Neurogastroenterol Motil (2006) 18, 507519

doi: 10.1111/j.1365-2982.2006.00803.x

REVIEW ARTICLE

Pelvic floor: anatomy and function

A. E. BHARUCHA

Clinical Enteric Neuroscience Translational and Epidemiological Research (C.E.N.T.E.R.), Program, Mayo Clinic College of
Medicine, Rochester, MN, USA

uterus, and rectum. These defects are closed by

connective tissue anterior to the urethra, anterior to
the rectum (i.e. the perineal body), and posterior to the
rectum (i.e. the postanal plate). Together with the
viscera (i.e. the bladder and anorectum), the pelvic floor
is responsible for storing and evacuating urine and
stool; these somatovisceral reflexes require coordination between visceral components (e.g. rectal contraction, rectal sensation, and internal sphincter
relaxation) and somatic components (e.g. external
sphincter contraction and relaxation).

Abstract The pelvic floor is a dome-shaped striated

muscular sheet that encloses the bladder, uterus, and
rectum, and, together with the anal sphincters, has an
important role in regulating storage and evacuation of
urine and stool. This article reviews the anatomy,
nerve supply, pharmacology, and functions of the anal
sphincters and the pelvic floor. The internal and
external anal sphincters are primarily responsible for
maintaining faecal continence at rest and when continence is threatened, respectively. Defecation is a
somato-visceral reflex regulated by dual nerve supply
(i.e. somatic and autonomic) to the anorectum. The
net effects of sympathetic and cholinergic stimulation
are to increase and reduce anal resting pressure,
respectively. Faecal incontinence and functional defecatory disorders may result from structural changes
and/or functional disturbances in the mechanisms of
faecal continence and defecation.

ANATOMY
Pelvic floor
The levator ani or pelvic diaphragm is subdivided into
four muscles, i.e. pubo-coccygeus, ileo-coccygeus, coccygeus, and puborectalis. These muscles are attached
peripherally to the pubic body, the ischial spine, and to
the arcus tendinus, a condensation of the obturator
fascia in between these areas (Fig. 1).
It is unclear whether the puborectalis should be
regarded as a component of the levator ani complex or
the external anal sphincter. Based on developmental
evidence, innervation and histological studies, the
puborectalis appears distinct from the majority of the
levator ani.1 On the other hand, the puborectalis and
external sphincter complex are innervated by separate
nerves originating from S2)4 (see below), suggesting
phylogenetic differences between these two muscles.2

Keywords fecal incontinence, constipation, defecation, anal sphincter, obstructed defecation, pelvic
floor, anatomy, functions.

INTRODUCTION
There is increasing enthusiasm for viewing the pelvic
floor from a global perspective, discounting the traditional segregation into anterior, middle, and posterior
compartments. The pelvic floor is a dome-shaped
muscular sheet that predominantly contains striated
muscle and has midline defects enclosing the bladder,
Address for correspondence
Adil E. Bharucha, MD, Mayo Clinic, Charlton 8-110,
200 First St SW, Rochester, MN 55905, USA.
Tel.: 507 266 2305; fax: 507 538 5820;
e-mail: bharucha.adil@mayo.edu
Received: 19 January 2006
Accepted for publication: 31 March 2006

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Rectum and anal canal

The rectum is 1520 cm long, and extends from the
recto-sigmoid junction at the level of third sacral
vertebra to the anal orifice (Fig. 2). The upper and
lower rectum are separated by a horizontal fold. The

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Figure 1 Pelvic view of the levator ani

demonstrating its four main components: puborectalis, pubococcygeus,
iliococcygeus, and coccygeus.
Reprinted with permission from Dyck
and Thomas.94

Obturator
internus

Levator
ani

Pelvirectal
space

Longitudinal
muscle
space

Circular
muscle
layer

Iliococcygeus

Transverse
folds

Pubococcygeus

Rectal
ampulla

Ischiorectal
fossa

Anal
columns

Gluteus
maximus
Semitendinosus

Deep
Superficial
Subcutaneous
Parts of
sphincter ani externus

Anal
sinuses
Skin
Sphincter
ani internus

Figure 2 Diagram of a coronal section

of the rectum, anal canal, and adjacent
structures. The pelvic barrier includes
the anal sphincters and pelvic floor
muscles. Reprinted with permission
from Bharucha.95

connective tissue, and is generally empty in normal

subjects, except during defecation. In humans, there
are fewer enteric ganglia in the rectum compared with
the colon and very few ganglia in the anal sphincter.4,5

upper rectum is derived from the embryological hindgut, generally contains faeces, and can distend towards
the peritoneal cavity.3 The lower part, derived from the
cloaca, is surrounded by condensed extra-peritoneal

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nerves to form the inferior hypogastric plexus, located

posterior to the urinary bladder. The inferior hypogastric plexus gives rise to the middle rectal plexus,
vesical plexus, prostatic plexus, and uterovaginal
plexus. The nerve supply to the rectum and anal canal
is derived from the superior, middle, and inferior rectal
plexus. Parasympathetic fibres in the superior and
middle rectal plexuses synapse with postganglionic
neurones in the myenteric plexus in the rectal wall. In
addition, ascending fibres from the inferior hypogastric
plexus travel via superior hypogastric and aortic plexuses to reach the inferior mesenteric plexus, ultimately
innervating the descending and sigmoid colon. After
entering the colon, these fibres form the ascending
colonic nerves, travelling cephalad in the plane of the
myenteric plexus to supply a variable portion of the left
colon.
Sacral parasympathetic pathways to the colon have
excitatory and inhibitory components.8 Excitatory
pathways play an important role in colonic propulsive
activity, especially during defecation. In other species
(e.g. guinea-pig), faeces transport may be entirely
organized by the enteric nervous system; spinal and
supraspinal reflexes are also involved in the process.9
Inhibitory pathways allow colonic volume to adapt to
its contents, and also mediate descending inhibition,
that initiates colonic relaxation ahead of a faecal bolus.

The anal canal is an anterioposterior slit, with its

lateral walls in close contact. The literature describes a
longer (approximately 4.04.5 cm) surgical or clinical
anal canal and a shorter (approximately 2.0 cm) anatomical or embryological anal canal. The anal valves
and the distal end of the ampullary part of the rectum
mark the proximal margin of the short and long anal
canal respectively. The proximal 10 mm of the anal
canal is lined by columnar, rectal-type mucosa. The
next 15 mm (which includes the valves) is lined by
stratified, or a modified columnar epithelium. Distal to
that is about 10 mm of thick, non-hairy, stratified
epithelium (the pecten). The most distal 510 mm is
lined by hairy skin.
The anal canal is surrounded by the internal and
external anal sphincters. The internal sphincter is not
merely a thickened extension of the circular smooth
muscle layer surrounding the colon. Indeed, in dogs,
the rectal circular muscle layer is tightly packed with
poorly defined septa while the internal anal sphincter
contains discrete muscle bundles separated by large
septa.6 In the rectum, the interstitial cells of Cajal
(ICC) are organized in dense networks along the
submucosal and myenteric borders. In the internal
anal sphincter, the ICCs are located along the periphery of the muscle bundles within the circular layer.
The external sphincter is composed of superficial,
subcutaneous and deep portions; the deep portion
blends with the puborectalis.3 In men, this trilaminar
pattern is preserved around the sphincter circumference. In contrast, among women, the external sphincter appears as a single muscle bundle anteriorly. The
external sphincter is enveloped by conjoint longitudinal fibres in men and women.

Somatic innervation
Cortical mapping with transcranial magnetic stimulation suggests that rectal and anal responses are
bilaterally represented on the superior motor cortex,
i.e. Brodmann area 4.10 There are subtle differences in
the degree of bilateral hemispheric representation
between subjects. Motor neurones in Onufs nucleus,
which is located in the sacral spinal cord, innervate
the external anal and urethral sphincters. Though
they supply striated muscles under voluntary control,
these motor neurones are smaller than usual a-motor
neurones and resemble autonomic motor neurones;11
however, the conduction velocity in pudendal nerve
fibres is comparable with that of peripheral nerves. In
contrast to other somatic motor neurones in the spinal
cord, these neurones are relatively spared in amyotrophic lateral sclerosis, but affected in ShyDrager
syndrome.12,13 Somatic branches originating from
Onufs nucleus travel in the pudendal nerve, muscular
branches and in the coccygeal plexus. The pudendal
nerve branches into inferior rectal, perineal, and posterior scrotal nerves. The inferior rectal nerve conveys
motor fibres to the external anal sphincter, and sensory
input from the lower anal canal as also the skin around

NERVE SUPPLY TO THE PELVIC FLOOR

Sympathetic and parasympathetic innervation
The anorectum and pelvic floor are supplied by sympathetic, parasympathetic and somatic fibres.7 Sympathetic preganglionic fibres originate from the lowest
thoracic ganglion in the paravertebral sympathetic
chain and join branches from the aortic plexus to form
the superior hypogastric plexus (Fig. 3). The alternative
term for this plexus (i.e. presacral nerve) is misleading
because it is seldom condensed, and does not resemble
a single nerve. The superior hypogastric plexus provides branches to the uteric and ovarian (or testicular)
plexus, and divides into right and left hypogastric
nerves. The hypogastric nerves unite with preganglionic parasympathetic fibres originating from ventral
rami of the second, third, and often the fourth sacral

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Figure 3 Sympathetic, parasympathetic and pudendal nerve supply to the

anorectum. Reprinted with permission
from Dyck and Thomas.94

Motor fibres of the right and left pudendal nerves

have overlapping distributions within the external
anal sphincter. Sherrington observed that stimulation
of the right pudendal nerve caused circumferential
contraction of the external anal sphincter. Conversely, tonic external sphincter activity, sphincter
inhibition during colonic distention, and the cutaneo-

the anus. The perineal nerve divides into posterior

scrotal (or labial) branches and muscular branches.
The posterior scrotal branches innervate the skin,
while muscular branches are distributed to the
transverse perinei, bulbospongiosus, ischiocavernosus,
urethral sphincter, anterior part of the external anal
sphincter, and the levator ani.

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as they are more likely to lack resting activity and

respond to pressure increments with a wider range of
discharge frequency.23,24 Janig and Morrison identified three different classes of mechanosensitive visceral afferents in the cat colon.22 Tonic afferents
fired throughout colonic distention and accurately
encoded the intensity of distention between 20 and
100 mmHg. Phasic colonic afferents generally discharged at the onset, and occasionally at the cessation of a distention stimulus. Tonic afferents were
predominantly unmyelinated slowly-conducting C
fibres while most phasic afferents were faster conducting myelinated Ad fibres. The afferents innervating the anal canal responded to shearing stimuli, but
not colonic or anal distention.
Two different theories have been proposed to
explain visceral pain perception. Proponents of the
specificity theory suggested that pain was a distinct
sensory modality, mediated by sequential activation
of visceral nociceptors and central pain-specific neurones in the spinal dorsal horn. However, in the cat
colon, Janig and Koltzenburg found no afferent fibres
that were selectively activated by noxious stimuli,
arguing against the specificity theory. The alternative
hypothesis for pain perception, i.e. pattern or intensity theory, attributes pain perception to spatial and
temporal patterns of impulses generated in nonspecific visceral afferent neurones.14 However, electrophysiological studies of visceral afferent fibres in
other organs, including the colon, have documented
high threshold visceral afferent fibres that only
respond to noxious mechanical stimuli. Subsequently, Cervero and Janig reconciled these opposing
concepts in a convergence model wherein input from
low- and high-threshold mechanoreceptors converge
on spinothalamic and other ascending tract cells.25
Physiological processes are generally accompanied by
low level activity, mediation of regulatory reflexes,
and transmission of non-painful sensations. Highintensity stimuli increase firing of low-threshold
afferents and also activate high-threshold afferents,
thereby activating nociceptive pathways and triggering pain.25
More than 90% of all unmyelinated pelvic afferents
are silent, being activated by electrical stimulation, but
not even by extreme noxious stimuli.22 Silent afferents
can respond to chemical stimuli or tissue irritation,
becoming responsive to even innocuous mechanical
stimuli after sensitization.26 These neurophysiological
changes are detectable within minutes after tissue
irritation, are likely to persist for the duration of
irritation and have been implicated to explain visceral
hypersensitivity.

anal reflex were not affected by sectioning either

pudendal nerve.
The nerve supply to the puborectalis has been the
subject of controversy. The early literature based on
dissections by several workers suggested that the
puborectalis was innervated from below by the
pudendal nerve, or jointly by the inferior rectal and
perineal branches of the pudendal nerve. Therefore,
the puborectalis was regarded as being derived not
from the levator ani but from the external anal
sphincter. However, an electrophysiological study
concluded that preoperative stimulation of the
sacral nerves above the pelvic floor invariably (i.e.
19 of 20 experiments) resulted in electromyogram
(EMG) activity in the ipsilateral puborectalis, but not
in the external anal sphincter. 2 Thus, further
investigations are necessary to clarify this important
point.

Sensory innervation
In contrast to colonic distention, which generally
evokes ill-defined discomfort and eventually pain,
rectal distention is perceived as a more localized
sensation of rectal fullness, interpreted by the patient
as a desire to pass wind or motion. The anal canal
responds to distention and to innocuous mucosal
proximo-distal mechanical shearing stimuli.14 In addition to mucosal nerve endings, there are also low
threshold, slowly adapting mechanoreceptors in the
guinea-pig rectum. These intraganglionic laminar endings detect mechanical deformation of the myenteric
ganglia.15,16 The anal canal is lined by numerous free
and organized nerve endings (i.e. Meissners corpuscles, Krause end-bulbs, Golgi-Mazzoni bodies and
genital corpuscles), perhaps explaining why it is
exquisitely sensitive to light touch, pain and temperature. Sensory traffic is conveyed by unmyelinated
small C fibres and larger A fibres.
Animal models and clinicopathological findings in
humans suggest that pelvic nerves travelling to the
sacral segments are more important for conveying
non-noxious and noxious colonic sensations than
lumbar colonic (sympathetic) nerves.8,1719 There are
more afferent neurones supplying the colon in the
sacral, compared with lumbar segments in the cat, i.e.
7500 vs 4500 neurones.20,21 However, the number of
spinal visceral afferent neurones is relatively small,
i.e. only 2.5% or less of the total number of spinal
afferent neurones supplying skin and deep somatic
structures.22
In general, sacral afferents may be better suited for
conveying afferent information than lumbar afferents,

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essential for the reflex, as it is preserved in patients

with cauda equina lesions or after spinal cord
transection. However, extrinsic nerves may modulate
the reflex, as relaxation is more pronounced and
prolonged in children with sacral agenesis.33 The
RAIR is probably mediated by nitric oxide (NO);
morphological studies reveal an efferent descending
nitrergic rectoanal pathway.34 Other nonadrenergicnoncholinergic neurotransmitters, i.e. vasoactive
intestinal peptide (VIP) and ATP may also participate
in the RAIR.35,36

ANAL SPHINCTER TONE AND REFLEXES

Internal anal sphincter
The internal sphincter is primarily responsible for
ensuring the anal canal is closed at rest.8,27 The other
contributors to anal resting tone include the external
anal sphincter, the anal mucosal folds and the puborectalis muscle. Penninckx et al. estimated that anal
resting tone was generated by nerve-induced activity in
the internal sphincter (45% of anal resting tone),
myogenic tone in the internal sphincter (10%), the
external sphincter (35%) and the anal haemorrhoidal
plexus (15%).28 These figures should be regarded as
estimates, because they were obtained, in part, from
complex studies in which anal resting pressure was
sequentially recorded before surgery (i.e. abdominoperineal resection), after curarization, and in the
resected specimen before and after verapamil. Moreover, the relative contributions of these factors to anal
resting tone are influenced by several factors, including
the size of the probe and the location at which pressure
was measured.
Frenckner and Ihre investigated the contribution of
myogenic tone and the extrinsic (sympathetic and
parasympathetic) nerves to anal resting tone by assessing anal pressure at rest and in response to rectal
distention under baseline conditions, after low spinal
anaesthesia (L5S1), and after high spinal anaesthesia
(T6T12).27 A separate study assessed anal pressures
before and after pudendal nerve blockade. The decline
in anal resting pressure was significantly greater after
high (32 3.2 mmHg) than low (11 7.1 mmHg)
anaesthesia or after pudendal nerve blockade
(10 3.9 mmHg), suggesting there is a tonic excitatory
sympathetic discharge to the internal anal sphincter in
humans. However, the anal pressure during rectal
distention was similar among the three groups, suggesting that this excitatory sympathetic discharge does
not contribute to anal pressure during rectal distention.
Conversely, sympathetic stimulation either evoked
internal anal sphincter relaxation,2830 or contraction
followed by relaxation.31
Anal resting pressure is not stationary but varies
during the day. In addition to spontaneous relaxation of
the internal sphincter, circadian variations that are
dependent on the sleepwake cycle and ultradian (20
40 min in length) rhythms that are independent of the
sleepawake cycle have also been described.32
Anal relaxation induced by rectal distention [i.e.
the recto-anal inhibitory reflex (RAIR)] is mediated by intrinsic nerves. This reflex is absent in
Hirschsprungs disease. The extrinsic nerves are not

External anal sphincter

Though resting sphincter tone is predominantly attributed to the internal anal sphincter, studies under
general anaesthesia or after pudendal nerve block
suggest the external anal sphincter generally accounts
for 25%, up to 50% of resting anal tone. When
continence is threatened, the external sphincter contracts to augment anal tone, preserving continence.
This squeeze response may be voluntary, or induced
by increased intra-abdominal pressure,37 or by merely
moving a finger across the anal canal lining.38 Conversely, the external sphincter relaxes during defecation.
The only other striated muscles that display resting
activity are the puborectalis, external urethral sphincter, cricopharyngeus and the laryngeal abductors.
Resting or tonic activity depends on monosynaptic
reflex drive, perhaps explaining why resting anal
sphincter tone is reduced, but voluntary contraction
of the external sphincter is preserved in tabes dorsalis.39 The fibre distribution also favours tonic activity; type 1 (i.e. fatigue-resistant, slow twitch) fibres
predominate in the human anal sphincter,40 while cats
and rabbits predominantly contain type 2 or fast-twitch
muscle fibres.41 External sphincter fibres are circumferentially oriented, and very small, separated by
profuse connective tissue.40

Puborectalis
The tonically active puborectalis muscle maintains the
resting anorectal angle. Moreover, puborectalis contraction during a sudden rise in abdominal pressure
reduces the anorectal angle, preserving continence.
While cadaveric studies suggested the puborectalis was
supplied by the pudendal nerve, electrophysiological
stimulation studies in humans suggest this muscle is
supplied, strictly ipsilaterally, by branches originating
from the sacral plexus above the pelvic floor.2 Disruption of the puborectalis inevitably causes significant

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gic agonists either contracted or relaxed internal anal

sphincter strips in humans.44 In the vervet monkey,
muscarinic receptor stimulation contracted internal
sphincter strips, but relaxed them after muscarinic
receptors were blocked, probably via non-adrenergic
non-cholinergic mechanisms.46 Nicotinic agonists also
relaxed internal sphincter strips, probably via nonadrenergicnon-cholinergic mechanisms.
Nitic oxide mediates internal sphincter tone and
the RAIR. A recent study using knockout mice
suggests that the isoforms of nitric oxide synthase
(NOS), i.e. neuronal (nNOS) and endothelial (eNOS),
modulate distinct facets of internal sphincter functions.47 While basal internal anal sphincteric tone
was comparable in nNOS)/) and wild mice, it
was significantly (approximately twofold) higher in
eNOS)/) mice and also significantly (approximately
25%) lower in mice that lacked c-Kit expressing ICC
(i.e. W/Wv mice). The RAIR was preserved in eNOS)/)
and W/Wv mice but was absent in nNOS)/) mice,
which is consistent with the selective loss of nNOS
and the RAIR in Hirschsprungs disease. Other studies have confirmed that nNOS is primarily responsible for mediating relaxation of the internal anal
sphincter, in mice and humans. While VIP may also
contribute to relaxation of the internal sphincter, the
role played by carbon monoxide in this process is
controversial.48,49
The effects of neurotransmitters on the internal anal
sphincter vary among species. Thus, angiotensin II
contributes to basal tone and contracts the internal
anal sphincter in rats50 but not in the opossum.45
Table 1 summarizes the effects of neurotransmitters
and pharmacological agents that modulate internal
anal sphincter tone.

incontinence, underscoring the importance of this

muscle in maintaining continence.

Sacral reflexes
The pelvic floor striated muscles contract reflexly in
response to stimulation of perineal skin (i.e. a somatosomatic reflex) or anal mucosa (i.e. a viscerosomatic
reflex). The cutaneoanal reflex is elicited by scratching
or pricking the perianal skin and involves the pudendal
nerves and S4 roots. Electrophysiological recordings
reveal both short- latency and long-latency responses;
the latter corresponds to the visible anal sphincter
contraction.42 Sacral reflexes also regulate anal sphincter tone during micturition. Thus, electrical activity of
the internal anal sphincter increases during urinary
bladder emptying in humans, returning to normal after
micturition.43 Conversely, the external anal sphincter
relaxed during micturition in humans, cats and dogs.

PHARMACOLOGY
In contrast to non-sphincteric regions, sympathetic
nerves excite while parasympathetic nerves inhibit the
sphincters. The internal anal sphincter is densely
innervated by adrenergic nerves in humans and monkeys. Stimulation of adrenergic a and b receptors
contracted and relaxed human internal sphincter strips
respectively (Table 1).44 All three b adrenoreceptor
receptor subtype (b1, b2 and b3) agonists relax the
opossum internal anal sphincter; the b3 receptor effect
is mediated by a cyclic guanylate monophosphate
(GMP)-mediated pathway similar to NO.45
The internal anal sphincter is more sensitive to
adrenergic compared to cholinergic agonists; choliner-

Table 1 Effects of pharmacological modulation on anal sphincter tone and pressures

Pharmacological agent
Adrenergic agents44
Phenylephrine (a1 agonist)53,

54

b (b1, b2 and b3) adrenoreceptor agonists81

Acetylcholine,44,82
Nicotine44
Bethanechol83
Loperamide84
Others glucagon, ketanserin, diltiazem,
enkephalin, somatostatin,28 diltiazem83
Angiotensin II50

Model

Effects

In vitro human and monkey

Healthy subjects and
incontinent patients
In vitro opossum
In vitro human and monkey
In vitro human and monkey

a contraction; b relaxation
Resting pressure in healthy subjects;
did not improve FI
Resting pressure
Either contraction, relaxation or no change
Relaxation upper anal canal
No change lower anal canal
Resting pressure
Resting pressure
Resting pressure

Healthy human subjects

Incontinent patients
Healthy human subjects
Rat internal anal sphincter

FI, faecal incontinence; , increased; , reduced.

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Contributes to basal tone

Resting pressure

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Denny-Brown and Robertson observed that rectal

distention evoked rectal contraction and anal sphincter
relaxation, facilitating evacuation.17 The pelvic floor,
particularly the puborectalis, also generally relaxes
during defecation (Fig. 4). Simultaneous assessments of
intrarectal pressures and pelvic floor activity (by
manometry, EMG or imaging) reveal that increased
intrarectal pressure and anal relaxation are required for
normal defecation. However, the relative contributions
of increased intra-abdominal pressure generated by
voluntary effort56 and rectal contraction57 to the
propulsive force during defecation are unclear, partly
because a barostat rather than manometry is necessary
to optimally characterize rectal contractions, which
are of relatively low amplitude. Current concepts
suggest that minimal straining to initiate defecation
is not abnormal because many asymptomatic subjects
strain to initiate defecation.58 However, excessive
straining and particularly a Valsalva manoeuvre, may
impede evacuation because while a Valsalva manoeuvre may increase intrarectal pressure, the pelvic
floor muscles also contract, increasing outlet resistance.59 Thus, it is necessary to assess the balance
between these two sometimes opposing forces by
measuring the net recto-anal force during evacuation.60
One possibility is that the relative contributions of
voluntary effort and rectal contraction to defecation
vary, depending on the circumstances prior to defecation. For example, the voluntary effort may range
from being negligible when stool is soft to considerable
when stool is hard and situated in the upper rectum.
If defecation is inconvenient, it can generally be
postponed. The rectal contractile response to distention normally subsides as the rectum accommodates or
relaxes. The external sphincter and/or puborectalis can
be contracted voluntarily. This contractile response
requires the ability to perceive stool in the rectum and
perhaps also in the anal canal. Indeed, the anal

APPLIED PHARMACOLOGY
Because anal fissures are often associated with increased anal resting tone, per-anal exogenous nitrates
(i.e. 0.2% glyceryl trinitrate) have been extensively
tested and widely used to treat anal fissures. The
experience from numerous clinical trials is discussed
in detail elsewhere.51 However, in earlier controlled
studies, the controls were frequently not treated with
standard conservative therapy (i.e. fibre supplementation, sitz baths). Moreover, approximately 60% of
patients so treated developed headaches with nitroglycerine and approximately 25% of patients had a
relapse. Topical calcium channel blockers (e.g., 0.2%
nifedipine or 2% diltiazem) are probably more effective
than nitrates for treating anal fissures with a lower
incidence of side effects. Bethanechol and botulinum
toxin have also been used to treat anal fissures.
The beneficial effects of loperamide in faecal incontinence (FI) may be attributable not only to reduced
diarrhoea, but also to increased anal resting tone.52 The
a1 adrenoreceptor agonist phenylephrine applied to the
anal canal increased anal resting pressure by 33% in
healthy subjects and in incontinent patients.53 However, phenylephrine did not significantly improve
incontinence scores or resting anal pressure compared
with placebo, in a randomized double-blind placebocontrolled crossover study of 36 patients with FI.54

MECHANISMS OF CONTINENCE AND

DEFECATION
Faecal continence is maintained by anatomical factors
(i.e. the pelvic barrier, the rectal curvatures and
transverse rectal folds), recto-anal sensation, and rectal
compliance. Stool is often transferred into the rectum
by colonic high-amplitude propagated contractions,
which often occur after awakening or meals.55
Rest

Rest

Evacuation

Evacuation

Figure 4 Sagittal dynamic MRI images of normal puborectalis relaxation (left panel, subject 1) and puborectalis contraction (black
arrow, right panel, subject 2) during rectal evacuation. In both subjects, evacuation was associated with perineal descent (2.6 cm in
subject 1, 1.7 cm in subject 2) and opening of the anorectal junction. During evacuation, the anorectal angle increased by 36 in
subject 1 and declined by 10 in subject 2. Reprinted with permission from Bharucha et al.96

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expulsion forces, recent studies have demonstrated a

wide spectrum of anorectal sensorimotor disturbances
(e.g. hypertensive anal sphincter, increased perineal
descent, reduced or increased rectal sensation) in
patients with symptoms of difficult defecation.6466
Indeed, a detailed characterization of anorectal sensorimotor functions and pelvic floor motion assessed by
magnetic resonance imaging (MRI) followed by a
principal component analysis in 52 patients with a
functional defecatory disorder revealed that three
factors best explained the phenotypic variance among
patients.66 These factors were primarily weighted by
perineal descent during evacuation, anorectal location
at rest and resting anal pressure. These findings are
consistent with the concept that patients with impaired relaxation of the anal sphincter and pelvic floor
tend to have impaired perineal descent while patients
with normal (or excessive) relaxation of the pelvic floor
with a hypertensive anal sphincter have increased
perineal descent. Thus, there is considerable evidence
that functional defecatory disorders do not comprise a
single entity.

sphincter may also relax independent of rectal distention, allowing the anal epithelium to periodically
sample and ascertain whether rectal contents are
gas, liquid or stool.61
These mechanisms underscore that defecation is an
integrated somato-visceral reflex. Indeed, the central
nervous system plays a greater role in regulating
anorectal sensorimotor functions compared with other
regions of the gastrointestinal tract. The elaborate
somatic defecation response depends on centres above
the lumbo-sacral cord, and probably craniad to the
spinal cord itself. However, Garry observed that
colonic stimulation in cats induced colonic contraction and anal relaxation even after destruction of the
lumbo-sacral cord, concluding that the gut seems not
to have wholly surrendered its independence.62

APPLIED ANATOMY AND FUNCTIONAL

DISORDERS OF DEFECATION AND
CONTINENCE
Functional disorders of defecation
Functional defecation disorders are characterized by
paradoxical contraction or failure of relaxation of the
pelvic floor muscles during attempted defecation (dyssynergic defecation) or inadequate propulsive forces
during attempted defecation (inadequate defecation).
Alternative terms for dyssynergic defecation (e.g. anismus, puborectalis dyssynergia) are preferably avoided
because the muscle dysfunction can affect either or
both muscles.
The traditional paradigm of a functional defecatory
disorder was limited to constipated patients with
pelvic floor dyssynergia.63 In addition to inadequate

Faecal incontinence
While most attention has focused on anal sphincter
weakness, disturbances of rectal compliance and perception, of stool consistency, mental faculties and
mobility often contribute to FI.
Anal sphincter pressures are reduced in most, but
not all incontinent patients (Table 2).67 While most
attention has focused on anal sphincter weakness,
recent studies using a dynamometer68 and dynamic
MRI69 also demonstrated weakness of the puborectalis
in FI. Moreover, the inward traction exerted by the

Table 2 Structural and functional disturbances of the human anal sphincters in disease
Sphincter condition

Finding (method)

Internal and external sphincters FI

Sphincter defects, scarring and atrophy (US and MRI)69,85

Reduced anal resting and/or squeeze pressures
Exaggerated transient relaxation of internal sphincter86
Thinning of the internal sphincter (US)87
Rectal fibrosis (histology)
Loss of smooth muscle and fibrosis (histology)88
Reduced response to pharmacological agents (e.g. catecholaminergic and muscarinic
agents but not 5-HT) and EFS89,90
Hypertrophy with polyglucosan inclusions (US and histology)91

Rectum and internal sphincter

scleroderma and FI
Internal sphincter neurogenic FI
Internal sphincter neurogenic FI
Internal sphincter proctalgia fugax
and constipation
Internal sphincter pruritus ani
Internal sphincter chronic anal fissure

Abnormal transient relaxation (ambulatory manometry)92

Increased resting pressure and less frequent transient anal relaxation (ambulatory
manometry)93

FI, faecal incontinence, US, ultrasound; 5-HT, 5-hydroxytryptamine; EFS, electrical field stimulation.

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shown that a subset of patients with a defecatory

disorder have excessive perineal descent, which is
associated with POP.72 Indeed, it is conceivable that
excessive straining during defecation may predispose
to POP. The relationship between perineal descent,
straining, and pudendal neuropathy needs to be further
clarified in prospective studies.

puborectalis was reduced in FI, correlated more closely

with symptoms than squeeze pressures, and improved
after biofeedback therapy.68
However, anal sphincter pressures do not always
distinguish continent from incontinent subjects,
underscoring the importance of rectal compliance and
sensation for maintaining continence. Impaired rectal
sensation allows stool to enter the anal canal, and
perhaps leak before the external sphincter contracts.67,70 On the other hand, exaggerated rectal
sensation, perhaps a marker of coexistent irritable
bowel syndrome, is associated with reduced rectal
compliance, repetitive rectal contractions during rectal
distention, external sphincter weakness, and exaggerated anal sphincter relaxation during rectal distention.67 The rectal capacity (i.e. the balloon volume at
the maximum imposed pressure) is also reduced in a
subset of women with idiopathic FI.69 Moreover,
reduced rectal capacity was associated with the symptom of urgency and with rectal hypersensitivity. Thus,
FI is a heterogeneous disorder; patients often suffer
from more than one deficit.

Surgical implications
From a therapeutic perspective, an understanding of
anatomy is particularly important for managing anal
fistulae, preventing nerve injury during surgical dissection, and understanding the consequences of rectal
resection. Left-sided colectomy may result in postoperative colonic transit delays in the unresected segment; this probably represents parasympathetic
denervation, as ascending intramural fibres travel in a
retrograde manner from the pelvis to the ascending
colon. The sigmoid colon and rectum are also supplied
by descending fibres that run along the inferior mesenteric artery. These nerves may be disrupted during a
low anterior resection, leaving a denervated segment
that may be short or long depending on whether the
dissection line includes the origin of the inferior
mesenteric artery.75 A long denervated segment is
more likely to be associated with non-propagated
colonic pressure waves and delayed colonic transit
than a short denervated segment. In addition to colonic
denervation, a low anterior resection may also damage
the anal sphincter and reduce rectal compliance;76 in
contrast to anal sphincter injury, rectal compliance
may recover with time.77 Defecation may also be
affected after surgical section of pelvic nerves in
humans.78,79
Denonvilliers fascia is intimately adherent to the
anterior mesorectal fat but only loosely adherent to the
seminal vesicles. During anterior rectal dissection, the
deep parasympathetic nerves situated in the narrow
space between the rectum and the prostate and seminal
vesicles may be damaged, leading to impotence.80 For
benign disease, most surgeons will tend to stay
posterior to Denonvilliers fascia in an attempt to
protect the pelvic nerves. For malignant disease, the
choice is less straightforward because dissection
behind, rather than in front of the fascia may, in
theory, be associated with incomplete resection and/or
local recurrence.

Global pelvic floor dysfunction

Based on the predominant manifestation, pelvic floor
disorders are traditionally classified into those affecting the anterior, middle and posterior compartment,
and managed separately by urologists, gynaecologists,
and gastroenterologists/colorectal surgeons respectively. It is conceivable that pelvic organ prolapse
(POP) and FI are associated, because both conditions
share similar risk factors, particularly obstetric trauma.
Moreover, it is conceivable that in subjects with POP,
excessive perineal descent may cause a pudendal
neuropathy, which in turn may cause anal sphincter
weakness, predisposing to FI.71 However, despite a
higher prevalence of risk factors for pelvic floor injury,
a recent controlled study demonstrated that women
with FI had a lower risk of severe POP compared with
age-matched women without FI.72 These findings
suggest that FI is predominantly caused by anorectal
dysfunctions rather than by generalized pelvic floor
weakness. An association between faecal and urinary
incontinence has been observed in case series73 and a
population-based study.74
An association between functional defecatory disorders and dysfunctional urinary voiding has also been
demonstrated. Thus, symptoms (e.g. straining to begin
or complete voiding and the sense of incomplete
emptying) and objective disturbances of voiding
occurred more frequently in women with a defecatory
disorder than in healthy controls. Other studies have

ACKNOWLEDGMENTS
The author is supported by grants RO1-HD-41129 and
RO1-DK-68055 from the National Institutes of Health.

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