Anatomy and Physiology of Continence 1

Adil E. Bharucha, Roberta E. Blandon

Introduction ration between the rectum and the urogenital tract. The upper portion of the is derived from Webster’s dictionary defines continence as “the abil- endoderm and is supplied by the inferior mesenteric ity to retain a bodily discharge voluntarily”. The artery, which supplies the . The lower third of word has its origins from the Latin continere or the anal canal has ectodermal origins and is supplied tenere, which means “to hold”. The anorectum is the by the rectal arteries, which are branches of the inter- caudal end of the , and is nal pudendal artery [2]. responsible for fecal continence and defecation. In humans, defecation is a viscero somatic reflex that is often preceded by several attempts to preserve conti- Anatomy nence. Any attempt at managing anorectal disorders requires a clear understanding of the anatomy and Pelvic Floor the integrated physiologic mechanisms responsible for maintaining continence. The pelvic floor is a dome-shaped muscular sheet [4] that predominantly contains striated muscle and has midline defects enclosing the bladder, the uterus, and the rectum. These defects are closed by connective tissue anterior to the urethra, anterior to the rectum The primitive gut is formed during the third week of (i.e., the perineal body), and posterior to the rectum gestation. The anorectal region in humans derives (i.e., the postanal plate). Together with the viscera (i.e., from four separate embryological structures: the the bladder and anorectum), the pelvic floor is respon- hindgut, the , the proctodeum, and the anal sible for storing and evacuating urine and stool. tubercles [1]. The hindgut forms the distal third of The levator ani and the coccygeus muscle com- the transverse colon, the descending colon, the sig- prise the two muscular components of the pelvic moid, the rectum, and the upper part of the anal floor or pelvic diaphragm. The muscles that consti- canal to the level of the anal valves [2]. The end of the tute the levator ani complex are the puborectalis, the hindgut enters into the cloaca, an endoderm-lined pubococcygeus, and the ileococcygeus. These mus- cavity that is in direct contact with the surface ecto- cles originate at different levels of the pubic bone, the derm. The cloaca is initially a single tube that is sub- arcus tendineus fascia pelvis (condensation of the sequently separated by caudad migration of the obturator internus muscle fascia), and the ischial into anterior urogenital and poste- spine. These muscles are inserted at the level of the rior intestinal passages. During the 10th week of rectum, the anococcygeal raphe (levator plate), and development, the external anal sphincter is formed the coccyx (Fig. 1). from the posterior cloaca as the descent of the uro- It is unclear whether the puborectalis should be genital septum becomes complete. By the 12th week, regarded as a component of the levator ani complex the internal anal sphincter is formed from a thick- or the external anal sphincter. Based on developmen- ened extension of rectal circular muscle [3]. The tal evidence, innervation, and histological studies, proctodeal portion of the disinte- the puborectalis appears distinct from the majority grates to form the anal tubercles that join posteriorly of the levator ani [1]. On the other hand, the pub- and migrate ventrally to encircle a depression, orectalis and external sphincter complex are inner- known as the anal dimple or proctodeum. The anal vated by separate nerves originating from S2–4 (see tubercles join the urorectal septum and genital tuber- below), suggesting phylogenetic differences between cles to form the perineal body, completing the sepa- these two muscles [5]. 4 A.E. Bharucha, R.E. Blandon

Fig. 1. Pelvic view of the levator ani de- monstrating its four main components: puborectalis, pubococcygeus, iliococ- cygeus, and coccygeus. Reprinted with permission from [6]

rectums are separated by a horizontal fold. The Rectum and Anal Canal upper rectum is derived from the embryological hind gut, generally contains feces, and can distend toward The rectum is 15- to 20-cm long and extends from the the peritoneal cavity [7]. The lower part, derived recto sigmoid junction at the level of third sacral ver- from the cloaca, is surrounded by condensed extra tebra to the anal orifice (Fig. 2). The upper and lower peritoneal connective tissue and is generally empty

Fig. 2. Diagram of a coronal section of the rectum, anal canal, and adjacent structures. The pelvic barrier includes the anal sphincters and the pelvic floor muscles. Reprinted with permission from [8] Chapter 1 Anatomy and Physiology of Continence 5 in normal subjects, except during defecation. In ing from ventral rami of the second, the third, and humans, there are fewer enteric ganglia in the rectum often the fourth sacral nerves to form the inferior compared with the colon and very few ganglia in the hypogastric plexus, which is located posterior to the anal sphincter [9, 10]. urinary bladder. The inferior hypogastric plexus The anal canal is an anteroposterior slit, with its gives rise to the middle rectal plexus, the vesical lateral walls in close contact. The literature describes plexus, the prostatic plexus, and the uterovaginal a longer (approximately 4.0–4.5 cm) “surgical” or “cli- plexus. The nerve supply to the rectum and anal nical” anal canal and a shorter (approximately 2.0 cm) canal is derived from the superior, middle, and infe- “anatomical” or “embryological” anal canal. The anal rior rectal plexus. Parasympathetic fibers in the supe- valves and the distal end of the ampullary part of the rior and middle rectal plexuses synapse with post- rectum mark the proximal margin of the “short” and ganglionic neurons in the myenteric plexus in the “long” anal canal, respectively. The proximal 10 mm rectal wall. In addition, ascending fibers from the of the anal canal is lined by columnar, rectal-type inferior hypogastric plexus travel via superior mucosa. The next 15 mm (which includes the valves) hypogastric and aortic plexuses to reach the inferior is lined by stratified, or a modified columnar, epithe- mesenteric plexus, ultimately innervating the lium. Distal to that is about 10 mm of thick, non descending and sigmoid colon. After entering the hairy, stratified epithelium (i.e., the pecten). The colon, these fibers form the ascending colonic nerves, most distal 5–10 mm is lined by hairy skin. traveling cephalad in the plane of the myenteric The anal canal is surrounded by the internal and plexus to supply a variable portion of the left colon. external anal sphincters. The internal sphincter is a Sacral parasympathetic pathways to the colon thickened extension of the circular smooth muscle have excitatory and inhibitory components [14]. layer surrounding the colon that contains discrete Excitatory pathways play an important role in muscle bundles separated by large septa [11]. In the colonic propulsive activity, especially during defeca- rectum, the interstitial cells of Cajal (ICC) are organ- tion. In other species (e.g., guinea pig), feces trans- ized in dense networks along the submucosal and port may be entirely organized by the enteric nervous myenteric borders. In the internal anal sphincter, the system; spinal and supraspinal reflexes are also ICCs are located along the periphery of the muscle involved in the process [15]. Inhibitory pathways bundles within the circular layer. allow colonic volume to adapt to its contents, and The external sphincter is composed of superficial, they also mediate descending inhibition that initiates subcutaneous, and deep portions; the deep portion colonic relaxation ahead of a fecal bolus. blends with the puborectalis [7]. In men, this trilam- inar pattern is preserved around the sphincter cir- cumference. In contrast, the anterior portion of the Somatic Motor Innervation external sphincter in women is a single muscle bun- dle. External sphincter fibers are circumferentially Cortical mapping with transcranial magnetic stimu- oriented, very small, and separated by profuse con- lation suggests that rectal and anal responses are nective tissue [12]. bilaterally represented on the superior motor cortex, i.e., Brodmann area 4 [16]. There are subtle differ- ences in the degree of bilateral hemispheric repre- Nerve Supply to the Pelvic Floor sentation between subjects. Motor neurons in Onuf’s nucleus, which is located in the sacral spinal cord, Autonomic Innervation innervate the external anal and urethral sphincters. Though they supply striated muscles under volun- The anorectum and pelvic floor are supplied by sym- tary control, these motor neurons are smaller than pathetic, parasympathetic, and somatic fibers [13]. usual α-motor neurons and resemble autonomic Sympathetic pre ganglionic fibers originate from the motor neurons [17]; however, the conduction veloci- lowest thoracic ganglion in the paravertebral sympa- ty in pudendal nerve fibers is comparable with that of thetic chain and join branches from the aortic plexus peripheral nerves. In contrast to other somatic motor to form the superior hypogastric plexus. Because the neurons in the spinal cord, these neurons are rela- superior hypogastric plexus is not a single nerve, the tively spared in amyotrophic lateral sclerosis but are alternative term for this plexus, i.e., “presacral affected in Shy-Dräger syndrome [18, 19]. Somatic nerve”, should be avoided. The superior hypogastric branches originating from Onuf’s nucleus travel in plexus provides branches to the uteric and ovarian the pudendal nerve, the muscular branches, and the (or testicular) plexus, and divides into right and left coccygeal plexus. The pudendal nerve branches into hypogastric nerves. The hypogastric nerves unite inferior rectal and perineal and posterior scrotal with preganglionic parasympathetic fibers originat- nerves. The inferior rectal nerve conveys motor 6 A.E. Bharucha, R.E. Blandon

fibers to the external anal sphincter and sensory veyed by unmyelinated small C fibers and larger Aδ input from the lower anal canal and the skin around myelinated fibers that have slow and fast conduction the anus. The perineal nerve divides into posterior velocities, respectively [27]. scrotal (or labial) branches and muscular branches. Animal models and clinicopathological findings in The posterior scrotal branches innervate the skin, humans suggest that pelvic nerves traveling to the while muscular branches are distributed to the trans- sacral segments are more important for conveying verse perinei, the bulbospongiosus, the ischiocaver- non–noxious and noxious colonic sensations than nosus, the urethral sphincter, the anterior part of the are lumbar colonic (sympathetic) nerves [12, 28–30]. external anal sphincter, and the levator ani. There are more afferent neurons supplying the colon Motor fibers of the right and left pudendal nerves in the sacral, compared with lumbar segments in the have overlapping distributions within the external cat, i.e., 7,500 versus 4,500 neurons [31, 32]. However, anal sphincter. Sherrington observed that stimula- the number of spinal visceral afferent neurons is rel- tion of the right pudendal nerve caused circumferen- atively small, i.e., only 2.5% or less of the total num- tial contraction of the external anal sphincter [20]. ber of spinal afferent neurons supply skin and deep Conversely, tonic external sphincter activity, sphinc- somatic structures [33]. ter inhibition during colonic distention, and the In general, sacral afferents may be better suited for cutaneo anal reflex were not affected by sectioning conveying afferent information than are lumbar either pudendal nerve. afferents, as they are more likely to lack resting activ- The nerve supply to the puborectalis has been the ity and respond to pressure increments with a wider subject of controversy. The early literature based on range of discharge frequency [34, 35]. Janig and Mor- dissections by several workers suggested that the rison identified three different classes of puborectalis was innervated from below by the mechanosensitive visceral afferents in the cat colon pudendal nerve, or jointly by the inferior rectal and [33]. Tonic afferents fired throughout colonic disten- perineal branches of the pudendal nerve. Therefore, tion and accurately encoded the intensity of disten- the puborectalis was regarded as being derived not tion between 20 and 100 mmHg. Phasic colonic from the levator ani but from the external anal afferents generally discharged at the onset and occa- sphincter. However, an electrophysiological study sionally at the cessation of a distention stimulus. that preoperative stimulation of the sacral nerves Tonic afferents were predominantly unmyelinated, above the pelvic floor invariably (i.e., 19 of 20 exper- slowly conducting C fibers, while most phasic affer- iments) resulted in electromyogram (EMG) activity ents were faster-conducting myelinated Aδ fibers. in the ipsilateral puborectalis, but not in the external The afferents innervating the anal canal responded to anal sphincter [5]. Gross dissection studies in shearing stimuli, but not colonic or anal distention. humans, rats, and squirrel monkeys demonstrate Two different theories have been proposed to that the anal sphincter and levator ani muscle are explain visceral pain perception. Proponents of the innervated by separate nerves [21–23]. specificity theory suggested that pain was a distinct sensory modality, mediated by sequential activation of visceral nociceptors and central pain-specific neu- Somatic Sensory Innervation rons in the spinal dorsal horn. However, in the cat colon, Janig and Koltzenburg found no afferent fibers Rectal distention is perceived as a more localized that were selectively activated by noxious stimuli, sensation of rectal fullness, interpreted by the patient arguing against the specificity theory. The alternative as a desire to pass wind or motion. Colonic disten- hypothesis for pain perception, i.e., pattern or inten- sion, on the other hand, causes ill-defined discomfort sity theory, attributes pain perception to spatial and and eventually pain. The anal canal responds to dis- temporal patterns of impulses generated in non spe- tention and to innocuous mucosal proximo distal cific visceral afferent neurons [24]. However, electro- mechanical shearing stimuli [24]. In addition to physiological studies of visceral afferent fibers in mucosal nerve endings, there are also low threshold, other organs, including the colon, have documented slowly adapting mechanoreceptors in the guinea pig high-threshold visceral afferent fibers that only rectum. These intraganglionic laminar endings respond to noxious mechanical stimuli. Subsequent- (IGLEs) detect mechanical deformation of the myen- ly, Cervero and Janig reconciled these opposing con- teric ganglia [25, 26]. The anal canal is lined by cepts in a convergence model wherein input from numerous free and organized nerve endings (i.e., low- and high-threshold mechanoreceptors converge Meissner’s corpuscles, Krause end-bulbs, Golgi-Maz- on spinothalamic and other ascending tract cells zoni bodies, and genital corpuscles), perhaps [36]. Physiological processes are generally accompa- explaining why it is exquisitely sensitive to light nied by low- level activity, mediation of regulatory touch, pain, and temperature. Sensory traffic is con- reflexes, and transmission of nonpainful sensations. Chapter 1 Anatomy and Physiology of Continence 7

High-intensity stimuli increase firing of low-thresh- gesting that this excitatory sympathetic discharge old afferents and also activate high-threshold affer- does not contribute to anal pressure during rectal dis- ents, thereby activating nociceptive pathways and tention. Conversely, sympathetic stimulation either triggering pain [36]. evoked internal anal sphincter relaxation, [40, 41] or More than 90% of all unmyelinated pelvic affer- contraction followed by relaxation [42]. ents are silent, being activated by electrical stimula- Anal resting pressure is not stationary but varies tion, but not even by extreme noxious stimuli [33]. during the day. In addition to spontaneous relax- Silent afferents can respond to chemical stimuli or ation of the internal sphincter, circadian variations tissue irritation, becoming responsive to even that are dependent on the sleep/wake cycle and ultra- innocuous mechanical stimuli after sensitization dian (~20 to 40 min in length) rhythms that are inde- [37]. These neurophysiological changes are de- pendent of the sleep/awake cycle have also been tectable within minutes after tissue irritation, are described [43]. likely to persist for the duration of irritation, and Anal relaxation induced by rectal distention [i.e., have been implicated in explaining visceral hyper- the recto anal inhibitory reflex (RAIR)] is mediated sensitivity. by intrinsic nerves. This reflex is absent in Hirschsprung’s disease. The extrinsic nerves are not essential for the reflex, as it is preserved in patients Anal Sphincter Tone and Reflexes with cauda equina lesions or after spinal cord tran- section. However, extrinsic nerves may modulate the Internal Anal Sphincter reflex, as relaxation is more pronounced and pro- longed in children with sacral agenesis [44]. The The internal sphincter is primarily responsible for recto anal inhibitory reflex is probably mediated by ensuring that the anal canal is closed at rest [14, 38]. nitric oxide (NO); morphological studies reveal an The other contributors to anal resting tone include efferent descending nitrergic rectoanal pathway [45]. the external anal sphincter, the anal mucosal folds, Other nonadrenergic/noncholinergic neurotransmit- and the puborectalis muscle. Penninckx et al. [39] ters, i.e., vasoactive intestinal peptide (VIP) and estimated that anal resting tone was generated by adenosine triphosphate (ATP), may also participate nerve-induced activity in the internal sphincter (45% in the RAIR [46, 47]. of anal resting tone), myogenic tone in the internal sphincter (10%), the external sphincter (35%), and the anal hemorrhoidal plexus (15%). These figures External Anal Sphincter should be regarded as estimates, because they were obtained, in part, from complex studies in which anal Though resting sphincter tone is predominantly resting pressure was sequentially recorded before attributed to the internal anal sphincter, studies surgery (i.e., abdomino perineal resection), after under general anesthesia or after pudendal nerve curarization, and in the resected specimen before block suggest the external anal sphincter generally and after verapamil. Moreover, the relative contribu- accounts for ~25% up to 50% of resting anal tone. tions of these factors to anal resting tone are influ- When continence is threatened, the external sphinc- enced by several factors, including the size of the ter contracts to augment anal tone, preserving conti- probe and the location at which pressure was meas- nence. This “squeeze” response may be voluntary, or ured. it may be induced by increased intra-abdominal Frenckner and Ihre investigated the contribution pressure [48] or by merely moving a finger across the of myogenic tone and the extrinsic (sympathetic and anal canal lining [49]. Conversely, the external parasympathetic) nerves to anal resting tone by sphincter relaxes during defecation. assessing anal pressure at rest and in response to rec- The only other striated muscles that display rest- tal distention under baseline conditions after low ing activity are the puborectalis, the external urethral spinal anesthesia (L5–S1), and after high spinal anes- sphincter, the cricopharyngeus, and the laryngeal thesia (T6–T12) [38]. A separate study assessed anal abductors. Resting or tonic activity depends on the pressures before and after pudendal nerve blockade. monosynaptic reflex drive, perhaps explaining why The decline in anal resting pressure was significantly resting anal sphincter tone is reduced, but voluntary greater after high (32±3.2 mm Hg) than low (11±7.1 contraction of the external sphincter is preserved in mm Hg) anesthesia or after pudendal nerve blockade tabes dorsalis [50]. The fiber distribution also favors (10±3.9 mmHg), suggesting there is a tonic excitatory tonic activity; type 1 (i.e., fatigue-resistant, slow sympathetic discharge to the internal anal sphincter twitch) fibers predominate in the human anal in humans. However, the anal pressure during rectal sphincter [12], while cats and rabbits predominantly distention was similar among the three groups, sug- contain type 2 or fast-twitch muscle fibers [51]. 8 A.E. Bharucha, R.E. Blandon

Rest Evacuation Rest Evacuation

Fig. 3. Sagittal dynamic magnetic resonance images of normal puborectalis relaxation (left panel, subject 1) and puborectal- is contraction (arrow, right panel, subject 2) during rectal evacuation. In both subjects, evacuation was associated with per- ineal descent (2.6 cm in subject 1; 1.7 cm in subject 2) and opening of the anorectal junction. During evacuation, the anorec- tal angle increased by 36° in subject 1 and declined by 10° in subject 2. Reprinted with permission from [52]

Puborectalis rectal curvatures, and the transverse rectal folds), recto anal sensation, and rectal compliance. Stool is The tonically active puborectalis muscle maintains often transferred into the rectum by colonic high- the resting anorectal angle. Moreover, puborectalis amplitude-propagated contractions, which often contraction during a sudden rise in abdominal pres- occur after awakening or meals [54]. Denny-Brown sure reduces the anorectal angle, thus preserving and Robertson observed that rectal distention continence. As noted earlier, electrophysiological evoked rectal contraction and anal sphincter relax- stimulation studies in humans suggest this muscle is ation, facilitating evacuation [28]. The pelvic floor, supplied, strictly ipsilaterally, by branches originat- particularly the puborectalis, also generally relaxes ing from the sacral plexus above the pelvic floor [5]. during defecation (Fig. 3). Simultaneous assessments Disruption of the puborectalis inevitably causes sig- of intrarectal pressures and pelvic floor activity (by nificant incontinence, underscoring the importance manometry, EMG, or imaging) reveal that increased of this muscle in maintaining continence. intra rectal pressure and anal relaxation are required for normal defecation. However, the relative contri- butions of increased intra-abdominal pressure gen- Sacral Reflexes erated by voluntary effort [55] and rectal contraction [56] to the “propulsive” force during defecation are The pelvic floor striated muscles contract reflexly in unclear, partly because a barostat rather than a response to stimulation of perineal skin, (i.e., a manometry is necessary to optimally characterize somatosomatic reflex) or anal mucosa (i.e., a viscero- rectal contractions, which are of relatively low ampli- somatic reflex). The cutaneoanal reflex is elicited by tude. Current concepts suggest that minimal strain- scratching or pricking the perianal skin and involves ing to initiate defecation is not abnormal, because

the pudendal nerves and S4 roots. Sacral reflexes also many asymptomatic subjects strain to initiate defe- regulate anal sphincter tone during micturition. cation [57]. However, excessive straining, and partic- Thus, electrical activity of the internal anal sphincter ularly a Valsalva maneuver, may impede evacuation increases during urinary bladder emptying in because while a Valsalva maneuver may increase humans, returning to normal after micturition [53]. intrarectal pressure, the pelvic floor muscles also Conversely, the external anal sphincter relaxes dur- contract, increasing outlet resistance [58]. Thus, it is ing micturition in humans, cats, and dogs. necessary to assess the balance between these two sometimes opposing forces by measuring the net recto anal force during evacuation [59]. One possibil- Mechanisms of Continence and Defecation ity is that the relative contributions of voluntary effort and rectal contraction to defecation vary, The mechanisms that maintain fecal continence depending on the circumstances prior to defecation. include anatomical factors (i.e., the pelvic barrier, the For example, the voluntary effort may range from Chapter 1 Anatomy and Physiology of Continence 9 being negligible when stool is soft to considerable pressure compared with placebo in a randomized when stool is hard and situated in the upper rectum. double-blind placebo-controlled crossover study of If defecation is inconvenient, it can generally be 36 patients with fecal incontinence [66]. postponed. The rectal contractile response to disten- tion normally subsides as the rectum accommodates or relaxes. The external sphincter and/or puborectal- Surgical Considerations is can be contracted voluntarily. This contractile response requires the ability to perceive stool in the From a therapeutic perspective, an understanding of rectum and perhaps also in the anal canal. Indeed, anatomy is particularly important for managing anal the anal sphincter may also relax independently of fistulae, preventing nerve injury during surgical dis- rectal distention, allowing the anal epithelium to section, and understanding the consequences of rec- periodically “sample” and ascertain whether rectal tal resection. Left-sided colectomy may result in contents are gas, liquid, or stool [60]. postoperative colonic transit delays in the unresected These mechanisms underscore that defecation is segment; this likely represents parasympathetic den- an integrated somato visceral reflex. Indeed, the cen- ervation, as ascending intramural fibers travel in a tral nervous system plays a greater role in regulating retrograde manner from the pelvis to the ascending anorectal sensomotor functions compared with other colon. The sigmoid colon and rectum are also sup- regions of the gastrointestinal tract. The elaborate plied by descending fibers that run along the inferior somatic defecation response depends on centers mesenteric artery. These nerves may be disrupted above the lumbo sacral cord, and probably craniad to during a low anterior resection, leaving a denervated the spinal cord itself. However, Garry observed that segment that may be short or long depending on colonic stimulation in cats induced colonic contrac- whether the dissection line includes the origin of the tion and anal relaxation, even after destruction of the inferior mesenteric artery [67]. A long denervated lumbo sacral cord, and concluded that the gut segment is more likely to be associated with non- “seems not to have wholly surrendered its independ- propagated colonic pressure waves and delayed ence” [61]. colonic transit than is a short denervated segment. In addition to colonic denervation, a low anterior resec- tion may damage the anal sphincter and reduce rec- Pharmacological Considerations tal compliance [68]; in contrast to anal sphincter injury, rectal compliance may recover with time [69]. In contrast to non sphincteric regions, sympathetic Defecation may also be affected after surgical section nerves excite while parasympathetic nerves inhibit of pelvic nerves in humans [70, 71]. the sphincters. The internal anal sphincter has dense Denonvilliers’ fascia is intimately adherent to the adrenergic innervation in humans and monkeys. It is anterior mesorectal fat but only loosely adherent to also more sensitive to adrenergic compared with the seminal vesicles. During anterior rectal dissec- cholinergic agonists [62]. Cholinergic agonists either tion, the deep parasympathetic nerves situated in the contracted or relaxed internal anal sphincter strips in narrow space between the rectum and the prostate humans. and seminal vesicles may be damaged, leading to Anal administration of exogenous nitrates (i.e., impotence [72]. For benign disease, most surgeons 0.2% glyceryl trinitrate) has been extensively tested will tend to stay posterior to Denonvilliers’ fascia in and widely used to treat anal fissures, as these are an attempt to protect the pelvic nerves. For malig- often associated with increased anal resting tone nant disease, the choice is less straightforward, [63]. Topical calcium-channel blockers (e.g., 0.2% because dissection behind rather than in front of the nifedipine or 2% diltiazem) are probably more fascia may, in theory, be associated with incomplete effective than nitrates for treating anal fissures, with resection and/or local recurrence. a lower incidence of side effects. Bethanecol and Because vaginal delivery can damage the anal botulinum toxin have also been used to treat anal sphincters and the pudendal nerve, up to 10% of fissures. women develop fecal incontinence after a vaginal The beneficial effects of loperamide in fecal incon- delivery [73]. The incidence of post partum fecal tinence may be attributable not only to a reduction of incontinence is considerably higher (i.e., 15–59%) in diarrhea, but also to an increase of anal resting tone women who sustain a third-degree (i.e., anal sphinc- α [64]. The 1 adrenoreceptor agonist phenylephrine ter disruption) or a fourth-degree tear (i.e., a third- applied to the anal canal increased anal resting pres- degree tear with anal epithelial disruption) [74, 75]. sure by 33% in healthy subjects and incontinent The only prospective study that imaged the anal patients [65]. However, phenylephrine did not signif- sphincters before and after vaginal delivery demon- icantly improve incontinence scores or resting anal strated that anal sphincter defects and pudendal 10 A.E. Bharucha, R.E. Blandon

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treatment of faecal incontinence. Br J Surg 87:38–42 physiology of urinary incontinence, fecal incontinence 67. Koda K, Saito N, Seike K et al (2005) Denervation of and pelvic organ prolapse. In: Abrams P, Cardozo L et the neorectum as a potential cause of defecatory dis- al (eds) Incontinence. Health Publication, Paris, pp order following low anterior resection for rectal can- 425–484 cer. Dis Colon Rectum 48:210–217 75. Sultan AH (1999) Obstetrical perineal injury and anal 68. Batignani G, Monaci I, Ficari F et al (1991) What incontinence. Clin Risk 5:193–196 affects continence after anterior resection of the rec- 76. Sultan AH, Kamm MA, Hudson CN et al (1993) Anal- tum? Dis Colon Rectum 34:329–335 sphincter disruption during vaginal delivery. N Engl J 69. Williamson ME, Lewis WG, Finan PJ et al (1995) Med 329:1905–1911 Recovery of physiologic and clinical function after low 77. Carroli G, Belizan J (2006) Episiotomy for vaginal anterior resection of the rectum for carcinoma: myth birth [systematic review]. Cochrane Database of Sys- or reality? Dis Colon Rectum 38:411–418 tematic Reviews http://www.cochrane.org. Cited 15 70. Devroede G, Lamarche J (1974) Functional importance Nov 2006 of extrinsic parasympathetic innervation to the distal 78. Royal College of Obstetricians and Gynaecologists colon and rectum in man. Gastroenterology (2001) Management of third- and fourth-degree per- 66:273–280 ineal tears following vaginal deliveries. London 71. Scott HWJ, Cantrell JR (1949) Colonmetrographic 79. Fernando RJ, Sultan AH, Kettle C et al (2006) Repair studies of the effects of section of the parasympathetic techniques for obstetric anal sphincter injuries: a ran- nerves of the colon. Bull Johns Hopkins Hosp domized controlled trial. Obstet Gynecol 85:310–319 107:1261–1268 72. Lindsey I, Guy RJ, Warren BF et al (2000) Anatomy of 80. Sultan AH, Monga AK, Kumar D et al (1999) Primary Denonvilliers’ fascia and pelvic nerves, impotence, repair of obstetric anal sphincter rupture using the and implications for the colorectal surgeon. Br J Surg overlap technique. Br J Obstet Gynaecol 106:318–323 87:1288–1299 81. Norderval S, Oian P, Revhaug A et al (2005) Anal 73. Bharucha AE (2003) Fecal incontinence. Gastroen- incontinence after obstetric sphincter tears: outcome terology 124:1672–1685 of anatomic primary repairs. Dis Colon Rectum 74. Mostwin J BA, Haab F, Koelbl H et al (2005) Patho- 48:1055–1061 Invited Commentary

Peter J. Lunniss, S. Mark Scott

The comprehensive overview of the anatomy and cortical evoked potential, etc. [20–24], will provide physiology of faecal continence by Drs. Bharucha essential knowledge concerning the brain–gut axis. and Blandon provides an excellent summary of what Development and use of these physiological tools is increasingly acknowledged to be a highly complex has confirmed the importance of suprasphincteric area of human biology. Readers should also direct components to continence and defecation. Neverthe- their attention to Table 1 in Chapter 4 in this book. less, the pelvic floor and anal sphincters are “the final Historically, both research and clinical interest have common path”, and, certainly in the surgical setting, focused on the role of the anal sphincter complex in represent a frequent source of disturbed function. the maintenance of continence and the physiological There is no doubt that anal sphincteric disruption is changes within the sphincters and pelvic floor associ- the main pathogenic mechanism in acquired faecal ated with defecation. This is perhaps not surprising incontinence, but levator ani failure, including that because of both the relative inaccessibility to study of of the puborectalis, is increasingly recognised to be the colorectum itself and the lack of appropriate of aetiological importance [2, 25, 26]. Nevertheless, physiological tools to assess function. However, it is failure to study and address those other components becoming increasingly recognised, principally fundamental to continence will, not surprisingly, through the efforts of the Mayo Clinic group [1–3], lead to poor outcomes following intervention direct- our own group [4–6], and that of others [7, 8], that ed solely at sphincteric dysfunction. We recently the contribution of normal rectal sensorimotor and demonstrated how assessment of rectal sensorimotor biomechanical function may be equally crucial to the function can direct surgery for both incontinence maintenance of continence, as evident from recent (rectal “augmentation” with or without electrically studies showing loss of rectal reservoir function asso- stimulated gracilis neosphincter for urgency, associ- ciated with hypersensitivity, hypocompliance, hyper- ated with rectal hypersensitivity, low rectal compli- contractility, and hyperreactivity in faecal inconti- ance and exaggerated motor activity [4]) and consti- nence [1–8]. Conversely, an appreciation that pation (vertical rectal reduction for megarectum impaired sensation (hyposensitivity) and hypercom- associated with hyposensitivity and excessive com- pliance may underlie (notably, passive) incontinence pliance [27]), with functional success associated with in a proportion of patients is also gaining momen- normalisation of pathophysiology. It remains tum [9–14]. Introduction of the barostat and stan- unclear exactly how sacral nerve stimulation (SNS) dardised protocols for its use has facilitated this may improve both colonic motility (in cases of iner- greater understanding of rectal and colonic dynam- tia [28]) and continence (in incontinence [29]), but it ics, both in health and in disturbed bowel function [2, is apparent that the primary effect is certainly not on 8, 13]. Evaluation of colorectal motor function, sphincteric function [30, 31]. Effects on rectal senso- though still primarily restricted to the research set- rimotor activity are not consistent [30–32], and it ting, can now be reproducibly determined by a vari- may be that we simply do not have the right tools to ety of techniques, including the use of long catheters measure the physiologically significant effects of SNS placed either antegrade [15, 16] or retrograde [17, 18] (possibly central or spinal [21]) and, ultimately, to to assess pancolonic motility; other, less invasive, predict in whom the technique has a good chance of methods to assess colonic contractility and transit positive effect [29]. will soon be available [19]. Furthermore, the associa- Intuitively, anal sensation must be integral to nor- tion between cerebral activity and bowel function can mal continence. It was first systematically assessed now also be studied, and carefully constructed proto- by Duthie and Gairns in 1960 [33], since when its cols employing techniques such as functional mag- measurement and significance has been somewhat netic resonance imaging (f-MRI), the assessment of questioned [34]. It may be, however, that it is the 14 P.J. Lunniss, S.M. Scott

methodology with which we are currently assessing Although the gross anatomy of the musculature of anal sensation (usually electrostimulation) that is the anal canal is well known, the same cannot be said imperfect, as the multitude and density of nerve end- of innervation of the pelvic floor and anorectum. ings subserving different sensations within the anal Readers will be already highly familiar with the transitional zone beg a more influential role. Equally, debate concerning the influence of pudendal neu- one may argue that the key to normal anal motor ropathy on continence and defecation, its measure- function is the conjoined longitudinal muscle of the ment, and usefulness in directing therapy or advising anal canal. In the foetus, this structure is thicker than on prognosis following (especially surgical) interven- the internal sphincter. As it descends between the tion. Cadaveric studies have demonstrated three internal sphincter and the true intersphincteric space variations in pudendal nerve anatomy [49, 50], and (medial to the external sphincter), it sends exten- its innervation of the levator ani group of muscles sions medially across the internal sphincter to help remains controversial. In addition, how much vari- support the submucosa of the anal canal (notably the ability and asymmetry there is in external anal anal cushions), laterally and variably across the sphincter innervation has not been explored until external sphincter into the ischiorectal fossa and recently [51]. There is now, however, growing aware- pelvic side wall fascia, and caudally to insert into the ness that the concept of lateral dominance—asym- perianal skin [35]. It is, indeed, the anatomy of these metry in the neural contribution of a bilaterally lateral and distal extensions that define the compo- innervated midline structure—applies to pudendal nents of the external sphincter. Not only does such nerve innervation [52–54]. This may be particularly an arrangement provide a supporting meshwork for important in that damage to the dominant nerve, the other sphincter components, but the differential sustained through whatever injurious mechanism responses to neurotransmitters compared with the (e.g. traction injury), may leave the individual more internal sphincter [36] begs a more active functional susceptible to dysfunction of those structures inner- role, its contraction flattening the anal cushions, vated by the pudendal nerve with resultant inconti- shortening and widening the anal canal, and everting nence. In a similar vein, autonomic innervation to the anal orifice during defecation [37]. Thinning, loss the pelvic viscera remains poorly studied, particular- of muscle and fragmentation associated with ageing ly with reference to the exact neuroanatomy of affer- [38], and perhaps in a more accelerated way, in sub- ent pathways. Consequently, there remains consider- jects with pelvic floor weakness and prolapse, are able inconsistency in the literature when describing undoubtedly of significance. Another important con- the correct neurological nomenclature of afferent sideration was highlighted by the discovery of nona- neurones and pathways to the rectum. However, sig- drenergic, noncholinergic (NANC) fibres subserving nificant advances are being made: Drs. Bharucha and internal anal sphincter contraction, mediated Blandon have highlighted the finding of rectal intra- through the neurotransmitter nitric oxide [36, 39, ganglionic laminar endings (rIGLEs) in the guinea 40]. This heralded both the acknowledgement of the pig rectum that serve as slowly adapting mechanore- superspecialised function of this distal continuation ceptors [55], and other molecular mechanisms of the gut circular muscle and the advent of involved in mechanosensory transduction have also “reversible chemical sphincterotomy” [41] to reduce been identified. For example, rectal sensory nerve resting tone, as well as (less successful) attempts at fibres expressing the transient receptor potential augmenting sphincter tone with topical sympath- vanilloid 1 (TRPV1) receptor, which is believed to be omimetic agents [42]. involved in neuronal signalling, have been found to Further study is merited concerning the role of be increased in patients with urge faecal incontinence coordinated colorectoanal activity in normal conti- associated with rectal hypersensitivity [56]. The nence and defecation. It is clear that entry of stool or results of further study of both somatic and auto- gas into the rectum initiates a series of events nomic innervation may go some way to help resolve (including elicitation of reflexes), the consequences recurrent angst and sometimes anger at clinical and of which may or may not be consciously perceived. research meetings! Investigation of these reflexes may shed further light One other point that deserves consideration is that on our understanding of the pathophysiology of faecal incontinence and “constipation” frequently incontinence. For example, several parameters of coexist. This perhaps underscores the importance of the rectoanal inhibitory reflex (RAIR) may be quan- “normal” defecation to the preservation of conti- tified, and the RAIR has been shown to be attenuat- nence, in that passive (overflow) faecal leakage, or ed in patients with faecal leakage [43–45]. The sig- postdefecation incontinence, may occur as a conse- nificance of the rectoanal contractile reflex requires quence of incomplete rectal emptying secondary to a further research, particularly its relation to con- “mechanical” (i.e. anatomical, such as large recto- scious perception of anorectal distension [3, 46–48]. cele, intussusception, megarectum etc.) or “function- Chapter 1 Anatomy and Physiology of Continence · Invited Commentary 15 al” outlet obstruction (e.g. pelvic floor dyssynergia, 11. Gladman MA, Scott SM, Chan CL et al (2003) Rectal poor defecatory dynamics, nonrelaxing pelvic floor hyposensitivity: prevalence and clinical impact in etc.). As such, a comprehension of the normal patients with intractable constipation and fecal incon- process of defecation should be considered funda- tinence. Dis Colon Rectum 46:238–246 12. Rao SS, Ozturk R, Stessman M (2004) Investigation of mental to the clinical management of patients with the pathophysiology of fecal seepage. Am J Gastroen- faecal incontinence. terol 99:2204–2209 Finally, the complexity of these two biological 13. Gladman MA, Dvorkin LS, Lunniss PJ et al (2005) Rec- functions (continence and defecation), which we all tal hyposensitivity: a disorder of the rectal wall or the take for granted until something goes wrong, means afferent pathway? An assessment using the barostat. that the risk factors contributing towards disturbed Am J Gastroenterol 100:106–114 function are often multifactorial and that interven- 14. Gladman MA, Lunniss PJ, Scott SM et al (2006) Rectal hyposensitivity. Am J Gastroenterol 101:1140–1151 tions, especially surgical, that aim to restore primari- 15. Bampton PA, Dinning PG, Kennedy ML et al (2001) ly anatomy and thus, hopefully, function, are not Prolonged multi-point recording of colonic manome- associated with outcomes that are always satisfactory try in the unprepared human colon: providing insight to the patient. As professionals involved in health into potentially relevant pressure wave parameters. delivery, emphasis on research must continue and Am J Gastroenterol 96:1838–1848 expand as the basis for effective, targeted and indi- 16. Scott SM (2003) Manometric techniques for the evalu- vidualised treatment. ation of colonic motor activity: current status. Neuro- gastroenterol Motil 15:483–513 17. Herbst F, Kamm MA, Morris GP et al (1997) Gastroin- testinal transit and prolonged ambulatory colonic References motility in health and faecal incontinence. Gut 41:381–389 1. Salvioli B, Bharucha AE, Rath-Harvey D et al (2001) 18. Rao SS, Sadeghi P, Beaty J et al (2001) Ambulatory 24- Rectal compliance, capacity, and rectoanal sensation in h colonic manometry in healthy humans. Am J Physi- fecal incontinence. Am J Gastroenterol 96:2158–2168 ol Gastrointest Liver Physiol 280:G629–G639 2. Bharucha AE, Fletcher JG, Harper CM et al (2005) 19. 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Dis Colon Rectum 22. Harris ML, Hobson AR, Hamdy S et al (2006) Neuro- 44:192–198 physiological evaluation of healthy human anorectal 5. Chan CL, Scott SM, Williams NS et al (2005) Rectal sensation. Am J Physiol Gastrointest Liver Physiol hypersensitivity worsens stool frequency, urgency, 291:G950–G958 and lifestyle in patients with urge fecal incontinence. 23. Thompson DG (2006) Neurogastroenterology: imag- Dis Colon Rectum 48:134–140 ing of the sensory and motor control of the GI tract. J 6. Chan CL, Lunniss PJ, Wang D (2005) Rectal sensori- Psychosom Res 61:301–304 motor dysfunction in patients with urge faecal incon- 24. Mayer EA, Naliboff BD, Craig AD et al (2006) Neu- tinence: evidence from prolonged manometric stud- roimaging of the brain-gut axis: from basic under- ies. Gut 54:1263–1272 standing to treatment of functional GI disorders. Gas- 7. Sun WM, Donnelly TC, Read NW (1992) Utility of a troenterology 131:1925–1942 combined test of anorectal manometry, electromyog- 25. 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