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

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

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

123

Dig Dis Sci (2012) 57:1445–1464

DOI 10.1007/s10620-012-2071-1

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

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

1446 Dig Dis Sci (2012) 57:1445–1464

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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

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

Dig Dis Sci (2012) 57:1445–1464 1447

123

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

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.

1448 Dig Dis Sci (2012) 57:1445–1464

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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

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

Fig. 1 Flowchart to show the

principal events occurring

during defecation

Dig Dis Sci (2012) 57:1445–1464 1449

123

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

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

1450 Dig Dis Sci (2012) 57:1445–1464

123

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].

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

Dig Dis Sci (2012) 57:1445–1464 1451

123

[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

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

1452 Dig Dis Sci (2012) 57:1445–1464

123

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

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

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]

Dig Dis Sci (2012) 57:1445–1464 1453

123

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].

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

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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].

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

Dig Dis Sci (2012) 57:1445–1464 1455

123

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].

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].

1456 Dig Dis Sci (2012) 57:1445–1464

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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-

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.

Fig. 3 Normal evacuation

proctogram images during

defecation. At rest (a), the

posterior anorectal angle (dottedwhite line) measures 100�; the

level of the anorectal junction

(ARJ) is marked by the solidblack 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

Dig Dis Sci (2012) 57:1445–1464 1457

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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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