiber tracts are displayed matching the perineal body (PB) [18]
1.4 Neuroanatomy
1.4.1 Puborectalis and Deep Pelvic Floor
Even if the concept that pelvic floor muscles are innervated from the S2, S3 and S4 sacral roots is commonly recognized, some controversies regard the innervation of levator ani muscle by the pudendal nerve. Varuna Raizada et al. reported that the middle layer of LA ( puborectalis m.) is innervated by the pudendal nerve [19], whereas the deeper muscles (pubococcygeus, ileococcygeus and coccygeus) are innervated by the direct branches of sacral roots S3 and S4 [20]. Therefore they affirm that in human the levator ani muscle is innervated by the levator ani nerve [21]. It primarily arises from sacral spinal roots and travels along the intrapelvic face of the levator ani muscle with a high degree of variability in branching patterns. The consequence of this affirmation is that pudendal nerve damage may cause dysfunctions of puborectalis m, urethral and anal rhabdosphincters, responsible for urinary and fecal incontinence.
In humans, there is some controversy concerning whether or not the pudendal nerve also innervates the levator ani muscle [22, 23]. Several observations induce to describe a distinct special somatic motor innervation of the rhabdosphincters by the pudendal nerve vs. a typical skeletal motor innervation of the levator ani muscle by the levator ani nerve.
1.5 Peripheral Innervation of Urethral and Anal Rhabdosphincters
The motor neurons that innervate the striated muscle of the external urethral and the anal sphincters originate from a localized column of cells in the sacral spinal cord called Onuf’s nucleus, expanding in humans from the second to third sacral segment (S2–S3) and occasionally into S1. Within Onuf’s nucleus there is some spatial separation between motor neurons concerned with the control of the urethral and anal sphincters. Spinal motor neurons for the levator ani group of muscles seem to originate from S3–S5 segments and show some overlap [21]. Extensive studies of the urethral rhabdosphincter, anal rhabdosphincter, bulbocavernosus and ischiocavernosus muscles have shown that these muscles are innervated by the pudendal nerve. Traditionally the pudendal nerve is described as being derived from the S2–S4 anterior rami, but there may be some contribution from S1 and, possibly, little or no contribution from S4.
The nerve runs along the lateral aspect of the internal obturator and coccygeus muscles and through Alcock’s canal (Fig. 1.7). In this portion, it branches into the inferior rectal nerve (for the anal rhabdosphincter), the perineal nerve (for the urethral rhabdosphincter, the bulbospongiosus muscle, the ischiocavernosus muscle, the superficial transverse perineal muscle and the labial skin), and the clitoris dorsal nerve. The branches of the perineal nerve are more superficial than the latter, and, in most cases, travel on the superior surface of the perineal musculature.
Fig. 1.7
Pelvic floor innervation (Grant (1962) An atlas of anatomy)
Therefore, Thor and de Groat [24] conclude that the pudendal nerve does not innervate to a significant degree the major muscles of the pelvic floor, i.e., iliococcygeus, pubococcygeus or coccygeus muscles. As regards morphology, levator ani motor neurons are similar to other skeletal motor neurons, showing large α and small γ neuronal cells distributed in the sacral ventral horn. One distinguishing feature, however, are some projections from levator ani motor neurons into Onuf’s nucleus, the location of rhabdosphincter motor neurons: this ought to represent a mechanism of coordination between pelvic floor and rhabdosphincter functions. Unfortunately the position of the LA nerve at the level of the intrapelvic surface of the muscles may expose it to be damaged during the passage of fetal head during the 2nd stage of delivery, thus contributing to the correlations between parity and POP.
1.6 Reflex Activation of Urethral and Anal Rhabdosphincters
The activation of the segmental reflex by pelvic nerve stimulation related to bladder distension stimulates the urethral rhabdosphincter; therefore the afferent inputs from the urinary bladder have been emphasized as being of primary importance. This reflex is often referred to as the guarding reflex or continence reflex.
However, recent studies are placing greater emphasis on urethral afferent fibers [25], so that some researchers are speculating that the guarding reflex is actually activated more vigorously by urethral afferent fibers: if urine inadvertently begins to pass through the bladder neck and into the proximal urethra, a fast closure of the more distal urethral sphincter (against any urine loss) is requested more rapidly as compared with simple bladder distensions or increases in intravesical pressure. Since the pudendal nerve is composed even by some urethral afferent fibers (as well as rectal, genital, and cutaneous ones), we may argue that the spinal urethral sphincter activation by pudendal afferent stimulation is also a manifestation of the guarding reflex.
Internal anal sphincter is innervated by autonomic sympathetic (spinal nerves) and parasympathetic (pelvic nerves) terminations. The former originate from the lower thoracic ganglia and form the superior hypogastric plexus, whereas the latter take origin from the 2nd, 3rd and 4th sacral roots to form the inferior hypogastric plexus, giving rise to the nerves that supply the rectum and the anal canal, that is the superior, middle and inferior rectal nerves.
1.7 Inhibition of Urethral Rhabdosphincter Reflexes During Voiding
Voluntary micturition is a behavior pattern that starts with the relaxation of the rhabdosphincter and the pelvic floor muscles. This can be detected as a disappearance of all EMG activity, which precedes detrusor contraction. The striated anal sphincter relaxes similarly with defecation and with micturition. Voluntary pelvic floor muscles contraction during voiding can lead to a stop of micturition, probably because of collateral connections to detrusor control nuclei. As a matter of fact descending inhibitory pathways for the detrusor have been often demonstrated. Bladder contractions are also inhibited by other reflexes that can be activated by afferent input from the pelvic floor muscles, perineal skin, and anorectum.
In addition to supraspinal inhibitory mechanisms, a spinal, urine storage reflex inhibitory center (SUSRIC) was found: it inhibits the somatic and the sympathetic urine storage reflexes, acting on the urethral rhabdosphincter and smooth muscle, respectively. Activation of SUSRIC by electrical stimulation of the pelvic nerve afferent fibers occurs simultaneously with the activation of the urethral rhabdosphincter reflex itself. Possibly the inhibition of rhabdosphincter activity by distension of the bladder represents a physiological corollary of the high-frequency electrical stimulation of pelvic nerve afferent fibers.
1.8 Levator Ani Innervation Damage in Childbirth and POP (see also Chap. 9)
It is well known that childbirth represents a risk factor for development of POP. Various studies have indicated that the damage to the innervation of the pelvic floor muscles may be the initial pathological cause for pelvic descent and prolapse [26–30]. Many other studies [31, 32] have underlined that levator ani nerve damage follows parturition in about 25 % of women with approximately one-third of those showing a persistent nerve damage at 6 months after parturition. On the contrary, women undergoing elective cesarean section (CS) (i.e., without preceding labor) showed no signs of levator ani nerve damage, while damage occurred in similar proportions of women who had CS after protracted labor as the ones with vaginal delivery, i.e., without CS. Furthermore, changes in function of the urethral rhabdosphincter were also associated with pregnancy itself (i.e., before labor), and these remained evident at 6 months after childbirth. Some experimental studies on squirrel monkeys indicate that, in nulliparous animals, the pelvic floor muscles play a minor role in providing visceral support, thus suggesting that the connective tissue plays the major role. On the other hand, after childbirth and consequent stretching of the pelvic connective tissue, the muscle may play a compensatory role. The levator ani muscle stretching might induce a reflex muscle activity and hypertrophy.
Other lesion mechanism than neurogenic and structural damage, such as muscle ischemia, may also be operative during childbirth. Although muscle weakness may be a common consequence of childbirth injury, it is the strength of muscle contraction that defines its functional integrity. Parous women with stress urinary incontinence (SUI) are subject to significant reduction of duration of motor unit recruitment, unilateral recruitment of reflex response in the pubococcygeal muscle and paradoxical inhibition of continuous firing of motor units in pelvic floor muscles activation on coughing.
Another mechanism through which the pelvic muscular support may facilitate pelvic organ prolapse is the avulsion of the puborectalis muscle from the pubic rami in the multipara. This kind of damage is present in 18–70 % of multiparous women, the majority of them showing POP on clinical examination [33–35].
Although not proven in studies, it is reasonable to assume that motor denervation is accompanied also by sensory denervation of the pelvic floor muscles. In addition to denervation injury there may be some further temporary “inhibitors” of pelvic floor muscles activity, such as periods of pain and discomfort after childbirth, increased by attempted pelvic floor muscles contraction.
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