Spinal Cord (2001) 39, 193 ± 203

ã 2001 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/01 $15.00
www.nature.com/sc

Scienti®c Review

Bowel dysfunction following spinal cord injury

AC Lynch1,2, A Antony1, BR Dobbs1 and FA Frizelle*,1,2
1
Spinal Injuries Unit, Burwood Hospital, Department of Surgery, Christchurch Hospital, Christchurch, New Zealand;
2
Colorectal Unit, Department of Surgery, Christchurch Hospital, Christchurch, New Zealand

Study Design: Review.

Objectives: To outline the present knowledge of bowel dysfunction following spinal injury,
and look at future directions of management and research.
Setting: Spinal Unit and Colorectal Unit, Christchurch, New Zealand.
Methodology: Review.
Results: The underlying physiology of colorectal motility and defecation is reviewed, and
consequences of spinal cord injury on defecation are reported. A discussion of present
management techniques is undertaken and new directions in management and research are
suggested.
Conclusion: There is need for more intervention in regard to bowel function that could
improve quality of life, but there is also a need for more research in this area.
Sponsorship: Dr AC Lynch is a holder of a Royal Australian College of Surgeons
Foundation Research Scholarship and the research has been supported by the Canterbury
Medical Research Foundation, and the Burwood International Spinal Trust.
Spinal Cord (2001) 39, 193 ± 203

Keywords: spinal cord injury; bowel function

Introduction
Bowel dysfunction following spinal cord injury (SCI) is 1200 age and gender matched controls. The mean
increasingly recognised as an area of major physical faecal incontinence score was higher for SCI patients
and psychological diculty for SCI patients. Following than controls (P50.0001), and for complete SCI
spinal cord injury, changes in bowel motility, sphincter compared with incomplete injury (P=0.0023).8 Age
control, and gross motor dexterity interact to make or time since injury did not a€ect the faecal
bowel management a major life-style problem limiting incontinence score. Incontinence a€ected quality of
quality of life.1 Once the acute phase is over and life for 62% of SCI patients, compared with 8% of
patients have adapted to their loss of mobility, surveys controls. Faecal urgency and time spent at toilet were
have shown that approximately one third of subjects also signi®cantly higher for the SCI group. Thirty-nine
rank colorectal problems2±6
as worse than both bladder per cent of SCI patients use laxatives, compared to 4%
and sexual dysfunction. of controls (P50.0001). Haemorrhoidectomy was
Colorectal problems can be a signi®cant cause of more common in the SCI population (9% vs 1.5%
morbidity immediately after SCI, and chronic gastro- (P50.001)), particularly among those requiring
intestinal problems remain common, but may become manual evacuations. Stone et al. found that improved
more frequent with increasing time after injury.7 management of bowel dysfunction led to improved
Although many SCI patients achieve an adequate well-being.9
bowel frequency with drugs and manual stimulation, In order to understand why SCI patients have such
the risk and occurrence of faecal incontinence, problems it is important to review the normal anatomy
diculties with evacuation, and need for assistance and physiology, the relationship between the enteric
remain signi®cant problems. In a recent study, nervous system and autonomic nervous systems.
questionnaires were sent to 1200 SCI patients, and
Normal colon anatomy and physiology
The human colon is a compliant sac approximately
*Correspondence: FA Frizelle, Professor of Colorectal Surgery,
Department of Surgery, Christchurch Hospital, Christchurch, New 1.5 m long, closed at one end by the ileocaecal valve
Zealand and the anal sphincter at the other. It has two layers
 Bowel dysfunction
AC Lynch et al
194

of smooth muscle. The inner layer is circular and stretching of the puborectalis and the urge to
thickens to form the internal anal sphincter (IAS) in defecate. The distended rectum causes re¯ex relaxa-
the distal rectum. The outer layer is arranged in three tion of the IAS (rectoanal inhibitory re¯ex (RAIR))
distinct bands of longitudinal smooth muscle called resulting in faeces reaching the upper anal canal
the taeniae coli. Included in the pelvic ¯oor are the where receptors sample the rectal contents. Then
levator ani, which form a funnel from the sides of the voluntary EAS contraction maintains continence by
pelvis in which the pelvic organs sit. Just inside the mechanically sealing the rectal neck and mechani-
anus is the external anal sphincter (EAS) complex, cally preventing further relaxation of the IAS.
described by Sha®k as three counterpoised U-shaped Defecation is a coordinated event requiring simulta-
loops (Figure 1).10 The upper loop, formed mainly by neous relaxation of the puborectalis to widen the
puborectalis, arises from the symphisis pubis, loops anorectal angle, relaxation of the EAS, and rectal
around the upper part of the rectal neck and opens contraction.
ventrally. It is innervated by the inferior haemor-
rhoidal nerve. The intermediate loop, from the
The enteric nervous system
anorectal raphe and coccyx, opens dorsally and is
innervated by the perineal branch of the fourth sacral Nervous control of the gastrointestinal tract is by the
nerve. The basal loop, from the skin anterior to the enteric nervous system. This complex network of
anus, opens ventrally and encloses the lower rectal intrinsic neurons is able to sense information, process
neck. It is supplied by the inferior haemorrhoidal it by means of interneurons and then through motor
nerve.10,11 As each loop has its own separate bilateral neurons e€ect secretion or muscular contraction. It
nerve supply, each can function as a sphincter retains contact with the central nervous system through
independently. a€erent and e€erent extrinsic neurons of the sympa-
Continence is maintained by the resting tone and thetic and parasympathetic systems.12
re¯ex activity of the IAS, EAS and muscles of the There are two main ganglionated plexuses, the
pelvic ¯oor. The resting anal canal pressure is myenteric (Auerbach's) and submucosal (Meissner's).
maintained by tonic contraction of the IAS. Re¯ex The myenteric plexus lies between the longitudinal
contraction of the EAS complex on coughing or and circular layers of muscle for the entire length of
Valsalva prevents leakage by kinking the anal canal the gut. It provides motor innervation to the two
in opposing directions. Rectal distention produces muscle layers and secretomotor innervation to the
mucosa. There are also projections from the
myenteric plexus to the sympathetic ganglia. The
submucous plexus is located in the submucosa
between the circular muscle and the muscularis
mucosa. It plays an important role in secretory
control, especially in the small intestine. It also
innervates the muscularis mucosa, intestinal endo-
crine cells and submucosal blood vessels. Smaller
nerve ®bres emerge from these plexuses to form
nonganglionated plexuses in the circular and long-
itudinal muscle and muscularis mucosae.13
The neurons can contain not only acetylcholine and
norepinephrine, but also Substance P (SP), vasoactive
intestinal peptide (VIP), serotonin, somatostatin, and
other neuropeptides, often coexisting in the same
neurons.
The neurons of the enteric nervous system can be
classi®ed into intrinsic a€erent, interneurons and
motor neurons.
. Intrinsic a€erent neurons form the sensory limb of
intrinsic motor and secretomotor re¯exes by
projecting to interneurons in both nerve plexuses.
They are all cholinergic and may contain other
neurotransmitters such as SP.12
Figure 1 The external anal sphincter (EAS), summarising . Interneurons project either up or down the gut
the basic arrangement of its ®bres. Puborectalis (PR) forms
between the a€erent and motor or secretomotor
the upper loop (UL) and has decussating ®bres (dc) that
blend with the longitudinal ®bres of the rectum, or (dd) the neurons. They form multisynaptic pathways to
perineal body. The middle loop (ML) is attached to the control the propagation of peristaltic waves. There
anococcygeal raphe (acr), bulbospongiosus (bs), and trans- are several subgroups based on neurotransmitter
versus perinei profundus (tp). The basal loop (BL) is content, but their various physiological roles are
perforated by longitudinal ®bres of the rectum11 unknown.
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 Bowel dysfunction
AC Lynch et al
195

. Motor neurons are either excitatory or inhibitory. complex activities requiring both voluntary and re¯ex
The excitatory neurons project either locally or activity can be impaired.13
orally to the circular muscle, their main neuro- The control of colonic movement is largely
transmitters being acetylcholine or SP. The autonomous. Intrinsic rhythmic slow waves originat-
inhibitory motor neurons project to the circular ing in the submucous plexus occur sequentially along
muscle caudally and contain VIP and nitric oxide the colon. In the right colon slow waves of contraction
(NO).12 may travel in both directions to produce mixing and
kneading contractions of the circular muscle layer. The
slow waves in the distal colon are directed towards the
Neuropeptides
anus to produce a propulsive peristaltic force. Normal
Peptides destined for secretion by neurons are colonic transport is between 12 to 30 h from ileocaecal
synthesised in the cell body then transported intra- valve to rectum.15
axonally to the nerve endings where they are stored in Peristalsis results in the propulsion of intraluminal
synaptic vesicles until release. There is no evidence for contents over long lengths of small and large intestine.
a re-uptake and re-use pathway for neuropeptides. The process requires coordinated contraction of the
longitudinal muscle and inhibition of the circular
muscle ahead of the bolus and simultaneous long-
Substance P itudinal muscle relaxation and circular muscle con-
Substance P (SP) was the ®rst gut neuropeptide to be traction immediately behind the bolus. It can occur in
discovered in 1931. It occurs widely in brain, spinal an isolated segment of gut in vitro, implying it is
cord, gut nerves, and mucosal endocrine cells. It is a dependent on an intact integrative enteric nervous
dose-dependent excitatory neurotransmitter acting system.16 Activation of the longitudinal muscle ahead
within the myenteric plexus on cholinergic neurons of the bolus is produced by acetylcholine released from
and directly on smooth muscle to cause contraction in the myenteric plexus. Relaxation of the circular muscle
both longitudinal and circular muscle layers. It is is produced by increased discharge from the intrinsic
known to increase gut motility and may promote and inhibitory neurons. Contraction of the circular muscle
maintain the peristaltic mode of intestinal motility. SP behind the bolus may be a myogenic event following
also increases blood¯ow in gut, binds to speci®c synaptic shutdown of continuously active inhibitory
receptors on pancreatic acinar cells associated with neurons, or it could be produced by cholinergic
enzyme secretion, and inhibits acid secretion and excitatory input to the muscle, or both.
intestinal absorption.14 The best evidence for intrinsic inhibitory mechan-
Evidence for this role includes the observation that isms is in Hirschsprung's disease where there is spasm
carcinoid tumors are often associated with increased in an aganglionic section of colon. As no re¯ex
gut motility and diarrhoea. These tumours can relaxation is initiated, the aganglionic segment
synthesise and release large amounts of SP, and behaves like a sphincter, resulting in a functional
serotonin, known to lower the threshold for the obstruction to faceal transit. The failure of relaxation
peristaltic re¯ex in isolated segments of intestine, into of the diseased segment is accounted for by its lack of
the portal and systemic circulations. inhibitory neurons containing VIP and NO.

Parasympathetic supply to the colon, rectum and

Vasoactive intestinal peptide
anus
Vasoactive intestinal peptide (VIP) is present in a wide
range of neurons in both gut and elsewhere. It is a Parasympathetic out¯ow to the colon contains two
strong stimulant of intestinal secretion, and causes types of preganglionic axons. One leading to intramur-
gastrointestinal relaxation. Myenteric VIP neurons al cholinergic excitatory neurons and one connecting
project in an oral to anal direction and are compatible with intramural noncholinergic nonadrenergic inhibi-
with a role in descending inhibition.14 tory neurons.
Stimulation of the pelvic nerves elicits a contraction
in both colonic muscle layers, but if the cholinergic
Central and enteric nervous system interaction
®bres are blocked with atropine, parasympathetic
The coordination of transport, secretion and blood stimulation results in inhibition of contraction and
¯ow requires a high degree of extrinsic and intrinsic relaxation due to muscle cell hyperpolarisation. In
neuronal integration. The intrinsic neurons of the gut humans, this can be seen when sectioning of the pelvic
exhibit a sophisticated pattern of behaviour indepen- nerves may result in impaired defecation.17
dent of, but modulated by the extrinsic parasympa- Distribution of vagal input is debated;17 it may
thetic and sympathetic nervous system.14 The extrinsic project as far as the rectum, although some authors
system acts to modulate intrinsic re¯exes and feel only the ascending colon is innervated, and others,
coordinate gut activity with that of the whole up to the transverse colon. It acts to increase
organism. When the gut is disconnected from the contractile activity by modulating coordinated motor
central nervous system, its function is preserved, but responses from the enteric nervous system.
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 Bowel dysfunction
AC Lynch et al
196

Sacral input is transmitted by pelvic nerves to the dog, the ®ring of sacral parasympathetic neurons is
large intestine. It issues from spinal roots S2 ± S4 via modulated by the pontine reticular formation.20
the pelvic plexus (Figure 2). It is mediated by nicotinic Parasympathetic preganglionic neurons are also
cholinergic receptors and functions to reinforce mass in¯uenced by a€erents from both the urinary bladder
contraction of the terminal large intestine during and colon. The ®ring of parasympathetic neurons to
defecation.18 the colon is increased by activatin of colonic a€erents
The parasympathetic supply to the internal anal and decreased by that of vesical a€erents that
sphincter comes from the sacral spinal cord through reciprocally inhibit colonic parasympathetic neurons
the pelvic nerves. The parasympathetic e€ect is and excite vesical ones.21
sphincteric relaxation through activation of nonadre-
nergic noncholinergic intramural neurons and a
Sympathetic supply to the colon, rectum and anus
presynaptic action of cholinergic intramural neurons
on sympathetic nerve endings. Sympathetic supply consists of cholinergic preganglio-
nic neurons and noradrenergic postganglionic neurons
Extrinsic parasympathetic re¯exes located in either the sympathetic chain or prevertebral
ganglia (coeliac, superior mesenteric, or inferior
Mechanical stimulation of the colon or rectum elicits a mesenteric). Preganglionic axons from spinal roots
coordinated re¯ex contraction of the rectum that may T9-T10 synapse in the coeliac and superior mesenteric
result in defecation. The sacral parasympathetic centre ganglia. From there, postganglionic nerves innervate
is of major importance in organising colonic motility, the small intestine and from the superior mesenteric
especially during defecation.17 It is able to organise ganglion to the ascending and transverse colon (Figure
defecation even after upper spinal cord section.19 2). Sympathetics are inhibitory and function to
However the sacral parasympathetic centre is also decrease bloow ¯ow and slow motility by relaxing
in¯uenced by supraspinal nervous structures. In the the colonic wall to increase compliance. Sympathetic

Figure 2 Autonomic and somatic innervation of the colon, anal sphincters and pelvic ¯oor. Spinal cord segments and nerve
branches are illustrated. Dashed lines represent sympathetic pathways with prevertebral ganglia. Solid lines depict
parasympathetic pathways that synapse with ganglia in the enteric nervous system within the colonic wall. Dotted lines
represent mixed nerves supplying somatic musculature of the external anal sphincter (EAS) and pelvic ¯oor15

Spinal Cord
 Bowel dysfunction
AC Lynch et al
197

input acts on presynaptic terminals to prevent

Vesicoanal re¯ex
excitatory transmitter release within the enteric
nervous system.18 Vesical ®lling increases electromyelographic activity in
There is evidence that the spinal cord is the source the IAS, and after voiding it decreases. The re¯ex is
of tonic inhibition. In cats, after lumbar ventral root probably partly from the lumbar spinal cord and partly
removal and spinal cord removal, there was a decrease from the inferior mesenteric ganglion. Sphincter
in e€erent lumbar colonic nerve ®ring and a parallel pressure is unchanged after high cord section,
increase in colonic motility.22 This suggests e€erent implying supraspinal centres have very little in¯uence
inhibition from between T12-L5. This may not be the on IAS tone. A dual origin for excitation is proposed
only source of e€erent trac in the colonic nerves as in the cat as IAS electrical activity remains after section
there are tonically discharging neurons in the cat of sympathetic excitatory ®bres, but it is desynchro-
inferior mesenteric ganglion.23 nised. The implication is that motor activity is both
Somatovisceral re¯exes have been described such myogenic and neurogenic, the latter reinforcing the
as inhibition of intestinal motility in response to skin former by synchronising electrical activity of smooth
pinching. It appears to have a segmental organisa- muscle cells.
tion but its role in spinal patients is unclear although
defecation appears enhanced by rubbing arms
Sympathetic innervation of the external anal
and abdominal massage. This may indicate the
sphincter
presence of somatic a€erent pathways connected to
vegetative central neurons involved in gut motility, The EAS is a striated muscle innvervated from the
perhaps via the sympathetic chain. However, patients sacral cord via the pudendal nerves (S2-S4). Its
who have had a complete bilateral sympathectomy structure is shown in Figure 1. Some of the EAS
do not generally present with change in bowel motor neurones can be activated by stimulation of
habit.24 a€erent axons in pudendal nerve branches from the
Postganglionic sympathetic neurons in the prever- external urethral sphincter. Clinical experience with
tebral ganglia are the sympathetic ®nal common path patients following spinal cord injury does not seem to
for the integration of information from the periphery demonstrate a change in anal tone. This may be
and the CNS. Their function is complicated. because supraspinal centres do not in¯uence sphincter
Immunocytochemical data indicates that the nerve tone, the adaptation of remaining structures, or that a
processes contain VIP, encephalin, SP, somatostatin, single level sympathectomy is insucient to result in
CCK and bombesin.25,26 Each of the nerve trunks change.29
connected to ganglia contain speci®c peptidergic
pathways.25 These substances play a role in synaptic
Chronic changes in colonic function following
transmission within ganglia or as modulators of
spinal cord injury
neurotransmitter release.26
SP at low concentration has been shown to increase The extrinsic nervous system acts to modulate the
the excitability of guinea pig prevertebral ganglionic intrinsic system. It is these complex integrated activities
neurons such that a subthreshold EPSP (excitatory that require re¯ex and voluntary muscular control such
postsynaptic potential) will generate a spike potential as defecation that are a€ected most by spinal cord
or give rise to tonic discharge of spike potentials in injury. Peripheral nerve lesions have been shown to
postganglionic neurones in the absence of excitatory result in transsynaptic degeneration and Schwann cell
input. Moreover, administering either SP, one of its proliferation in the colonic wall, but local synaptic
analogs, or a SP-degrading endopeptidase inhibitor to remodelling after spinal injury has not been demon-
rats will result in a signi®cant increase in gastro- strated.17,30
intestinal transit.27 The level of the spinal cord lesion determines the
e€ect on colonic motility. A supraconal (Upper Motor
Neuron or UMN) SCI results in loss of conscious
Sympathetic innervation of the internal anal
sphincter sphincter control and an inability to signi®cantly
increase intraabdominal pressure. There is a loss of
The IAS receives sympathetic innervation from the voluntary control of defecation and a degree of
lumbar spinal cord through the lumbar splanchnic anorectal dyssynergy. This means that straining and
nerves and from the inferior mesenteric ganglion rectal contraction result in increased tone in the EAS.
through the hypogastric nerves. The sympathetic effect Loss of rectal sensation and a spastic EAS require
is excitatory, and tonic discharge maintains IAS defecation to be anticipated. Re¯ex defecation can be
closure. With rectal distension or digital stimulation, initiated by mucosal stimulation, either digitally or
the IAS relaxes probably due to the activation of with a suppository. Stimulation activates the rectoanal
intramural inhibitory nonadrenergic noncholinergic inhibitory re¯ex. It can be exploited to cause
neurons. There may be some extrinsic participation relaxation of the IAS, re¯ex relaxation of the EAS
since pelvic nerve stimulation induces sphincter and pelvic nerve mediated peristalsis. If there is no
relaxation.28 re¯ex relaxation of the EAS complex, re¯ex evacuation
Spinal Cord
 Bowel dysfunction
AC Lynch et al
198

will not occur or be incomplete. Manual evacuation or The conclusion is that the increase in colonic
enemata are often required in this situation. activity and decrease in compliance may be due to
Complete or partial injuries to the cauda equina loss of descending inhibitory input from the CNS. This
result in a lower motor neuron (LMN) pattern of is supported by animal studies in the cat where
injury. The EAS and pelvic muscle are ¯accid and sympathetic nerve activity via a2-adrenergic receptor
there is no re¯ex response to increased intraabdominal activation resulted in profound inhibition of colonic
pressure. The loss of parasympathetic control and motility,37 and sectioning of preganglionic splanchnic
re¯ex innervation of the IAS means a further sympathetic nerves produced an increase in colonic
reduction in resting anal tone and leads to faecal contraction.38
incontinence. A person with a LMN lesion following
SCI will have absent EAS tone and decreased re¯ex
E€ects of obstruction on motility and colonic
peristalsis. Valsalva can result in faecal leakage and neuropeptides
the rectum has to be kept empty to avoid faecal
incontinence. Stool has to be removed digitally, If the change in colonic motility was due to functional
assisted by Valsalva and abdominal massage. rectal obstruction secondary to anorectal dyssynergy
Patterns of gut dysmotility have been described for alone, we should expect changes such as those
di€erent levels and degrees of SCI. Lesions above T1 produced by mechanical obstruction of the colon.
result in delayed mouth-to-caecum time, but lesions Bowel muscle and ganglia hypertrophy, and if the
below this exhibit normal transit times to the obstruction is not removed, hypertrophy and contrac-
caecum.31 Beyond the ileocaecal valve, transit times tile e€orts continue until enzymatic mediator depletion
are markedly delayed. A LMN injury from a lesion occurs.39 Non-constricting obstructive bands in rats
a€ecting the conus, cauda equina or pelvic nerves produces histological changes such as ganglion cell
results in interruption of the parasympathetic supply elongation, probably due to bowel distension, but does
to the colon and reduced spinal cord-mediated re¯ex not result in signi®cant changes to the enteric nervous
peristalsis. Stool propulsion is by segmental colonic system.40
peristalsis only. An UMN lesion results in variable That said, obstruction has been shown to a€ect
changes in colonic transit. Marker transit studies and neurotransmitter levels.41 One study looked at ®ve
scintigraphy have demonstrated that patients with patients with decompensated ileus due to tumour
spinal cord lesions above the lumbar region have obstruction of the large bowel. Immediately after
slowed transit throughout the whole colon.32 One resection, samples were taken 10 cm proximally and
study involving 28 SCI patients also demonstrated distally to the tumour and SP and VIP levels were
distal small bowel dilatation in 10 patients, all of obtained by radioimmunoassay. A signi®cantly de-
whom had abdominal symptoms and nine of whom creased tissue level of both SP and VIP was found in
had a spinal cord lesion above T5.33 Radioisotope the prestenotic sample. The mechanisms that lead to
scintigraphy has shown the delay to involve the whole this decrease are unknown. Increased release of
colon. The velocity of the median position of bowel neurotransmitters due to endotoxins may be impor-
contents throughout the colon was signi®cantly slower tant. Decreased SP would impair motility by reducing
in SCI patients (0.63+0.33 cm/h in SCI, 2.58+1.2 cm/ bowel contractility. VIP may act by causing dysmoti-
h in controls, P50.001).32 lity due to loss of descending peristaltic inhibition.
The delay in transit may in part be due to loss of While the mechanical obstruction may be the major
colonic compliance. The colon of patients with complete cause of obstructive ileus, the ®nal rapid decompensa-
thoracic injury has been shown to have an abnormal tion may be due to alteration of gut neuropeptides.41
response to increasing volume. Distension with water to
generate a volume/pressure curve (colometrogram)
Role of neuropeptides in bowel dysfunction
produces a hyperre¯exic response similar to that
described in the bladder.34 With a spinal cord lesion There is a distinction in the intramural distribution of
above L1, the left colon is less compliant. Above T5, the regulatory neuropeptides within the bowel wall. SP is
right colon is also a€ected. The lack of compliance leads exclusively localised in nerves. Large quantities of SP
to functional obstruction, increased transit times, and and VIP are present in the lamina propria which is in
abdominal distension, bloating and discomfort. It close contact with the epithelium and muscularis
suggests that the CNS is necessary to modulate colonic mucosae.42 Large numbers of VIP and SP-containing
motility.35 Colonic myoelectric activity has been enteric nerves supply the ganglionated plexuses and
recorded in a group of SCI patients with injuries at are especially numerous in the circular muscle layer.
varying levels and controls. This demonstrated a They have a role in colon motility while those
signi®cantly higher level of basal colonic activity in supplying the mucosa are involved with electrolyte
SCI patients (12.6 spikes per 10 min vs 3.3), and no and ¯uid transport. SP has been shown to accelerate
demonstrable gastrocolic re¯ex.36 This would support the transit of a charcoal meal in rats.27 It increases
the assumption that the CNS exerts a tonic inhibitory intraluminal pressure mainly by circular muscle
in¯uence on basal colonic activity and is consistent with contraction by direct action on the muscle as well as
the hypertonicity seen on colometrograms.34 by simultaneous activation of excitatory cholinergic
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 Bowel dysfunction
AC Lynch et al
199

pathways and inhibitory VIP-independent, NO-regu- histological di€erences were found between colonic
lated pathways.43 specimens from SCI and control patients. The ratio of
SP is reduced in the colonic mucosa of patients with SP and VIP to NSE was qualitatively similar for both
chronic constipation and increased in patients with SCI patients and controls. There is still considerably
ulcerative colitis. In both cases there was a signi®cant more work to be undertaken in this area and it may
correlation between mucosal SP levels and the disease provide an interesting and possible novel means on
states.44 The elevated levels in ulcerative colitis may be intervention.
a reactive e€ect secondary to other in¯ammatory
factors. The fact that mucosal SP levels are associated
Relationship of anorectal and bladder function
with two disorders associated with colonic transit
suggests a role in the pathogenesis of intestinal transit There are similarities between the bladder and rectum
disorders. in terms of function and behaviour following spinal
A similar scenario exists with diabetic constipation cord injury. The dysmotility seen in spinal patients may
where SP in the rectal mucosa of diabetics with be due to decompensation of colorectal smooth muscle
constipation is signi®cantly lower than in diabetics following chronic colorectal distension, similar to
with normal bowel function.45 Both groups of diabetic detrusor decompensation seen with chronic bladder
patients exhibited greater SP levels than controls. outlet obstruction.29 Colonic compliance is reduced
These abnormalities the mucosal content of SP may be following thoracic SCI, and the uninhibited contraction
the result of degenerative changes in the submucosal of the bladder seen following distension produces a
plexuses of diabetics.46 cystometrogram analogous to the colonic compliance
While mucosal SP may be decreased with chronic curves. This perhaps re¯ects a similar interruption of
constipation, concentrations in the muscle layers may ascending somatosensory and descending visceral
be increased. Sjolund et al.47 examined tissue from the pathways.35
colon of 18 people with slow-transit constipation. We have explored a possible relationship between
Tissue concentrations of VIP and SP were measured patterns of anorectal physiology and patterns seen
by radioimmunoassay. Signi®cantly increased concen- with cystometrograms. Anorectal manometry was
trations of VIP and SP were found in the ascending performed on 37 SCI volunteers. Patterns of rectal
colon, and in the descending colon, SP was increased and sphincter function were identi®ed. These patterns
in the myenteric plexus. were then compared with questionnaire answers on
Dysfunctional colonic motility in children can result bowel function and cystometrograms to identify a
in severe constipation. A spectrum of dysganglionoses relationship between detrusor dyssynergy and anal
has been identi®ed of which Hirschsprung's Disease sphincter tone. Rectal compliance and basal resting
(HD) is a subgroup. There are morphological sphincter pressures were lower than normal values.
di€erences between groups but the functional implica- Ramp rectal in¯ation demonstrated patterns of
tion of this is unclear. One subgroup has been sphincter activity similar to that recorded in the
identi®ed from immuno¯uorescence studies of neuro- patients' cystometrograms. There is no de®nite
transmitters in full thickness colonic biopsies in relationship of bowel function to the ®ndings on
children with colonic constipation.48 These children manometry in SCI patients. We concluded that SCI
have a markedly reduced number of SP-immunoreac- patients have abnormal anorectal function, and that
tive nerve ®bres in the muscularis propria. This anorectal manometry results were able to be classi®ed
reduction in excitatory nerve ®bres may be the basis into four patterns relating to rectal pressure and
of their functional impairment.49 Intestinal Neuronal sphincter tone in response to rectal distension. The
Dysplasia is a malformation of the enteric plexus that patterns of anorectal manometry seen were similar to
clinically resembles HD. Its pathogenesis is unknown, those in cystometrograms, however there is no de®nite
but patients appear to have defective innervation of relationship to bowel dysfunction.
the neuromuscular junction that results in chronic
constipation.50
Mechanisms for bowel dysfunction following spinal
Enteric neurotransmitters such as SP and VIP cord injury
appear to have a role in disease states a€ecting
colonic transit. If this scenario is applied to colonic Colonic dysmotility has been noted, with delayed
transit following SCI, impaired colonic transit may be colonic transit times and a loss of colonic compli-
re¯ected in abnormal concentrations of SP or VIP in ance. It is more marked in those with complete cervical
the colonic muscle layers. This may result from injuries and can result in constipation, abdominal
chronic obstruction secondary to anorectal dyssy- distention and discomfort. This may be due to a loss
nergy, or chronic dysmotility secondary to a change of descending inhibitory modulation from the sympa-
in CNS and sympathetic neuromodulation. thetic nervous system. The observation that transit
Our recent preliminary work on colonic neurotrans- delays are more profound in higher injuries supports
mitters shows no di€erence in SP, VIP or NSE in SCI this assumption.
patients and controls.51 In this study, specimens were The intrinsic enteric nervous system appears intact.
obtained from four SCI and seven control patients. No No histological changes have been demonstrated to
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 Bowel dysfunction
AC Lynch et al
200

occur in colonic specimens from long-term SCI shown to result in faster colonic transit time. The main
patients.51 Nerve ®bres containing the intrinsic reason to have a high ®bre intake therefore is to
neurotransmitters SP and VIP appear to be present absorb excess water and keep the stool soft. Forty-
in qualitatively similar amounts in SCI patients and three per cent of SCI patients use ®bre sometimes or
control specimens.51 The colon may therefore continue regularly, compared with only 23.2% of controls.
to function independently of CNS modulation after Fibre use didn't change with time after injury and
SCI. users were on average younger than controls.
The diculties with defecation following high SCI Stool softeners other than ®bre, such as docusate
could be the result of discoordinate anal sphincter sodium (Coloxyl, [Fawns & McAllan]) increase the
function.52 The normal synergistic activity of colonic amount of water in stool without increasing volume
smooth muscle and pelvic striated muscle is lost. The and have no e€ect on bowel motility. They can also
conus-mediated increase in EAS tone with increasing a€ect the intestinal absorption of other drugs,
intraabdominal pressure was seen for all groups of resulting in higher plasma levels. The stool is more
SCI patients. The re¯ex relaxation of the IAS and likely to be liquid, so continence will not be improved.
EAS can be exploited in order to defecate.52 It can They are most useful where faecal incontinence is not
also lead to faecal incontinence as the anal sphincter a risk and straining is to be avoided, such as for those
may relax at relatively low rectal volume. Lower SCI patients with haemorrhoids or autonomic dysre¯exia.
can result in faecal incontinence secondary to reduced Stimulant laxatives act by increasing intestinal
sphincter tone that is unresponsive to changes in motility resulting in less time for water reabsorption.
intraabdominal pressure. A loss of rectal tone results Senna (Senokot, [Reckitt & Colman]) has a direct
in a capacious rectum and a reliance on the manual stimulant e€ect on the myenteric plexus and also
evacuation of stool. increases intraluminal ¯uid. Bisacodyl (Dulcolax,
The relationship between colonic dysmotility and [Boehringer Ingelheim]) has a similar mode of action
anorectal dysfunction is unknown. Does the functional and is often used as a suppository to initiate bowel
obstruction caused by dyssynergic EAS contraction evacuation. Dose dependent side e€ects can occur.
during defecation lead to a change in colonic motility? These include abdominal cramping, diarrhoea and
In constipated non-SCI patients correction of pelvic electrolyte imbalance. Chronic use of stimulant
¯oor abnormality often corrects abnormal transit laxatives, especially senna, can result in a progressive
time.53 Alternatively, does the colon fail to transport unresponsiveness. Osmotic laxatives such as lactulose
faeces to the rectum at a rate and volume sucient to (Duphalac, [Duphar]) draw ¯uid into the colon. They
generate sphincter relaxation and defecation? Patterns can result in more liquid stool and cause cramping.
of bladder and bowel dysfunction following SCI, Laxative use was almost ten times more frequent
demonstrate a common loss of coordination in re¯ex among the SCI patients, becoming even more frequent
and voluntary muscle functions.52 with increasing time from injury. This may suggest a
greater incidence of constipation.
Enemata are often employed when suppositories or
Current management strategies
digital stimulation fail. Long term use can result in
The approach to bowel management in the spinal enema dependence and side e€ects such as rectal
injured patient should address speci®c issues such as trauma and autonomic dysre¯exia can occur.
faecal incontinence, constipation, and functional Prokinetic agents such as cisapride (Prepulsid,
mobility. This must be within the context of the [Janssen-Cilag]) have been employed to reduce
patient as a whole person and consider their cultural, constipation in SCI patients. Transit times are
social, sexual and vocational roles. A bowel care improved, however, cardiac arrhythmias have been
regimen needs to be generated that ®ts the person's noted with long-term use.54
long-term routine. The aim should be e€ective colonic SCI patients with UMN lesions can exploit the
evacuation without faecal incontinence or other rectocolic re¯ex to e€ect defecation. Digital stimula-
complications. Regularity of evacuation prevents tion can result in a re¯ex wave of conus-mediated
excessive buildup of faeces and impaction. Appro- rectal peristalsis. The intact rectoanal inhibitory re¯ex
priate equipment, such as commode chairs and (RAIR) then causes IAS relaxation and defecation.
wheelchair able toilets, needs to be supplied for an Rectal sensation is reduced however, so defecation has
adequate long-term bowel programme. to be anticipated on a regular basis. Based on the
Dietary manipulation is important. Adequate water anorectal manometry data52 it is possible to identify
intake promotes transit by keeping the stool soft. those SCI patients who will re¯exly defecate at low
Fibre is promoted to give the stool bulk and rectal volume. These patients require a bowel manage-
plasticity.15 This is thought to assist colonic transit ment programme that keeps the rectum empty to
in neurologically intact patients, probably by promot- reduce the incidence of incontinence. Those patients
ing propulsive activity secondary to increased colonic with UMN lesions and an obstructed defecatory
wall distention. However, an increase in stool bulk pattern need a management plan that mimics
may mean more time spent with bowel care, and anorectal trauma but still allows adequate rectal
increasing ®bre intake for SCI patients has not been evacuation to avoid constipation.
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 Bowel dysfunction
AC Lynch et al
201

Patients with LMN lesions have an are¯exic bowel spina bi®da who had the LACE procedure, there was a
and reduced sphincter tone. The increase in sphincter consistently high level of functional continence achieved
pressure with Valsalva is reduced, leading to increased following surgery.65 The use of the procedure in spina-
risk of incontinence, especially with liquid stool. The bi®da has shown that this procedure may have an as yet
aim is therefore to keep stool consistency ®rm. Local unidenti®ed role in SCI patients.
anorectal re¯exes are often insucient to result in
defecation, and a compliant rectum acts as a large
Future objectives for the investigation and
reservoir, so stool is digitally removed.
management of bowel dysfunction
A Brindley sacral anterior nerve root stimulator
(S2 ± S4) can be used for electromicturition to achieve The SCI patients with bowel management problems are
regular, complete bladder emptying. Often deafferen- easy to identify. Interview and clinical examination can
tiation of the sacral posterior nerve roots is performed generate an impression of their general bowel function
before the stimulator is implanted to produce detrusor and identify problems such as constipation, faecal
are¯exia and interim urinary continence. The deaf- impaction, anal ®ssures, and haemorrhoids. Simple
ferentation also results in loss of the sacral re¯exes tests of anorectal function are available. These could be
necessary for defecation. The stimulator can be used to performed on all SCI patients in the same manner that
initiate defecation, not during stimulation, due to bladder dysfunction is investigated. Anorectal mano-
simultaneous rectal and sphincter contraction, but metry will identify those with dyssynergic sphincter
when stimulation stops and the EAS relaxes instanta- function. For those with abdominal bloating and
neously and the rectum relaxes slowly, resulting in constipation, abdominal X-ray and colonic motility
spontaneous defecation. This has been shown to result studies give further useful information.
in quicker, more controllable defecation than the re¯ex After 12 months from SCI, bowel function does not
method.55,56 seem to change either with increasing time after injury,
Colostomy may be an alternative for SCI patients or increasing age. This allows for early identi®cation
with ongoing bowel management diculties. It has of what may be ongoing problems.
been shown to result in improved quality of life, it is After the acute phase of spinal cord injury, prompt
accessible for those with poor hand dexterity, and identi®cation of those with bowel management
o€ers control of faecal incontinence. Risks and problems would be useful. Anorectal manometry
complications that are associated with any surgical could then be performed. Speci®c patterns identi®ed
procedure may not make it acceptable to all SCI may help determine future management.52 Those with
patients. A recent study by us has revealed that a compliant rectum and re¯exly relaxing sphincter can
patients with colostomies do not have their quality of employ digital stimulation to re¯exly defecate. Patients
life impaired.57 A standardised previous validated with high rectal compliance (pattern 4) may require
question designed to assess quality of life in spinal regular manual evacuation to ensure their compliant
injured patients was sent to 26 spinal cord injured rectum is empty. Patients with increased rectal and
patients with colostomies and 26 spinal cord injured sphincter tone (pattern 1) will probably have high
patients without colostomy. The two groups were injuries and need to be identi®ed because this pattern
matched for level of injury, completeness of injury, may result in inadequate rectal evacuation. Anecdo-
length of time with injury, age (+5 years) and gender. tally, these would be the patients where manual
There was no signi®cant di€erence (P40.05) in the evacuation is dicult and often accompanied by
two groups of patients in regard to their general autonomic dysre¯exia.
wellness, emotional, social, or work functioning. Following SCI, the colonic nervous system may still
Further prospective studies are needed and we have be intact but functioning in an ummodulated way. The
one underway at present. existence of SP analogues and inhibitors of SP
The antegrade continence enema (ACE) procedure is degradation that are reactive in vitro and in vivo have
now widely accepted as an option in the treatment of already been used to demonstrate a reduction in
faecal incontinence in children who have not responded colonic transit time in rats.27 These compounds are
to medical management.58,59 The operation involves useful tools to further investigate the actions of
attaching the appendix to the surface of the abdomen as colonic neuropeptides. Increasing coordinated colonic
a catheterisable channel to enable regular antegrade peristalsis would be a useful therapeutic modality. This
colonic washouts. There have been a number of could be done either by direct stimulation of colonic
modi®cations to the ACE procedure including non- smooth muscle or by stimulation of SP and VIP
reversal of the appendix,60 various skin ¯ap techni- immunoreactive nerve endings.
ques,61 a simpli®ed laparoscopic technique (LACE),62,63 Although improving colonic motility and appro-
and the use of the procedure in older patients.64 The priate bowel management may help, there will be some
procedure appears to have a low incidence of SCI patients with ongoing bowel problems. Colostomy
complications and morbidity. It requires a motivated formation has been used to provide the patient with
patient with good hand function and is generally relief from constipation and anorectal dysfunction and
considered best in patients with a lax anal sphincter. an independent means of managing their own bowel
In a recent study we have undertaken children with function. Further research needs to be done into the
Spinal Cord
 Bowel dysfunction
AC Lynch et al
202

di€erences in quality of life and bowel function 9 Stone JM, Wolfe VA, Nino-Murcia M, Perkash I.
following colostomy formation in SCI patients. Colostomy as treatment for complications of spinal
Another focus of future investigation is the intrinsic cord injury. Arch Phys Med Rehabil 1990; 71: 514 ± 518.
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mechanism and the physiology of defecation. Dis Colon
on colonic neurotransmitters imply that the intrinsic
Rectum 1987; 30: 970 ± 982.
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(with respect to NSE, SP and VIP) following SCI. The sphincter revisited. Aust NZ J Surg 1996; 66: 626 ± 629.
way this muscle functions without spinal cord 12 Goyal RK, Hirano I. The enteric nervous system. New
modulation may form the basis for some of these Engl J Med 1996; 334: 1106 ± 1115.
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Spinal Cord
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