Endosonographic anatomy of the anal canal

77 Pages·2017·5.7 MB·English

Endosonographic anatomy of the anal canal:
In 1992 Tjandra et al. have performed elegant post-mortem and clinical studies and have identified the
anatomic layers that correspond to the anal ultrasound images. Bartram confirmed these studies in 2008
(Tjandra et al., 1992; Bartram, 2008). On ultrasound, five hypoechoic and hyperechoic layers can be seen
in the normal anal canal (Fig. 1). The ultrasonographer must have a clear understanding of what each of

these five layers represents anatomically (Santoro and Di Falco, 2006).
a b

Fig. 1: Normal ultrasonographic five-layer structure of the mid-anal canal.
a Axial image obtained by 2050 transducer (B-K Medical). b Schematic representation. (Santoro and Di Falco, 2010).

 The first hyperechoic layer, from inner to outer, corresponds to the interface of the transducer with
the anal mucosal surface.
 The second layer represents the subepithelial tissues and appears moderately reflective. The mucosa
as well the level of dentate line is not visualized. The muscularis submucosae ani can be
sonographically identified in the upper part of the anal canal as a low reflective band.
 The third hypoechoic layer corresponds to the internal anal sphincter (IAS). The sphincter is not
completely symmetric, either in thickness or termination. It can be traced superiorly into the circular
muscle of the rectum, extending from the anorectal junction to approximately 1 cm below the dentate
line. In older age groups, the IAS loses its uniform low echogenicity, which is characteristic of
smooth muscle throughout the gut, to become more echogenic and inhomogeneous in texture (Starck
et al., 2005).
 The fourth hyperechoic layer represents the longitudinal muscle (LM). It presents a wide variability in
thickness and is not always distinctly visible along the entire anal canal. The LM appears moderately
echogenic, which is surprising as it is mainly smooth muscle; however, an increased fibrous stroma
may account for this. In the intersphincteric space the LM conjoins with striated muscle fibers from
the levator ani, particularly the puboanalis, and a large fibroelastic element derived from the
endopelvic fascia to form the “conjoined longitudinal layer” (CLL) (Fig. 2) (Shafik, 1976). Its
fibroelastic component, permeating through the subcutaneous part of the external anal sphincter
(EAS), terminates in the perianal skin. According to the “Integral Theory” proposed by Papa Petros,
the CLL creates the downward force for bladder neck closure during effort, and stretches open the
outflow tract during micturition (Papa Petros, 2007).
 The fifth mixed echogenic layer corresponds to the EAS. The EAS is made up of voluntary muscle
that encompasses the anal canal. It is described as having three parts: (1) the deep part is integral with
the puborectalis (PR). Posteriorly there is some ligamentous attachment. Anteriorly some fibers are
circular and some decussate into the deep transverse perinei; (2) the superficial part has a very broad
attachment to the underside of the coccyx via the anococcygeal ligament. Anteriorly there is a
division into circular fibers and a decussation to the superficial transverse perinei; (3) the
subcutaneous part lies below the internal anal sphincter (Shafik, 1975).
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a b

Fig. 2: Anatomy of conjoint longitudinal muscle
a puboanalis (PA) rises from the medial border of the
pubococcygeous muscle (PC) (cPrimal Pictures Ltd,
with permission).
b Fibers from the longitudinal muscle run through the
internal anal sphincter to form the muscularis
submucosae
ani (MSA).
c Coronal image of the anal canal obtained by 2050
transducer (B-K Medical). (SP) symphysis pubis. The
PA joins the longitudinal muscle layer (LL) of the
rectum to form the conjoined longitudinal layer (CLL).
c (Santoro and Di Falco, 2010).

Ultrasound imaging of the anal canal can be divided into three levels of assessment in the axial plane
(upper, middle, and lower levels), referring to the following anatomical structures (Figs. 3, 4):
 Upper level: the sling of the PR, the deep part of the EAS and the complete ring of IAS.
 Middle level: the superficial part of the EAS (complete ring), the CLL, the IAS (complete ring), and
the transverse perinei muscles.
 Lower level: the subcutaneous part of the EAS.
The muscles of the lower and the upper part of the anal canal are different. The first ultrasonographic
image recorded is normally the PR muscle and is labeled upper level. The PR slings the anal canal instead of
completely surrounding it. At its upper end, the PR is attached to the funnel-shaped levator ani muscle and
the levator ani anchors the sphincter complex to the inner side of the pelvis. The deep part of the EAS is
similar in echogenicity to the PR and cannot be differentiated from it posteriorly. Anteriorly, the circular
fibers of the deep part of the EAS are not recognizable in females, whereas in males thin arcs of muscle
from the deeper part of the sphincter may be seen extending anteriorly (Santoro and Di Falco, 2006; Stoker
et al., 2001; Kumar and Scholefield, 2000; Hussain et al., 1996).
Moving the probe a few millimeters in the distal direction will show an intact anterior EAS forming just
below the superficial transverse perinei muscles, imaged at 11 o’clock and 1 o’clock (Fig. 5). This image is
a mid-anal projection where the IAS, CLL, and superficial EAS all are identified. This image will be labeled
middle level. In females, fibers between the transverse perinei fuse with the EAS, so that there is. no plane
of dissection between these two structures. In males a plane of fat persists between the transverse perinei and
the EAS. EAUS is not able to precisely assess the perineal body because of the lack of clear limits. Also the
proposed use of a finger introduced into the vagina as a landmark seems to be of poor benefit, altering its
normal configuration due to the digital compression on the central perineum. At this level, the anococcygeal
raphe is seen as a posterior hypoechoic triangle (Fig. 5) (Zetterstrom et al., 1998; Oberwalder et al.,
2004).
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Fig. 3: Three levels of assessment of the anal canal in the axial plane.
Right side of the image is left side of the patient. EAS, external anal sphincter; IAS, internal anal sphincter; PR, puborectalis. Scan
obtained by 2050 transducer (B-K Medical). (Santoro and Di Falco, 2010).
a b

Fig. 4: Three levels of assessment of the anal canal in sagittal plane.
The internal sphincter ends at the level of the junction between the superficial (level II) and subcutaneous (level III) external
sphincter. a Schematic representation. b Coronal image obtained by 2050 transducer (B-K Medical). EAS, external anal sphincter;
IAS, internal anal sphincter; PR, puborectalis muscle (Santoro and Di Falco, 2010).

When the probe is pulled further out, the image of the IAS will disappear and only the subepithelium and
the subcutaneous segment of the LM and EAS will be seen. This last image will be labeled lower level (Fig.
4). The anterior part of the EAS differs between genders, and anatomic studies have shown that this
difference is already present in the fetus. In males, the EAS is symmetrical at all levels; in females, it is
shorter anteriorly, and there is no evidence of an anterior ring high in the canal (Fig. 6). In examining a
female subject, the ultrasonographic differences between the natural gaps (hypoechoic areas with smooth,
regular edges) and sphincter ruptures (mixed echogenicity, due to scarring, with irregular edges) occurring at
the upper anterior part of the anal canal must be kept in mind. Three-dimensional longitudinal images are
particularly useful to assess these anatomic characteristics of the EAS (Fig. 6) (Williams et al., 2000;
Regadas et al., 2007; Bollard et al., 2002; Gold et al., 1999).

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a b

Fig. 5: Images of the transverse perinei muscles (TP) in the axial plane in male (a) and female (b).
The anococcygeal ligament is seen as a posterior hypoechoic triangle.
Scan obtained by 2050 transducer (B-K Medical) (Santoro and Di Falco, 2010).
a b

c d

e f

Fig. 6: The ventral part of the external sphincter differs between males (a, c, e) and females (b, d, and f) (see text).
a, b Schematic representations; C–f Three-dimensional endosonographic reconstructions in the longitudinal plane. The distance
between the anterior anorectal junction and the external sphincter is called the gap (arrows). EAS, external anal sphincter; IAS,
internal anal sphincter.Scans obtained by 2050 transducer (B-K Medical) (Santoro and Di Falco, 2010).
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Anatomical differences between sexes:
On 3D studies, no significant difference in length between the sexes was found for the puborectalis (mean of
23.9 mm in men, 27.1 in women), nor for the internal sphincter (mean 34.4 mm, 33.2 mm, respectively), but
there was a significant difference in the length of the external sphincter in all planes (anterior – 30.1:15.6;
coronal – 31.6:19.5; posterior – 29.3:16.5, respectively). This confirms that the external sphincter is
generally shorter; particularly anteriorly in women (Fig. 7), which is supported by endoanal MR studies
(Williams et al., 2000; Rociu et al., 2000).

Fig. 7: Sagittal view of the moderately reflective external sphincter (EAS) caudal to the low reflective perineal body (PB)
showing how this is shorter anteriorly in the female. (Santoro and Di Falco, 2010)
Endosonographic anatomy of the Rectum:
The rectal wall consists of five layers surrounded by perirectal fat or serosa (Fig. 8). On ultrasound the
normal rectal wall is 2–3 mm thick and is composed of a five-layer structure (Santoro and Di Falco, 2006)
There is some debate as to what the actual layers represent anatomically. In 1986, Hildebrandt et al.
believed that three layers are anatomical, while the other layers represent interfaces between the anatomical
layers. Beynon and colleagues in 1986, however, have produced both experimental and clinical evidence
that the five anatomic layers are recognizable. Good visualization depends on maintaining the probe in the
center lumen of the rectum and having adequate distension of a water-filled latex balloon covering the
transducer to achieve good acoustic contact with the rectal wall. It is important to eliminate all bubbles
within the balloon to avoid artifacts that limit the overall utility of the study. The rectum can be of varying
diameters and therefore the volume of water in the balloon may have to be adjusted intermittently (Santoro
and Di Falco, 2006; Hildebrandt et al., 1986; Beynon et al., 1986).

Fig. 8: Diagrammatic representation of the five-layer structure of the normal rectal wall.
1, mucosa; 2, submucosa; 3, muscularis propria/circular layer; 4, muscularis propria/longitudinal layer; 5, serosa/perirectal fat
(Santoro and Di Falco, 2010)
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 The first hyperechoic layer corresponds to the interface of the balloon with the rectal mucosal
surface.
 The second hypoechoic layer corresponds to the mucosa and muscularis mucosae.
 The third hyperechoic layer corresponds to the submucosa.
 The fourth hypoechoic layer corresponding to the muscularis propria (in rare cases seen as two
layers: inner circular and outer longitudinal layer).
 The fifth hyperechoic layer corresponding to the serosa or to the interface with the fibro-fatty tissue
surrounding the rectum (meso-rectum). The meso-rectum contains blood vessels, nerves, and
lymphatics and has an inhomogeneous echo pattern. Very small, round to oval, hypoechoic lymph
nodes should be distinguished from blood vessels which also appear as circular hypoechoic
structures (Fig. 9) (Santoro and Di Falco, 2006).
a b

Fig. 9: Normal ultrasonographic appearance of
five layered structure of rectum
a Schematic ultrasound representation of the rectal
wall (T, transducer).
b The five layers in the axial plane correspond to:
1, acoustic interface with mucosal surface;
2, mucosa; 3, submucosa; 4, muscularis propria;
5, serosa/perirectal fat interface.
c Three-dimensional reconstruction of the rectal
wall in the coronal plane. Scans obtained by 2050
transducer (B-K Medical) (Santoro and Di Falco,
c 2010)

Endorectal ultrasound allows an accurate visualization of all pelvic organs adjacent to the rectum: the
bladder, seminal vesicles, and prostate in males (Fig. 10), and the uterus, cervix, vagina, and urethra in
females. Intestinal loops can also be easily identified as elongated structures (Fig. 11) (Santoro and Di
Falco, 2006).

Fig. 10 Coronal view of the bladder (B), seminal vesicles (SV), Fig. 11 Sonographic view of the intestinal loops (IL).
prostate gland (P), urethra (U), and obturator foramen (OF). Scans obtained by 2050 transducer (B-K Medical)
Scans obtained by 2050 transducer (B-K Medical)
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Introduction:
Normal continence and defecation is achieved through a complex interaction between peroral intake, the
upper gastrointestinal tract (digestion, secretion and propulsion), and colorectoanal function. Accordingly,
continence and defecation can be severely disturbed secondary to abnormal eating patterns or disturbed
digestion and propulsion in the small bowel. In clinical practice anorectal function cannot be interpreted
without considering colonic function. The main functions of the colorectum are absorption (water,
electrolytes, and short-chain fatty acids), transport, and storage. Absorption occurs mainly in the right colon.
The main function of the left colon is storage of stools and, together with the rectum, the pelvic floor, and
the anal canal, it is responsible for continence and defecation. The mechanisms underlying continence and
defecation are interdependent, and in the majority of patients with functional problems both are affected to a
varying degree (Laurberg & Krogh, 2010).
General Aspects of Colorectal Motility:
 Colonic Motility
Peristaltic activity is regulated by the enteric nervous system, which coordinates smooth muscle activity to
create receiving and propulsive segments. In the receiving segment, the longitudinal muscles “ahead” of the
intraluminal bolus contract and the circular muscles relax, causing the lumen to expand and receive the
bolus. Circular smooth muscles in the propulsive segment “behind” the bolus contract and the longitudinal
muscles relax. A variety of gut motility patterns has been described. Contractions are either phasic or tonic
[(Gregersen & Ehrlein, 1996)]. Phasic colonic contractions are well defined, having a definite beginning
and ending. Phasic contractions are the mechanical response of smooth muscle cells to spike potentials.
They last a few seconds and cause elevated intraluminal pressure (Gregersen & Ehrlein, 1996; Mandrek &
Golenhofen, 1990). Different patterns of phasic colonic contractions have been identified. It may be
segmental contractions or Propagating contractions. Segmental contractions occur typically at a rate of 3
cycles/ min and represent the majority of colonic motility. On average, segmental contractions create
pressure changes of between 5 and 50 mmHg. These contractions may occur as single events or as a group
of waves. It is thought that less than 6% of segmental contractions are rhythmic, the rest being
uncoordinated or arrhythmic (Bassotti et al., 2005). Even though the net effect of these uncoordinated
segmental contractions is propulsion in an aboral direction, boluses can be propelled in a retrograde manner
over short segments. This haphazard pattern of movement is the basis of the prolonged colonic transit time,
allowing extensive exposure of the luminal content to the mucosa, optimising absorption by the colon (Cook
et al., 2000). Propagated contractions may be either low amplitude (LAPC) or high-amplitude propagated
contractions (HAPC). LAPCs occur approximately 100 times a day, causing pressure changes in the bowel
of less than 50 mmHg. The probable main function of these contractions is the transport of liquid luminal
content and flatus through the colon. LAPCs are thought to be initiated by distension of the colonic lumen,
occur more frequently after meals, and are also closely related to sleep–wake patterns (Bassotti et al., 1996;
Rao et al., 2001). HAPCs are infrequent contractions occurring approximately six times per day, generating
pressures of greater than 100 mmHg. The main function of these contractions is to shift large quantities of
content along long segments of the colon and their frequency and amplitude is reduced in patients with slow
transit constipation. Greater than 95% of propulsion occurs in an aboral direction. The propulsion of these
large volumes in an aboral direction can be a defaecatory stimulus, with the large pressure gradient
potentially resulting in a defaecatory urge (Ritchie, 1971). The tonic contractions are less well-defined,
longer lasting – usually several minutes – and may or may not be associated with increased luminal
pressures (Gregersen & Ehrlein, 1996; Mandrek & Golenhofen, 1990). Movements of colonic contents are
often not associated with detectable pressure changes and may be due to changes in colonic tone (Cook et
al., 2000). Two types of tone have been described: a tetanic tone that is generated by fused phasic
contractions, and a specific tone that is regulated mainly by chemical processes (Gregersen & Ehrlein,
1996).
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Diurnal Variation in Colon Function:
Colonic motility in healthy individuals varies considerably through the course of a day. Studies have shown
the colon to be quiescent for long periods, interrupted by bouts of spontaneous activity. Twenty-fourhour
electromyogram (EMG) studies have shown twofactors in particular to have a significant impact on gut
motility: (1) sleep–wake patterns and (2) meals (Wyman et al., 1978).
i Effect of Sleep
Sleep has an important inhibitory effect on both segmental and propagated contractions of the colon
(Furukawa et al., 1994). Colonic activity during sleep is dramatically reduced and can disappear for long
periods of time. Between 10 pm and 6 am, bowel motility is at its most quiescent. Emerging evidence shows
that during the rapid eye movement phase of sleep, arousal or sudden awakening, there is an increase in
bowel activity. The central nervous system directly influences colonic motility via the autonomic nervous
system, providing a plausible explanation of how emotional states and phases of sleep influence gut motility
(Rao et al., 2001). Soon after waking, colonic contractions increase threefold (explaining the urge to have a
bowel action that some people experience on waking) before reaching a basal level by afternoon. During the
course of the daytime, the transverse to descending colon demonstrates greater levels of motor activity than
the rectosigmoid (Furukawa et al., 1994).
ii Effect of Meals
Ingestion of food is a major physiological stimulant of colon motor activity. Meals increase both segmental
and propagated contractions in the colon, and also increase overall smooth muscle tone. There are two
phases to this postprandial increase in colonic motility. The gastrocolic (early) phase, when the increased
colonic motor activity starts directly after, and possibly even before, ingestion (1–3 min). The intestinal
(late) phase, which correlates to the intestinal phase of digestion, occurring at least 1 h after eating. The
degree of motility initiated in the gastrocolic phase is increased with large-volume intake (via a mechanism
involving increased gastric distension) (Wiley et al., 1988). A high calorie intake and fatty content of the
meal increases the intestinal phase of motility, while meals with high amino acid and protein content
decrease it. The mechanism by which ingestion exerts its effect on the colon is not fully understood. Neither
an intact stomach nor nervous system is required to elicit this response. The physiological changes are
thought to be initiated by mechanoreceptors and chemoreceptors on the gastroduodenal wall. An intricate
interaction of neurohumeral mediators then acts to elicit a response from the colon. The mediators of the
response are thought to include vagal cholinergic pathways, regulatory peptides (protein peptide YY – PYY,
gastrin, cholecystokinin, neurotensin), prostaglandins and serotoninergic pathways. There is growing interest
in PYY and its influence on the gut. It is released in response to bile, fat, glucose and amino acids detected
in the terminal ileum. PYY acts to alter gut transit time and is thus named the “ileal brake” (Cuche et al.,
2000; Cherbut et al., 1998).
iii Effect of Stress
Physical and psychological stress can profoundly influence gut function. Whilst external stressors induce
gastric stasis, they accelerate colonic transit. In particular, stress promotes prolonged propagated
contractions across several sections of the colon. This effect occurs in the absence of an autonomic response,
the effect being mediated via the release of corticotropin-releasing factor released from the hypothalamus.
This peptide hormone stimulates colonic motility directly via modulation of vagal and sacral
parasympathetic outflow (Tache et al., 1999). Interestingly, the motility effect outlives the psychological
stressor, providing a possible explanation for how psychological stress may influence long-term colonic
functional symptoms. In contrast to psychological stress, physical stress induces simultaneous contractions,
defined as pressure waves occurring in several areas of the colon. Again, in contrast to psychological stress,
physical stressors tend to be associated with a systemic autonomic response, and colonic motor activity
ceases after the stress has ceased (Rao et al., 1998).
 Rectal Motility
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Rectal motility resembles the colonic pattern, with some colonic mass contractions progressing to the
rectum, often initiating defecation (Rao et al., 2001; Rao & Welcher, 1996). There are, however, some
differences. There are 3 different patterns of phasic rectal contractions. This includes isolated contractions,
short clusters of contractions and powerful phasic contractions. The physiological significance of isolated
contractions and short clusters of contractions (often with a low amplitude and a frequency of
approximately 5–6 contractions per minute) is as yet unknown. Powerful phasic contractions within the
rectum have been termed the rectal motor complex (RMC) (Ferra et al., 1993; Rao et al., 2001). The RMC
is usually seen every 60–120 min, it lasts several minutes and its contractions have a frequency of 3–10 per
minute (Fig. 12) (Rao et al., 2001). They are very similar to phase three of the migrating motor complex
within the small bowel. RMCs are often restricted to a single short segment of the rectum, but they may
propagate either orally or anally, and they are often associated with contractions of the colon and the anal
canal (Rao et al., 2001). Accordingly, their main function may be to prevent defecation. Two types of
change in rectal tone have been described: rapid volume waves and slow volume waves. Rapid volume
waves last less than 2 min and are associated with increased luminal pressure. They are not affected by
eating. Slow volume waves last more than 2 min, are not associated with changes in intraluminal pressure but
their frequency increases after a meal. Slow waves may increase rectal sensation to luminal contents (Ferra
et al., 1993).
 The Rectum as Storage Conduit:
The rectum acts as a conduit for storage prior to defaecation. Faeces that are propelled from the distal colon
into the rectum increase the rectal volume, eliciting a desire to defaecate. This can be voluntarily suppressed
if required. In response, a receptive relaxation occurs and the rectal defaecatory contractions subside. This
receptive relaxation allows the rectum to accommodate larger volumes without a significant rise in rectal
pressure. The neural basis for rectal accommodation is thought to be via inhibitory nerves, which allow large
rectal volumes to be stored without the urge to defaecate. There is a process of negative feedback with
increasing rectal volumes such that gastric emptying is inhibited and the frequency of colonic propagated
contractions is reduced, with the overall effect of prolonging stomach-to-rectum transit time (Shafik et al.,
2006). Changes in rectal pressure with changes in volume can be quantified clinically by the assessment of
“compliance”. Compliance varies in several functional and organic disorders. For example, in patients who
have had pelvic radiotherapy, compliance is reduced as the rectum becomes fibrotic and non-distensible.
These patients tend to suffer with urgency to relatively small rectal volumes (van Duijvendijk et al., 2002).

Fig.12: Rectal Motor Complex. (Laurberg & Krogh, 2010)
On the other hand, patients with a mega-rectum have increased compliance and are able to tolerate large
volumes without the urge to defaecate (Williams et al., 2000). In addition, rectal compliance can be the
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focus of therapy, such as in biofeedback, when faecally incontinent patients with urgency can undergo

behavioural therapy to increase compliance and decrease urge perception (Shafik et al., 2006).
Generation and Control of Colorectal Motility:
Smooth muscle cells within the circular and longitudinal colorectal muscle layers are arranged in bundles
that are connected by gap junctions. Bundles fuse at many points and thereby function as a syncytium. The
resting membrane potential of the smooth muscle cells (−50 to −60 mV) is not constant, but undergoes small
undulating changes called slow waves. These are generated by the pacemaker cells (interstitial cells of
Cajal) (Daniel & Berezin, 1992). The slow waves do not cause contractions, but they do influence the
frequency of spike potentials. Spike potentials are action potentials occurring when the resting membrane
potential becomes more positive than about −40 mV. During spike potentials, calcium enters the smooth
muscle cell causing contraction of the colorectal wall. Several factors influence the occurrence of spike
potentials, either by depolarisation making the membrane potential more positive, and thus the cells more
excitable, or by hyperpolarisation making it more negative and the cells less excitable. Depolarisation of the
membrane potential is caused by stretching of the muscle cells, acetylcholine and several gastrointestinal
hormones. Hyperpolarisation is caused by epinephrine and norepinephrine. Colorectal motility is controlled
by the nervous system, hormones, and the immune system. The neuronal system modifies colorectal motility
at four levels (Wood et al., 1999):
1. The enteric nervous system (ENS)
2. The prevertebral sympathetic ganglia
3. The parasympathetic and sympathetic systems within the brainstem and spinal cord
4. The higher brain centers
 The Enteric Nervous System (ENS)
The ENS contains about the same number of neurons as the spinal cord. Enteric nerves within the
intermuscular plexus (Auerbach’s plexus) mainly control colorectal motility and those within the
submucosal plexus (Meissner’s plexus) mainly control mucosal secretion and blood flow. The ENS
generally consists of three types of neurons: sensory neurons, interneurons and motor neurons Its sensory
neurons are specialized for the detection of mechanical stimuli, temperature, and chemical properties.
Through multiple interneurons, such stimuli affect the motor neurons that finally stimulate or inhibit smooth
muscle cells. Interneurons also integrate stimuli from the ENS with the extrinsic nerve system and
hormones. Reflexes within the ENS can thus be activated by both local and extrinsic stimuli. Thus efferent
parasympathetic fibres within the vagal and splanchnic nerves can stimulate motility over large distances of
the gastrointestinal tract. The ENS integrates several local reflexes (i.e., the distension reflex where
distension registered by mechanoreceptors cause contractions orally and relaxation distal to the site). These
reflex patterns can be modified by the autonomic nerve system via interneurons. Many different
neurotransmitters either stimulate (e. g., acetylcholine, histamine, serotonin, cholecystokinin, motilin,
gastrin) or inhibit (e. g., dopamine, noradrenalin, glucagon, vasoactive intestinal peptide, enkephalin,
somatostatin) motility. Moreover, receptors for several of these transmitters (e. g., histamine and serotonin)
have been divided into several subgroups, and specific agonist and antagonist have been developed that
have, or in future may have, a clinical role (Wood et al., 1999).
 The Prevertebral Sympathetic Ganglia
The second level of integration and control is within the prevertebral sympathetic ganglia and nerves. These
are considered to be the most important mediators of the gastrocolic response mediating colorectal phasic
and tonic activity after a meal (Wood et al., 1999).
 The Parasympathetic and Sympathetic System Within the Brainstem and Spinal
Cord
The vagus nerve provides parasympathetic input from the oesophagus to the splenic flexure of the colon
(Devroede & Lamarche, 1974). The pelvic nerves carry parasympathetic fibres from S2–S4 to the rest of the
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