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The Physiology of Human Defecation

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Dig Dis Sci (2012) 57:1445–1464
DOI 10.1007/s10620-012-2071-1
REVIEW
The Physiology of Human Defecation
Somnath Palit • Peter J. Lunniss • S. Mark Scott
Received: 3 June 2011 / Accepted: 23 January 2012 / Published online: 26 February 2012
 Springer Science+Business Media, LLC 2012
Abstract Human defecation involves integrated and
coordinated sensorimotor functions, orchestrated by cen-
tral, spinal, peripheral (somatic and visceral), and enteric
neural activities, acting on a morphologically intact gas-
trointestinal tract (including the final common path, the
pelvic floor, and anal sphincters). The multiple factors that
ultimately result in defecation are best appreciated by
describing four temporally and physiologically fairly dis-
tinct phases. This article details our current understanding
of normal defecation, including recent advances, but
importantly identifies those areas where knowledge or
consensus is still lacking. Appreciation of normal physi-
ology is central to directed treatment of constipation and
also of fecal incontinence, which are prevalent in the
general population and cause significant morbidity.
Keywords Defecation
Rectal evacuation

Physiology of defecation
Rectal sensorimotor function

Colonic motor activity
Introduction
Continence and defecation are inextricably linked, with
common anatomical, physiological, and neurological
S. Palit
P. J. Lunniss
S. M. Scott
Academic Surgical Unit (GI Physiology Unit), Barts and the
London School of Medicine and Dentistry, Blizard Institute,
Queen Mary University, London, UK
S. Palit (&)
GI Physiology Unit, Royal London Hospital, Wingate Institute
of Neurogastroenterology, 26 Ashfield Street,
London E1 2AJ, UK
e-mail: s.palit@qmul.ac.uk
bases. However, although continence is ultimately depen-
dent upon sphincteric function (as long as anal pressure is
greater than rectal pressure, continence is maintained),
defecation appears to be a much more complex process.
Disordered defecation and incontinence are both associated
with significant economic and personal burdens [1].
Rational directed management of the individual consti-
pated patient is suboptimal [2], primarily because our
understanding of defecation is incomplete; this may reside
in a combination of lack of appropriate investigative tools,
over-reliance on acceptance of various mechanisms
believed to contribute to defecation through received wis-
dom, lack of focused research, and lack of consensus over
what constitutes ‘‘normal.’’ This review describes con-
temporary understanding of the processes involved in
defecation in humans and identifies gaps in our knowledge.
Such understanding is fundamental to the definition/clas-
sification and management of patients presenting with
symptoms of constipation characterized by evacuatory
dysfunction.
Frequency of Normal Defecation
Infrequency of defecation is often used to define consti-
pation. A community questionnaire survey involving more
than 1,800 volunteers found that the most common bowel
pattern was once a day in both sexes, but this pattern was
present in only 40% of men and 33% of women [3];
another 7% of men and 4% of women had a regular twice
or thrice daily bowel habit [3]. Inquiring the bowel
symptoms of 1,455 healthy adults, Connell et al. [4] found
that over 99% had between three motions per day to three
motions per week. Similar findings were reported by Hardy
et al., in a study involving 440 nurses [5]. Based on these
123
1446
studies, it is generally accepted that in adults the ‘‘normal’’
frequency ranges between a maximum of three times per
day to a minimum of three times per week [6]. However,
less than three motions per week has been considered
normal if this is not associated with discomfort [7]. It is
important to note that patients’ perception of what is
‘‘normal’’ and what is constipation can differ from their
clinicians [8, 9]. While clinicians usually define constipa-
tion by decreased stool frequency, patients tend to define it
in terms of disordered function (e.g. need to strain), and
passage of hard stool [10].
In children, the frequency of bowel movements
decreases with age; the decline occurs during the first
3 years and is most rapid from the first months postpartum
[11]. By the age of 4, bowel frequency is equivalent to that
of adults [12]. The average frequency of defecation in
children is 6.3 ± 1.3 times per week (range, 4–9 per week)
[13]. The frequency of high amplitude propagating con-
tractions (HAPCs), which have been linked to colonic mass
movements (see below), is significantly higher in young
children when compared to children older than 4 years of
age [14]; this correlates with the increased number of
bowel movements observed in young children [14].
Factors Influencing Evacuation
Influence of Psycho-Behavioral Factors and Voluntary
Suppression of Defecation
There is now increasing recognition that a variety of psycho-
behavioral factors can affect gastrointestinal function.
Influence of psychological trait on bowel habit has long been
appreciated [15], and several studies have shown that the
incidence of constipation is higher in patients with psycho-
logical impairment [16–18] or a history of traumatic life
events including sexual and physical abuse [19, 20]. The
influence of mental state, such as short-term anxiety and
stress, also impact on bowel habit. Furthermore, it is well
known that stool ‘‘withholding’’ behavior, often triggered by
an instinct to avoid painful evacuation, is one of the main
causes of defecatory dysfunction in children [21–23]. Two
separate studies have reported that up to 97% of constipated
children display stool withholding behavior [24, 25]. Other
associated findings were the presence of a rectal/abdominal
mass and a history of earlier painful defecation [21, 24, 25].
There is evidence that constipation and painful defecation
not only precede toileting refusal [26], but also help in
maintaining this behavior [27, 28], which manifests as
‘‘retentive posturing’’ where toddlers hold an erect posture
and forcefully contract their gluteal and pelvic floor mus-
culature [24] until the defecatory urge disappears due to
rectal accommodation. It is hypothesized that stool in the
123
Dig Dis Sci (2012) 57:1445–1464
rectum gradually hardens and becomes more difficult to
evacuate causing a vicious cycle that can ultimately lead to
chronic rectal distension [29]. Ignoring the defecatory urge
may be a conscious decision or an unconscious automatic
habit of the child resulting from altered or diminished brain
processing of urge sensations due to loss of attention [30].
Such ‘‘conditioning’’ behavior has also been reported in
adults [31], many of whom display toilet avoidance behavior
due to pain, or to the lack of the ‘‘sanctum’’ of one’s private
lavatory [32]. In a seminal study, Klauser et al. compared
frequency of defecation and colonic transit in 12 healthy
male volunteers during a 2-week study where 1 week of
normal defecation and 1 week of voluntary suppression of
defecation followed each other in a randomized order [33].
Voluntary suppression of defecation led to decrease in stool
frequency, stool volume, and increases in total colonic and
recto-sigmoid transit times, a finding which suggests that
constipation can be ‘‘learned’’ [33].
Appropriate toilet training also appears necessary for
normal defecation. Improper training has been implicated as
a cause of constipation in children. Studies have shown that
toilet training is now initiated at an older age than it was in
the past [34]. In the 1940s, toilet training usually started
before 18 months of age, whereas today, training often starts
between 21 and 36 months, and only 40–60% children
complete toilet training by the age of 3 [35, 36]. One study
reported that girls develop toileting skills earlier than boys
[37]. Lack of successful toilet training by 42 months of age
is associated with toileting refusal behavior [36].
Toilet training is initiated and completed significantly
earlier in urban areas as compared to rural areas [38]. Race
and income are independent predictors of the age at which
parents believe they should initiate toilet training; Cauca-
sians and higher income group parents are more likely to
start toilet training at a later stage as compared to other
races and lower income groups [39]. Parents play a key role
in toilet training; they need to provide the direction,
motivation, and positive reinforcement in addition to set-
ting aside time and having patience during the process [40].
Influence of Posture on Defecation
The defecatory position that a subject assumes is dictated
by a number of factors, including the type of toilet avail-
able (if available), physical and mental ability, and cultural
factors. In Western countries, sitting on a toilet seat
(commode) is common, whereas in Africa and Asia
squatting is the preferred position.
Using defecography (simulated defecation of a neostool
under continuous fluoroscopic screening), it has been
demonstrated that the anorectal angle becomes more obtuse
(opens up) with increasing hip flexion, making evacuation
easier [41]. In a study which compared the time and sense
Dig Dis Sci (2012) 57:1445–1464
of satisfactory rectal emptying in three postures (sitting on
a Western standard commode; sitting on a similar com-
mode with a 10 cm stool under the subjects’ feet, effec-
tively lowering the height of the commode; and in the
squatting posture), it was found that evacuation was
quickest and afforded a more complete sense of bowel
emptying in the squatting posture and was most difficult on
the standard Western type commode [42]. As expected,
other studies have shown that evacuation is also easier
when sitting compared to lying [43, 44]. The latter of these
studies also showed, perhaps not surprisingly, that com-
pared to the sitting posture, the frequency of dyssynergia
(uncoordinated pelvic floor activity) during evacuation was
greater when lying down [44].
Influence of Colonic Transit, Volume, and Consistency
of Stool
Stool volume and consistency are directly related to gas-
trointestinal (GI) transit time [45]. Co-ordinated colonic
motor activity drives transit, and hence the rate at which
colonic contents are delivered to the rectum, as well as the
physical and chemical nature of the feces itself.
As a general rule (though not absolute), loose stools are
associated with rapid GI/colonic transit [46, 47] whereas
constipation may be associated with slow GI transit and
reduced motility [48]. Degen and Phillips, who assessed
transit in 32 healthy volunteers with scintigraphy and
radio-opaque markers [45], concluded that hard stools
correlated significantly with slower intraluminal movement
and loose stool with faster transit. Other studies have
reported that constipation may be associated with greater
levels of (uncoordinated) contractile activity in the pelvic
colon in comparison to patients with diarrhoea [49]. Intu-
itively, reduced colonic motor activity, and hence delayed
transit should allow greater water absorption from intra-
luminal contents, desiccating the stool, and reducing vol-
ume, resulting in harder motions that are more difficult to
expel. In a study investigating constipated children, Ben-
ninga et al. found a significant association between the
presence of a palpable rectal mass and a colonic transit
time of[100 h [50]; these children suffered from nocturnal
‘‘overflow’’ fecal soiling. Conversely, increased and co-
ordinated motor activity can deliver larger quantities of
more liquid fecal material into the rectum, which may
overpower the continence mechanism. In constipated
patients, stool form correlates well with whole gut [47] and
colonic transit [51]. In constipated subjects, a mean Bristol
stool form [47] of \3 (indicating hard stools, ranging from
pellet-like or ‘‘nuts,’’ to sausage- or snake-like, with cracks
on its surface) is specific and sensitive for the diagnoses of
delayed whole gut and colonic transit [51]. This relation-
ship may be absent in healthy individuals [51]. In contrast
1447
to stool form, frequency of defecation is poorly correlated
with whole gut or colonic transit [47, 51], in that true slow
transit is usually associated with infrequency, but frequent
bowel actions does not imply fast transit, i.e. a constipated
patient may revisit the toilet repeatedly [52]. Likewise, in
children, stool frequency has been shown to correlate with
total gastrointestinal transit time, but not all children with
prolonged transit have reduced bowel frequency [13].
Very few studies have compared the effect of stool
volume or form on evacuation. Bannister et al. demon-
strated that evacuation of small hard spheres mimicking
pellet-like stool required more effort (measured as longer
time and higher intrarectal pressures) than the expulsion of
a compressible 50 ml balloon, used as a surrogate of soft
stool [53]. In a more recent study [44], only 4% of subjects
were unable to expel a silicone stool-substitute in the sit-
ting position, while 16% were unable to expel a 50 cc
balloon. Moreover, balloon expulsion time was signifi-
cantly longer than expulsion of the stool substitute.
Influence of Diet and Intraluminal Contents
Ingestion of a meal is regarded as the most potent physi-
ological stimulus influencing colonic/gastrointestinal tran-
sit and motor activity. A meal-induced increase in colonic
motor activity is more pronounced in the transverse/
descending colon than the recto-sigmoid colon [54–56].
Studies performed around 30 years ago showed that overall
colonic response to a meal is excitatory and follows a
biphasic pattern, with a first peak of activity seen within the
first 10–50 min and a second peak occurring within 70 and
90 min of having a meal [57–59]. A fatty meal stimulates
colonic motor activity [54, 57, 58, 60] to a greater extent
than a carbohydrate-rich [54, 58] or a protein-rich meal
[58]. However, fatty meals also stimulate retrograde colo-
nic activity which may result in a net decrease in colonic
transit [54]. The stimulatory effect of a carbohydrate-rich
meal has a more rapid onset than that of a fatty meal [54]
but is shorter lived. Ingestion of a protein and amino acid-
rich meal actually inhibits colonic motor activity [58, 59].
Likewise, alcohol has been shown to have an inhibitory
effect on recto-sigmoid motility [61, 62]. Patients in whom
the colonic intraluminal contents have a high osmotic load
(e.g. bile salt malabsorption, lactose intolerance, etc.) have
a rapid colonic transit [63]. It should be noted that the
effect of dietary components on colonic motor functions
using contemporary methodologies (pancolonic manome-
try/scintigraphy) has not been reproduced.
Although it is generally agreed that an increase in die-
tary fibre intake is beneficial for constipation [64–66], there
have been concerns about the adverse effects of a high fibre
diet in children, including a resultant lowering of calorie
intake [67–69], increased fecal energy loss [66, 69], and
123
1448
decreased bioavailability of minerals [70]. Dietary fibre
intake can also lead to excessive gas formation resulting in
abdominal bloating and cramping, though it has been
reported that if fibre content in diet is increased gradually
rather than acutely, excessive gas formation can be reduced
[71].
Influence of Age and Gender
Age and gender are also known to effect evacuation [72];
epidemiological studies indicate that the incidence of
constipation is characterized by two peaks—one during
early childhood and the second after the age of 60–65 (see
below). In childhood constipation, one study has shown
that half of the affected children develop constipation
within the first year of their life [73], with transition from
breast milk to formula feeding being proposed as the
possible cause [74]. Other studies have reported a peak
incidence between 3 and 5 years [75–78]. The second
peak, occurring in geriatric patients [9, 79], has been var-
iously attributed to aging with consequent loss of tissue
elasticity [80], increased evidence of neuropathy with age
[81], pelvic floor weakness and laxity [81], reduced
mobility, polypharmacy [82], etc.
With regard to gender, incidence of childhood consti-
pation is reported to be similar between boys and girls [13,
83, 84], or slightly higher in boys [85]. However in adults,
constipation is much more common in women [3, 9, 79,
86]. It is not clear why this change occurs. However,
gender specific differences in pathophysiologic mecha-
nisms and the increased incidence of constipation in
association with pregnancy and delivery have been impli-
cated [85]. Colonic transit time is faster in males compared
to females [87, 88], and females are also more likely to
pass hard stools [3, 45], perhaps making them more sus-
ceptible to constipation [3]. Increased perineal descent,
reflecting a less supportive pelvic floor (likely a conse-
quence of parity), has been noted in elderly females com-
pared to younger females, and there is a decreased ability
among both sexes to evacuate 18-mm spheres with
advancing age [80]. Other possible causes for a female
preponderance in the adult population include the influence
of female hormones [3], the menstrual cycle [96–99],
parity and childbirth, pelvic floor function [100], and pelvic
surgery (e.g. hysterectomy) [89], but for the sake of brevity
will not be addressed in further detail.
Other Influences
There are several other important factors relating to
ability to defecate, not least intact cognition [90] and
mobility [91, 92], as evidenced by studies of the insti-
tutionalized [93], as well as fluid intake [90, 92], and
123
Dig Dis Sci (2012) 57:1445–1464
access to sanitation [94, 95]. Cultural and lifestyle fac-
tors are likely to have major influence, but obviously are
more difficult to study.
Circulating hormones (like somatostatin) and humoral
factors (like substance P, vasoactive intestinal peptide,
peptide YY, cholecystokinin, etc.) are also known to be
important as they can influence gastrointestinal motility
that underscores efficient defecation [101–106]. Sec-
ondary constipation is a well known consequence of
systemic disorders including diabetes, hypothyroidism,
hypercalcemia, several form of myopathies and neurop-
athies, etc.
Additionally, in patients with intractable constipation a
reduction in the number of interstitial cells of Cajal [107–
110], which are regarded as intestinal pacemakers [111,
112], morphological changes or reduction in number of
ganglia and/or glial cells [110, 113, 114], and an abnormal
nerve fibre density in the circular muscle layer [115] have
all been identified. The mechanistic significance of such
findings is however unclear.
Gaps in Our Knowledge
• The precise influence of psychobehavioral factors,
particularly according to underlying subject state or
trait;
• The force vectors that are endowed by changes in
posture, and that positively influence evacuatory
efficiency;
• Why colonic transit is longer in females;
• The influence of diet on colonic motor function using
contemporary methodologies;
• Why there is no gender specific difference in the
prevalence of constipation in children, yet constipation
is more prevalent in adult women.
The Phases of Defecation
The multiple factors that ultimately result in defecation
are best appreciated by describing four temporally and
physiologically fairly distinct phases: (1) the basal phase,
(2) a pre-defecatory phase, leading to generation of a
defecatory urge, (3) the expulsive phase, during which
evacuation occurs, and finally, (4) termination of defe-
cation (Fig. 1).
The Basal Phase
Prior to the events that specifically lead up to defecation, a
comprehension of normal colo-rectal motor functions, in
the absence of a desire to defecate, requires description.
Dig Dis Sci (2012) 57:1445–1464
Fig. 1 Flowchart to show the
principal events occurring
during defecation
Colonic Motor Activity
Colonic functions relevant to normal defecation include:
absorption of water from intraluminal contents, net ante-
grade propulsion of colonic contents at an adequate rate,
and temporary storage of feces until convenient to expel
them. After delivery of chyme from the terminal ileum into
the caecum, luminal contents are transported distally while
gradual desiccation and mixing occurs, making them pro-
gressively more solid [116]. This transport is facilitated by
complex colonic motility patterns.
Colonic motor activity shows a circadian pattern, in that
it increases after awakening [117] and is higher during the
day compared to the night [117–120]. Colonic activity also
increases after meals (see above) [117, 120, 121]. Patients
with constipation may lack the nocturnal suppression of
1449
colonic activity [122] and exhibit reduced colonic respon-
ses to food [122–125], as well as lacking spatio-temporal
organization of colonic contractile patterns [126].
Colonic motor functions can simplistically be subdi-
vided into ‘‘transit’’ (i.e. intra-luminal movement), mea-
sured clinically either by radio-opaque marker studies,
colonic scintigraphy, or more recently by wireless tele-
metric capsule methods [127–129], or ‘‘contractile activi-
ties,’’ the sum of which underlies the shift in intra-luminal
content. This is best measured by intraluminal manometry
[116]. Although colonic manometry remains a research
tool in adults, it been used to influence clinical manage-
ment in highly selected pediatric cases [130–133].
From transit studies the upper limit of normal colonic
transit time has been determined to be around 72 h in
adults [134]. Colonic transit is faster in children [12], being
123
1450
reported as less than 57 h [13, 135–137]. ‘‘Slow transit’’
refers to a clinical condition likely resulting from ineffec-
tive colonic propulsion. Abnormalities of colonic transit
are often expressed as segmental (right colonic, left colonic
or recto-sigmoid delay) or pan colonic in nature [138–140].
Colonic motor activity is characterized by brief (phasic)
contractions and also sustained (tonic) contractions (best
measured with a barostat) [127]. Phasic contractions are
further classified as propagating or non-propagating con-
tractions, or sequences, based on whether or not they
propagate along the colon. Non-propagated contractions
appear to be the most common event and can occur as
isolated, seemingly random contractions or in ‘‘bursts’’
[116, 118]. They have a frequency of between 2 and 4
cycles per minute [141] and an amplitude of between 5 and
50 mm Hg [117]. The duration of these contractions can
either be short (\15 s) or long (15–60 s) [116, 142, 143].
‘‘Bursts’’ of non-propagated pressure activity, lasting 3 min
or more can also occur [116]. These contractions can either
be rhythmic (occurring at frequencies of 2–3 cycles/min or
6–8 cycles/min) or arrhythmic [116, 118]. As a caveat, it
should be noted however, that the majority of colonic
manometries have been performed with recording sites
spaced 10 cm or more apart. A recent study using high
resolution manometry with 1 cm sensor spacing indicates
that manometric pressure patterns often propagate for less
than 10 cm [144], which indicates propagated activity may
have been previously ‘‘mislabeled’’ as non-propagated
[141]. Although the role of non-propagated activity in
luminal transport is not fully understood [141], it is thought
to aid mixing of intraluminal contents by local propulsion
[145, 146] and retropulsion [147] of the fecal bolus.
Propagated colonic activity can be retrograde (oral
propagation) or antegrade (aboral propagation). Retrograde
colonic activity is thought to be less frequent than ante-
grade activity [117, 122] and appears mostly confined to
the proximal colon [147]. The frequency of retrograde
propagated activity may be higher in patients with consti-
pation than in healthy individuals [122] indicating that the
ratio between retrograde and propagated contractile activ-
ity may be an important pathophysiological mechanism of
delayed colonic transit.
Among propagated sequences, there are sets of propa-
gated pressure waves that are distinct by virtue of their
elevated amplitude. These waves, known as high amplitude
propagated sequences (HAPSs; or contractions: HAPCs)
have been widely and variously defined [116, 148], but
typically have amplitudes [100 mmHg [147, 149, 150]. In
adults, HAPCs occur, on average, 5–6 times a day (range
2–24) [116], whereas the frequency of HAPCs is signifi-
cantly greater in children younger than 4 years of age [14],
which likely correlates to the increased number of bowel
movements in infants/toddlers. Although HAPCs can
123
Dig Dis Sci (2012) 57:1445–1464
originate anywhere in the colon, they do so mostly in the
proximal colon and then migrate distally for a variable
distance [117, 120, 121, 147]. The distance of propagation
correlates with the proximity of the site of origin to the
caecum [120, 121, 147]. One study found that only a third
of the HAPSs reached the anus, the remainder terminating
at the rectosigmoid region [117]. HAPSs are often tem-
porally associated with defecation [117, 148, 151] or
passing flatus [117]. They help in propulsion of the fecal
bolus [147] and are the manometric equivalent of ‘‘mass
movements’’ noted radiologically (i.e. a rapid shift of a
considerable volume of intraluminal content) [152, 153].
Frequency of HAPSs is often reduced in patients with
constipation [122–125, 140, 151, 154, 155], and this is the
most consistent motor abnormality described is such
patients.
The majority of the colonic propagated activity is
characterized by low amplitude propagated sequences
(PSs; or low amplitude propagated contractions: LAPCs).
These typically have amplitude \50 mmHg [156], occur
40–120 times in a 24 h period [117, 147, 157], and prop-
agate for distances \22.5 cm [121]. Studying the relation
between frequency of PSs and constipation, some authors
have found a reduced frequency in obstructed defecation
[122] and slow transit constipation [155]; others have
found no difference [151]. In healthy individuals, propa-
gating sequences display a spatio-temporal or ‘‘regional
linkage’’ (where two consecutive PSs, originating from
different colonic regions overlap) [120, 158]. The signifi-
cance of this finding lies in the fact that although a single
PS does not span the entire length of the colon, a series of
‘‘regionally linked’’ PSs can. This linkage has been found
to be absent in patients with constipation [126, 158].
The sigmoid colon primarily exhibits cyclical bursts of
contractions (though they occur throughout the rest of the
colon also), called motor complexes (MC) or ‘‘periodic
colonic motor activity’’; these may be important in mod-
ulating the delivery of fecal material into the rectum. These
MCs typically have amplitudes of 15–60 mm Hg, last
3–30 min, and recur at 80–90 min intervals [159]. By
conventional manometry, up to 70% of these are non-
propagating, approximately 18% propagate aborally, and
15% migrate orally [117]. Another feature of the sigmoid is
that when distended, it contracts, with concomitant relax-
ation of the recto-sigmoid junction; this mechanism likely
facilitates progression of feces into the rectum [160]. The
presence of a sphincter between the sigmoid and the rectum
(the recto-sigmoid sphincter of O’Beirne) [161] has long
been debated. Although the evidence of a convincing
anatomical sphincter is lacking, a high-pressure zone with
unique contractile properties (in response to sigmoid and
rectal distension/contraction) has been shown in the distal
sigmoid, which supports the idea of a physiological
Dig Dis Sci (2012) 57:1445–1464
sphincter [161–164]. The role of the recto-sigmoid junction
in normal defecation is still unclear. However, it is inter-
esting to note that many severely constipated patients have
an empty rectum on rectal examination [165, 166].
Rectal Motor Activity
Rectal motor activity, like the sigmoid, is characterized by
recurrent motor complexes. The frequency of rectal MCs
appears unaffected by meal intake [117]. The role of these
motor activities is not fully understood [141]. However,
rectal MCs are seen to propagate in a retrograde direction
[167]; it has thus been postulated they help to keep the
rectum empty by acting as a ‘‘braking mechanism’’ to
untimely flow of colonic contents [167]. It has been pro-
posed that MC activity may be used as a marker of enteric
neuromotor function as their presence is independent of
intact extrinsic innervation [116, 159, 168]. In healthy
volunteers, during the basal phase, the rectum remains
mostly empty [169] or can contain a variable amount of
feces without conscious awareness [170].
Pelvic Floor and Puborectalis Activity
At rest, the levator ani, the puborectalis, and the external anal
sphincter remain in a state of continuous contraction. This
reflex is known as the postural reflex [171] and it helps to
support the weight of the pelvic viscera. The reflex is main-
tained through the lower lumbar and sacral spinal cord [171].
In relation to defecation, among the pelvic floor mus-
cles, the puborectalis is probably the most relevant. It
originates from the posterior surfaces of the pubis, passes
around the anorectal junction inferolaterally, and decus-
sates with its fibers from the opposite side to form a sling
behind the anorectal junction. The puborectalis derives its
nerve supply from direct branches of the anterior roots of
S3 and S4 [63, 172–174].
At rest, the contractile traction of puborectalis maintains
the anorectal angle (angle between the long axis of the
rectum and the long axis of the anal canal) at approxi-
mately 90 [175]. While this angulation helps in preser-
vation of continence [176], increased acuity has been
related to obstructed defecation [177, 178].
Anal Canal Activity
At rest, the anal canal remains closed to preserve conti-
nence. The anal sphincter complex is extremely dynamic
and is influenced by a variety of reflexes and modulation by
higher centers in such a way that rather than acting as a
passive barrier, it provides an airtight seal at all times
except when the subject wants to pass flatus or defecate
[179].
1451
The anal canal is normally closed by the tonic activity of
the internal and external anal sphincters, together with the
anal cushions. The internal anal sphincter (IAS) is chiefly
responsible for continence at rest [180], and is predomi-
nantly composed of slow-twitch, fatigue-resistant smooth
muscles. Electromyographic study of the IAS demonstrates
a constant activity at rest [181–183], which is unaffected
by respiration or administration of a general anaesthesia
[184]. The contribution of the IAS to anal canal tone is
debated, but has been reported as being as much as 85% at
rest, 65% during constant rectal distension, and 40% after
sudden rectal distension [185]. Other studies estimate a
lesser influence, in that approximately 55% of resting anal
tone is due to IAS activity [186]. The external anal
sphincter is also in a state of constant tonic activity at rest
[187], and this generates approximately 30% of the basal
resting anal tone [186]. The anal vascular cushions,
including the superior hemorrhoidal plexus, contribute to
approximately 15% of the resting anal tone [186], but
importantly provide the ‘‘hermetic seal’’ which cannot be
achieved by sphincteric muscle tone alone.
Integral to the dynamic nature of anal canal activity is
the intermittent, transient relaxation of the internal anal
sphincter, which allows descent of distal rectal contents
into the upper anal canal, endowing a subconscious or
conscious perception of their physical nature. This so-
called sampling reflex occurs approximately seven times
per hour [188] in healthy control subjects, but less fre-
quently in patients with incontinence [189]. This reflex can
be reproduced under laboratory conditions, where rectal
distension causes reflex relaxation of the internal anal
sphincter (in this case know as the ‘‘recto-anal inhibitory
reflex’’: RAIR), as well as contraction of the external anal
sphincter.
In vivo, the consequence of the sampling reflex is a drop
in upper anal canal pressure, so that rectal pressure
becomes greater than or equal to mid anal pressure [188].
Lower anal canal pressure, however, remains virtually
unchanged [190], and overall, maximal intra-anal pressure
remains higher than intra-rectal pressure to preserve con-
tinence [191]. The net effect of this pressure change is to
briefly expose the anal sensory area to the rectal contents so
that sampling can occur [188, 190]. The reflex is controlled
by the enteric nervous system [180, 192, 193], with a
degree of regulation from the sacral cord [192], and is
absent in patients suffering from Hirschsprung’s disease
[194].
The anal canal epithelium is lined by highly sensitive
nerve endings derived from sensory, motor and autonomic
nerves, in addition to the enteric nervous system [63]. The
anal sensory area contains specialized sensory end organs,
including Krause end bulbs, Golgi Mazzoni bodies, genital
corpuscles, Meisnner’s corpuscles, and Pacinian corpuscles
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1452
[195]. It is important to note, however, that this informa-
tion was derived from studies performed over 50 years ago,
using techniques which may now be regarded as outdated.
Few other data are available. Slowly adapting afferents that
remain silent in basal conditions, but are sensitive to cir-
cumferential stretch, exist in the IAS of guinea pigs [196].
Lynn et al. also demonstrated that in guinea pigs, rectal
nerve axons to the IAS predominantly end in extensive
varicose arrays within the circular muscle [196]. Mecha-
notransduction sites were strongly associated to these
varicose arrays [196].
Gaps in Our Knowledge
• Manometric methods for studying pancolonic motor
activity have thus far been suboptimal. The use of high
resolution manometry may unravel the complexity of
motor activities present in the human large intestine;
• The physiological function of motor complex activity;
• The existence or not of a true recto-sigmoid sphincter
and how this regulates movement into the rectum;
• The contributions of feedback reflexes to normal (and
abnormal) motor functions;
• Characterization of human anal sensory receptors and
afferent pathways.
The Pre-Expulsive Phase
During this phase, specific motor events occur, which
culminate in an awareness by the subject of an urge to
defecate, the ‘‘call to stool.’’
Origin of the Defecatory Urge
In order to achieve normal defecation, the importance of a
defecatory urge cannot be overemphasized. The voluntary
process involved in defecation starts with a sensation of
‘‘call to stool.’’ Although our knowledge on the origin of
this urge has increased significantly in the last few decades,
the precise location of the receptors responsible and con-
tribution of the organs involved are still debated. It is likely
that the colon, rectum, anus, extra-rectal tissue, and the
puborectalis may all contribute to varying degrees (see
below).
Role of the Colon
In healthy subjects, there is a close relationship between
HAPSs and urge to evacuate, a relationship that is often
absent in patients with constipation [197]. In one study in
volunteers, it was shown that out of 27 instances of per-
ceived urge to defecate, 26 were associated with a
123
Dig Dis Sci (2012) 57:1445–1464
propagated sequence, of which 62% were associated with
HAPSs [121]. This study also showed that propagated
sequences were more likely to result in urge during the 1 h
pre-expulsive phase (as compared to the basal phase), and
that sequences that propagated further were more likely to
result in an urge. During the pre-expulsive phase, propa-
gated sequences often start as unperceived colonic con-
tractions in the proximal colon, and migrate distally while
increasing in amplitude to become a ‘‘full blown’’ HAPS,
that is then associated with an urge to defecate [148]. It is
feasible that increased colonic activity seen during the pre-
expulsive phase leads to movement of colonic contents
distally, which in turn stimulates distal colonic afferents (or
indeed perhaps rectal) [148], possibly by distension,
resulting in sensory perception. However, balloon disten-
sion of the colon in healthy individuals typically results in a
colicky or ‘‘windy’’ pain rather than the usual defecatory
urge [198, 199]. Goligher et al. reported that performing
balloon distension of the terminal colonic segment in
patients with colostomies typically resulted in periumbili-
cal or suprapubic pain rather than the typical ‘‘rectal-type’’
sensation associated with an urge to defecate [199].
Role of the Rectum, the Pelvic Floor, and the Extra-Rectal
Tissues
The rectum is regarded as the primary site of origin of the
defecatory urge. Gradual distension of the rectum produces
a graded sensory response starting with an initial awareness
of filling [200]. With continued distension, this is followed
by a constant sensation (likened to the desire to pass wind)
that is replaced by a sustained urge to defecate, and finally
by a sense of discomfort and an intense urge to defecate as
the maximal tolerable volume/pressure is reached [201–
203]. Rectal-type sensation similar to a desire to defecate
can be elicited by distension of the bowel up to 15 cm from
the anal verge, whereas distension above this level typi-
cally leads to a colonic-type sensation similar to wind pain
or suprapubic pain [199]. In patients with residual rectum
following colectomy (and colorectal anastamosis), balloon
distension below the suture line results in a normal defe-
catory urge [199]. In another surgical study, following a
unique procedure in which the anorectum was mobilized
on its neurovascular pedicle and transposed to the anterior
abdominal wall to preserve intestinal length in patients
with short bowel syndrome, balloon distension through an
abdominal wall stoma provoked sensation of pelvic filling
[204].
In support of an extra-rectal origin of urge sensation, it
has been shown that defecatory desire can be provoked by
stimulating nerve endings and stretch receptors in pelvic
floor muscles including the puborectalis, and from struc-
tures adjacent to the rectum [205]. It has also been shown
Dig Dis Sci (2012) 57:1445–1464 1453

that anesthetizing the rectal wall with Lignocaine has no

effect on perception if rectal distension is rapid (although
the threshold for perception is increased if distension is
gradual) [206]. Additionally, in patients following rectal
excision and colo-anal anastamosis, it has been observed
that a sense of impending defecation is preserved [207,
208]. A study of filling sensations in patients who had
undergone restorative proctocolectomy with pouch-anal
anastamosis concluded that neorectal filling thresholds
were comparable to normal individuals [203]. However,
the nature of sensation in these patients appeared different
from their sense of call to stool prior to surgery [199, 207,
208]. This led Abercrombie et al. [209] to suggest that the
receptors are likely located in the rectal wall and that after
rectal excision, patients adapt to new sensations and
associate them to a sense of impending defecation.
In summary, based on these observations, it can be
concluded that both the rectum and the pelvic floor have a
role in the generation of normal filling sensation, and also
in the urge to defecate.

Role of the Anal Canal

Although intact anal canal sensation is essential for

‘‘sampling’’ of fecal contents, whether it directly contrib-
utes to the generation of a defecatory urge is unclear.
Golligher et al. studied the nature of defecatory urge in
healthy volunteers and in a series of patients who had
undergone colectomy with a variable length of anorectum
left in situ [199]. In healthy volunteers, inflation of a bal-
loon in the anal canal led to a sensation of stool escaping
from the anus rather than a typical defecatory urge. This
work also showed that in patients with a colo-anal anas-
tomosis, where the anal canal distal to the mucocutaneous
junction was preserved, balloon distension most commonly
elicited a sense of ‘‘wind’’ or perineal or sacral discomfort,
and rarely a very vague sensation akin to rectal stimulation
[199]. Thus the anus informs the subject in a direct somatic
way of the contents impinging upon it.
Colonic Motor Activity (Up to 1 h Before Defecation)
During the pre-expulsive phase, there is a distinct change
in colonic motor activity characterized by a progressive,
time-dependent increase in the frequency and amplitude of
propagated sequences [148, 197]. This is absent in con-
stipated patients (Fig. 2) [122, 197]. Between 60 and
15 min before defecation, there is distal shift in the site of
origin of PSs, which move from the transverse colon or
splenic flexure towards the descending colon [148, 197].
However, this pattern reverses in the final 15 min preced-
ing defecation, when a retrograde shift in the site of origin
of PS occurs (Fig. 2) [120, 148, 197]. Little is known about
Fig. 2 Pancolonic manometric tracings during defecation. In a
healthy volunteer (a), stool expulsion is preceded by several PSs.
The site of origin of each subsequent PS is seen to originate from a
site more proximal than the preceding sequence. Such activity is
absent in a constipated patient (b). (Kindly reproduced with
permission from Gastroenterology 2004;127:49–56) [197]
the initiating stimulus, mechanism, or function of this
organized migration in the site of origin of these PSs, but it
has been hypothesized that it may be due to the effect of
long colo-colonic reflex pathways [148]; during the initial
phase of antegrade migration, movement of luminal con-
tents distally may stimulate distal colonic afferents, which
in turn may initiate progressively retrograde PSs as well as
a sensation of urge [148].
Rectal Sensorimotor Activity
During this phase, rectal filling occurs. Impaired (blunted)
perception of rectal distension, or rectal hyposensitivity, is
often associated with an attenuated ‘‘call to stool’’ and
constipation [16, 210–213], with or without overflow
incontinence [201, 214–217]. Conversely, rectal hyper-
sensitivity, reflecting increased perception of distension, is
associated with a heightened sense of urge, allied to fecal
urgency, with or without incontinence [218–221].
Responding appropriately to the ‘‘call to stool’’ appears
fundamental to normal defecation. Furthermore, normal

123
1454
functioning of rectal afferent nerves and normal rectal wall
biomechanical properties appear critically important for
perception of rectal fullness and ultimately a defecatory
urge [222]. It is postulated that habitual suppression of the
defecatory urge may lead to attenuation of the call to stool
resulting in rectal fecal impaction and secondary dilation,
potentially culminating in a megarectum [223–226]. Nev-
ertheless, the clinical importance of impaired peripheral
sensations in children has been questioned [30]. Although
earlier studies reported that larger rectal distension vol-
umes were needed to trigger rectal sensation in constipated
children [227, 228], more recent studies found no differ-
ence in sensory function in children with functional con-
stipation when compared to healthy volunteers [229, 230],
although rectal compliance (stretch response to an imposed
force) was greater (i.e. the rectum was more lax) in con-
stipated individuals. Alternatively, megarectum may be
secondary to other disordered neuromuscular dysfunctions
[231–233]. Whether idiopathic megarectum is a primary or
secondary phenomenon is unknown [223], but it is likely
that psychological [234], behavioral, and neurophysio-
logical factors may all play a part [223].
In consideration of the perception of rectal filling, it has
been postulated that in vivo, the incoming fecal bolus, likely
transported by PS activity, deforms the rectal wall, altering
stress and strain, and thus activating mechanoreceptors that
then induce reflex rectal contractions [235, 236]. The
amplitude of the rectal contraction increases with higher
rectal volumes [191]. It has been proposed in some studies
that rectal sensation does not occur unless accompanied by
rectal contractions [201, 237]. Furthermore, the duration of
rectal contractile activity correlates well to the duration of
rectal sensation [201]. Reduced rectal contractility has been
reported in constipated patients [165, 238]. Rectal sensation,
and by implication contraction of the rectum, is also an
important determinant of reflex external anal sphincter con-
traction [201], and hence maintenance of continence [239].
In order to evaluate whether volume, pressure or weight
of rectal contents provides the main trigger for rectal sen-
sation, Broens et al. compared the sensation generated by
inflating a rectal balloon with 60 ml of air, water, and
mercury [202]. The study demonstrated a constant rela-
tionship between level of rectal sensation and the pressure
in the rectal balloon. Sensation levels were independent of
both the weight and the volume of the rectal contents. They
concluded that rectal sensation is sensitive to intrarectal
pressure changes which triggers tension-activated stretch
receptors [202]. However more recent studies suggest that
rectal wall deformation rather than intrarectal pressure is
the direct stimulus, since mechanoreceptors are stimulated
by circumferential strain and shearing forces that cause
deformations in rectal wall morphology [240–242], which
may be secondary to intraluminal pressure changes [242].
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Dig Dis Sci (2012) 57:1445–1464
Our understanding of the morphology of visceral affer-
ent nerve endings potentially responsible for generation of
rectal sensation is far from complete [243], and most of our
knowledge is based on animal studies. In the myenteric
ganglia of the guinea pig rectum, specialized nerve termi-
nals with branched, flattened lamellar endings, called rectal
intraganglionic laminar endings (rIGLEs), have been
identified as mechanotransduction sites of low threshold,
stretch-sensitive mechanoreceptors [244, 245]. Their den-
sity decreases significantly proximally along the distal gut
[244]. Functionally, rIGLEs are probably independent of
the enteric nervous system since they have been shown to
function normally in the rectums of piebald lethal mice
devoid of any enteric ganglia [246]. In addition, medium-
to-high threshold mechanoreceptors sensitive to local
compression and stretch are present in close association
with intramural and extramural blood vessels of major
viscera including the colon [247].
It has been shown that rectal sensation is preserved after
bilateral pudendal nerve block [185, 248]. However, low
spinal anaesthesia (L5–S1) abolishes rectal sensation,
which is then perceived only as a vague abdominal dis-
comfort at higher levels of rectal filling. Rectal sensation,
including abdominal discomfort, is fully abolished by high
spinal anaesthesia (T6–T12) [249]. This shows that the
sacral outflow plays a key role in the perception of rectal
sensation while the thoracolumbar outflow has a lesser role.
It has also been shown that the sense of rectal distension is
impaired in patients with bilateral excision of sacral nerve
roots (preserving S1–2 bilaterally) [250]. The importance
of the lower sacral cord and the S3 nerve root in particular
is emphasized by the preservation of bowel and bladder
function by preserving at least one S3 nerve root during
sacral resection [251].
Current neuroanatomical thinking indicates that spinal
afferents travel in parallel with the sympathetic and sacral
parasympathetic pathways from the rectum, in nerves
passing in the lateral ligaments, through the pelvic plexus
and the pelvic splanchnic nerves (nervi erigentes) to reach
the sacral segments of the spinal cord, with the majority of
the sensory information entering the S3 and S4 nerve roots
[250, 251]. However, a proportion of rectal sensory infor-
mation is conveyed via lumbar afferents which run from
the inferior mesenteric ganglion into the hypogastric
nerves, down through the pelvic ganglia, entering the rec-
tum via the rectal nerves. This pathway is probably
responsible for the perception of abdominal discomfort
associated with rectal distension [249].
Integrity of afferent neuronal pathways can be assessed
using cerebral evoked potentials [252, 253] whereas
efferent pathways can be evaluated using motor evoked
potentials [254]; alterations have been suggested in patients
with colorectal dysfunction. By measuring cerebral evoked
Dig Dis Sci (2012) 57:1445–1464
potentials in response to rectal balloon distension, Loening-
Baucke et al. found that children with chronic constipation
and encopresis have significantly prolonged latencies sug-
gestive of a defect in the afferent pathway from the rectum
[255]. Other than integrity of the afferent pathway, evoked
potentials may also depend on the degree of stimulation
from surrounding structures [253], the differences in cor-
tical neuronal orientation or volume, the state of myelina-
tion of the nerves, and type and diameter of nerve fibers
constituting the pathway [256].
In addition to rectal afferent nerve function, rectal wall
biomechanical properties are central to governing rectal
sensitivity. The healthy rectum is compliant, i.e. it can
accommodate increases in volume with little change in
pressure [174]. This allows the rectum to distend in
response to incoming fecal material, a phenomenon known
as adaptive relaxation [257], which enables it to serve as a
temporary storage organ (i.e. its ‘‘reservoir’’ function).
Rectal distensibility depends on both passive and active
properties of its walls [258]. Passive mechanical distension
(stress relaxation) depends on the viscoelastic properties of
the rectal wall [259], which is influenced by its collagen
content and the state of contraction of the smooth muscle
fibers within it [231, 240]. Active distension occurs by
adaptive relaxation [257], which is influenced by neuron-
controlled smooth muscle relaxation [258]. It is also
influenced by the properties of the extrarectal tissues [260].
In healthy subjects, gradual balloon distension causes an
initial phase of rapid increase in rectal cross-sectional area,
followed by a slow increase until a steady state is reached
[261]. Circumferential rectal wall tension shows a linear
increase, and rectal compliance a non-linear decrease with
increasing distension pressure [261]. If the distending
stimulus persists, it is possible that the rectal wall may
continue to relax [262], to an extent that a loss of urge to
defecate occurs [263].
In studying a group of patients with constipation and
rectal hyposensitivity to simple balloon distension,
Gladman et al. found that a subgroup of these patients
had increased rectal capacity and/or compliance (i.e.
excessive laxity) with normal rectal mucosal electro-
sensitivity (used as a direct measure of afferent nerve
function), while another subgroup had normal wall bio-
mechanical properties, but a significantly elevated rectal
mucosal electrosensitivity threshold [241, 257]. Thus
hyposensitivity can result from: (a) abnormal rectal wall
properties where afferent nerve function may be intact
(i.e. a secondary disorder due to inadequate stimulation)
or (b) from impaired afferent function (i.e. a primary
disorder) [222], which can occur at any level of the
pathway from receptor to higher centers of the central
nervous system [222].
1455
Pelvic Floor Activity
As in the basal phase, the pelvic floor continues to remain in a
state of continuous contraction, thus preserving continence.
When a defecatory urge occurs, and if defecation is not con-
venient, the external anal sphincter and the pelvic floor muscles
including puborectalis can be further voluntarily contracted
[171, 199]. This increases the acuity of the anorectal angle,
elevates the pelvic floor, and lengthens the high pressure zone
of the anal canal [264]. Whether such activity actually results in
retropulsion of rectal contents into the sigmoid is unknown.
Anal Canal Activity
Whether there is a change in frequency (or characteristics)
of the sampling reflex during the pre-expulsive phase is
unknown. However, personal human experience teaches
that with increased rectal filling, there is increased anal and
conscious awareness of intra-luminal contents. Broens
et al., who studied anal canal relaxation allied to rectal
filling sensation, showed that at a filling volume which
elicited a constant sensation, the upper anal canal diameter
was 3.2 cm, which increased to 4 and 4.4 cm at urge and
maximum tolerable volumes, respectively [265]. Thus,
with increasing rectal filling, the voluntary muscles acting
to preserve continence (i.e. occlusion of the distal anal
canal) play an increasingly important role.
Gaps in Our Knowledge
• The relative contributions of the different organs/
structures involved in generation of a defecatory urge;
• Understanding the relationship between rectal contrac-
tile activity and rectal sensation;
• Characterization of the nerve endings responsible for
generation of human rectal sensation;
• The process of rectal filling from the sigmoid—bolus or
piecemeal—and what governs this;
• Mechanisms responsible for change in colonic motor
activity.
The Expulsive Phase
Facilitated by the sampling reflex, and in the presence of a
defecatory urge, if a conscious decision to evacuate is
made, rectal contents and a variable quantity of colonic
contents are evacuated during this phase. Efficacy of
expulsion may be influenced by additional voluntary
straining and assumption of an appropriate posture. The
final common path is effected by an elevation in intra-
rectal pressure and relaxation of the pelvic floor and anal
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1456
canal. Even in the healthiest of subjects, it is important to
note that voluntary suppression of defecation may be
overcome according to physical nature and volume of the
stool.
Colonic Activity
During defecation, a variable portion of the colon, as well
as the rectum, empties [266]. A scintigraphic study of
defecation in 11 healthy volunteers showed that the mean
percentage of segmental evacuation was: right colon 20%,
left colon 32%, and rectum 66% [266]. In healthy adults,
35–40% of all HAPSs in a day occur during or immedi-
ately preceding defecation [117, 126], and virtually all
episodes of defecation are associated with HAPSs [121,
267]; this is compatible with the radiological concept of
mass movement [152, 153]. Performing simultaneous
scintigraphy and left colonic and anal manometry during
defecation in a healthy volunteer, Kamm et al. showed an
equivalent propulsive pattern to swallowing, i.e. colonic
(c.f. oesophageal body) peristaltic wave with simulta-
neous anal (c.f. lower oesophageal) sphincter relaxation
[268].
Rectal Activity
In order for rectal contents to be evacuated, intra-rectal
pressure must exceed anal canal pressure. Normal defeca-
tion is thus associated with an increase in intra-rectal
pressure [269, 270] and a necessary relaxation of the anal
canal resulting in decreased anal pressure. Straining during
evacuation raises intra-pelvic and hence intra-rectal pres-
sure. Intuitively, simultaneous rectal contractions would
likely augment evacuation, but whether this is true or not
has not been clearly demonstrated [141]. One group
reported no appreciable rise in intra-rectal pressure in
relation to intra-pelvic pressure during evacuation [271]
and suggested that evacuation is not accompanied with
rectal contraction. Others have suggested that the rectum
can contract during evacuation [272]. It is probable that
evacuation is effected by both voluntary straining and
cooperative colorectal contractions; the relative contribu-
tion of each likely depends on circumstances, such as
volume and consistency of the stool [273], and behavioral
and cultural influences (including the timing of attempted
defecation in relation to onset of the defecatory urge). One
study showed that subjects who displayed stronger rectal
contractile activity in response to rectal filling needed to
strain less and had larger amplitude rectal contractions
during evacuation (rectal-contraction-type evacuators), in
contrast to strain-type evacuators, in whom rectal con-
tractile activity during filling and during evacuation were
proportionally less [272].
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Dig Dis Sci (2012) 57:1445–1464
Pelvic Floor Activity
During this phase, there is reflex inhibition of pelvic floor
tonic activity [274]. How this is mediated is not entirely
clear. Muscle spindles have been found in the human
pelvic floor [275], and it has been suggested that increased
abdominal pressure (stretch stimulus), although initially
excitatory to the pelvic floor, becomes inhibitory when
prolonged beyond a critical level [171]. More recently it
has been suggested that higher centers modulate pelvic
floor reflex pathways, and that there may be a ‘‘gating
mechanism’’ that allows or prevents stimuli from various
sources (like increased intra-abdominal pressure, pelvic
organ distension, etc.) to excite or inhibit the motor neu-
rons [274]. Adequate pelvic floor relaxation is essential for
effective evacuation, failure of which is a recognized cause
of disordered defecation (i.e. pelvic floor dyssynergia, or
dyssynergic defecation) [231, 264, 270, 276, 277]. Relax-
ation of the pelvic floor coupled with high intra-abdominal
pressure causes it to descend [178], assuming a funnel
shape with the tip of the funnel located at the anorectal
junction. The anorectal angle straightens due to relaxation
of the puborectalis part of the pelvic floor; such straight-
ening of the angle is also helped by the posture assumed
during defecation, which usually involves a degree of hip
flexion.
Anal Canal Activity
During the expulsive phase, anal canal relaxation occurs.
Inadequate relaxation of the anal sphincter is also a rec-
ognized cause of pelvic floor dyssynergia [231, 270, 276,
278], seen in both adults and in children. It has been sug-
gested that infants with constipation fail to coordinate the
increased intra-abdominal pressure with adequate pelvic
floor relaxation [279]. In fact they may even inappropri-
ately contract their external anal sphincter during defeca-
tion [227, 280–282]; whether this behavior is primary or
secondary to chronic fecal retention is unclear. Dyssyner-
gic defecation is often screened by the balloon expulsion
test. A study by Loening-Baucke et al. reported that
chronically constipated children who were unable to expel
a rectal balloon were less likely to recover after conven-
tional laxative treatment [280]. In a separate study, bal-
loons of 30, 50, and 100 ml were used, and it was reported
that failure to expel the 100 ml balloon (but not smaller
volume balloons) within 1 min correlated with treatment
failure [281]. Another study by the same group found that
children with functional constipation and encopresis who
were able to expel the rectal balloon were twice as likely to
respond to treatment [283]. Nevertheless, the ability of the
balloon expulsion test to predict response was only slightly
better than by chance [283].
Dig Dis Sci (2012) 57:1445–1464
Internal anal sphincter relaxation occurs involuntarily in
response to rectal distension and the relaxation is propor-
tional to the intra-rectal pressure [180, 182]. After assum-
ing a posture convenient for defecation, the subject strains
by contracting the abdominal muscles and diaphragm
against a closed glottis (Valsalva maneuver). This is
associated with relaxation of the external anal sphincter. It
has been suggested that the levator plate (that inserts into
the posterior aspect of the rectum) and the longitudinal
muscles of the anus contract simultaneously during evac-
uation. The resultant force vector is directed posteriorly
and downwards resulting in the opening of the anorectal
angle [284] (Fig. 3). This is facilitated by contraction of the
pubococcygeus muscle that ‘‘splints’’ the perineal body,
effectively tensing the anterior wall of the anal canal,
allowing only the posterior wall to move backwards [284].
Contraction of the conjoint longitudinal muscles of the
anus also causes flattening of the anal vascular cushions
[285] and shortening of the anal canal [141]. The incoming
fecal bolus possibly further flattens the vascular cushions
by direct compression [285]. All these changes, occurring
simultaneously, decrease the anal canal pressure to a value
lower than the intrarectal pressure resulting in a pressure
gradient from the rectum to the outside. Expulsion occurs
and continues due to high intra-rectal pressure, augmented
by straining. It has been postulated that once defecation
starts, sensory input from the anus maintains the propulsive
activity until the rectum is empty [101, 286]. This is
probably due to a spinal reflex since rectal emptying, once
initiated, is nearly complete even in patients with spinal
injury [286].
Gaps in Our Knowledge
• The contribution of colonic and rectal contractile
activities to fecal expulsion;
• Mechanism of modulation of the postural reflex, with
pelvic floor contraction in response to increased intra-
Fig. 3 Normal evacuation
proctogram images during
defecation. At rest (a), the
posterior anorectal angle (dotted
white line) measures 100; the
level of the anorectal junction
(ARJ) is marked by the solid
black line; and the site of the
closed anal canal (AC) is
represented by the white arrow.
During expulsion (b), the
anorectal angle opens to 178,
the anorectal junction descends,
and the anal canal opens
1457
abdominal pressure during coughing, but relaxation to
the same stimulus during evacuation;
• Modeling of the colo-recto-anal force vectors generated
during evacuation;
• How ‘‘full’’ opening of the anal canal is effected—
passive stretching, active relaxation or both;
• The relative contributions of voluntary and involuntary
components to active defecation, and whether these
simply reflect behavioral differences (e.g. responding
appropriately to the call to stool, or going by routine).
Termination of Defecation
This phase begins under semi-voluntary control (the
sense of complete rectal emptying, with cessation of
those maneuvers aimed at increasing intra-pelvic pres-
sure), and thence by involuntary contraction of the
external anal sphincter and pelvic floor, which closes the
anal canal and reverses the pressure gradient towards the
rectum. When traction is applied to the anus and then
released (likened in vivo to passage of stool), the
external sphincter shows a momentary increase in
activity that tends to close the canal. This reflex is
known as the ‘‘closing reflex’’ [141, 171, 174, 287] and
is important at the end of defecation to provide the
internal sphincter, which is no longer inhibited by rectal
distension, time to recover its tone [287]. This reflex
seems to be cortically modulated since it is impaired in
patients with spinal injury [171]. Once straining ceases
and intra-abdominal pressure falls, the postural reflex in
the pelvic floor is reactivated [171], resulting in con-
traction of the puborectalis which increases its traction
on the anorectal junction, returning the angle to its basal
state. Simultaneous relaxation of the conjoint longitudi-
nal muscle elongates the anal canal and allows the anal
cushions to passively distend, resulting in full closure of
the anal canal.
123
1458
Summary
Defecation, akin to continence, is a complex event that is
influenced by a number of conscious and subconscious
processes. The contribution of higher center influences is
perhaps best exemplified by the contrasting defecatory
habits of man and higher mammals, in whom a socially
convenient time and place for the act predominate, over
lower species in whom such habits are absent. Although
defecation may be divided into various phases, and the
various components contributing to those phases identifi-
able, understanding of the coordinated interplay between
brain, spinal cord, peripheral nerves, and end organs
(colon, rectum, anus, and extraintestinal pelvic muscles)
remains limited. Our knowledge of motor activity in par-
ticular has seen major advances recently, but there remain
significant gaps in our understanding of other processes
(see above). Research into combined modality assessment
under ideal physiological circumstances is fundamental to
further comprehension of evacuatory function and dys-
function which, along with other ‘‘functional bowel dis-
eases’’ have significant impact on quality of life.
Conflict of interest None.
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