Colonic and anorectal dysfunction associated with multiple sclerosis

In a recent survey of 280 unse-Icctcd patients with multiple sclerosis, 68% reported constipation and/or fecal incontinence.. Tbis review outlines tbe clinical features and pathophysiolo

THE AMERICAN JOURNAL or GASTROENTEROLOGY

Copyright© I989by Am.Coll of Gaslrocnterology

Vol.84 No 6 1989 Printed in U.S.A.

Clinical review

Colonic and Anorectal Dysfunction Associated

with Multiple Sclerosis

John P, Hinds, M.B.Bch., and Arnold Wald, M.D.

Gastroenterology Unit Montefiore Hospital University of Pittsburgh School of Medicine Pittsburgh Pennsylvania

Gastrointestinal symptoms are common in patients

with multiple sclerosis In a recent survey of 280

unse-Icctcd patients with multiple sclerosis, 68% reported

constipation and/or fecal incontinence In contrast to

bladder dysfunction which has been extensively studied,

bowel dysfunction in tbis disease bas received relatively

little attention Tbis review outlines tbe clinical features

and pathophysiology of constipation and fecal

inconti-nence in multiple sclerosis and presents treatment

op-tions and suggesop-tions for investigation of colonic and

anorectai dysfunction in tbis population

INTRODUCTION Multiple sclerosis is a common neurological disease

aflecting approximately one-quarter million Americans

(1) The onset of the disease is usually during the third

and fourth decades: 60% of those affected are women

The characteristic pathological feature in multiple

scle-rosis is focal demyelination of axons leading to plaque

formation which can occur within any area of the white

matter of the brain and spinal cord The result is an

intermittent partial or complete block in nerve

conduc-tion: the clinical picture that ensues depends on the

location of the foci of demyelination within the central

nervous system (2)

Gastrointestinal symptoms are common in patients

with multiple sclerosis In a recent survey of 280

unse-lected subjects with multiple sclerosis (3), 68% reported

constipation and/or fecal incontinence, complaints that

were common even in mildly disabled subjects (Table

1) Upper gastrointestinal symptoms (4, 5), especially

difficulty with swallowing {6 7) are also features of the

disease, although these complaints were less prominent

in our survey population In contrast to bladder

dys-function, which is also common and has been

exten-sively studied (8-10), bowel dysfunction has received

relatively little attention

Received Nov W 1988: accepted Nov 10 1988.

In this review, we outline the clinical features and pathophysiology of constipation and fecal incontinence

in multiple sclerosis We also present various treatment options and suggestions for further studies of colorectal dysfunction in this disease

CONSTIPATION Constipation is a common complaint in patients witb multiple sclerosis and was present in 43% of our survey population We defined constipation as infrequent bowel movements (<3/wk) and/or rectal manipulation

to facilitate defecation {during >50% of bowel move-ments) and/or frequent laxative, enema, or suppository use (>l/wk) Constipation was more common in the moderately (48%) and severely (56%) disabled groups compared to the mildly disabled (24%) The high prev-alence even in the latter group su^ests that factors other than lack of mobility are important

Normal colonic motility

The two major functions of the colon are to retard tbe fecal stream, ensuring the absorption of fluid and electrolytes, and to act as a storage organ so that defe-cation can occur at a socially convenient time

The colon consists of an outer longitudinal and an inner circular smooth muscle layer between which lies the intrinsic nervous system (myenteric plexus) Tbe extrinsic nerve supply is via the autonomic nervous system The parasympathetic nerve supply to the as-cending colon and proximal one-half of the transverse colon is via the vagus nerve The remainder of the colon

is supplied by parasympathetic fibers from sacral nerves

2, 3, and 4 via the nervi erigentes These nerves synapse with intrinsic neurons, among them cholinergic nerves which release acetylcholine to muscarinic receptors on the muscle cells

The sympathetic innervation of the colon is supplied

by the lower six thoracic and first three lumbar seg-587

TARt_h I

Lower Bowel Sympioms in Muhiple Sclerosis (n = 280)

Splk» polmnllml

Symptoms Constipation

Fecal incontinence

Constipation and fecal incontinence

Constipation and/or fecal incontinence

Prevalence 43%

51%

25%

68%

TRANSUEyBRANE

ments of the spinal cord via the inferior and superior

mesenteric ganglia For the most part sympathetic

nerves are in contact with cholinergic nerves: they

inhibit release of acetylcholine rather than act on the

muscle cells directly There is also evidence for

non-adrenergic inhibitory' nerves in the colon Generally

SF>eaking, stimulation of the sympathetic nervous

sys-tem inhibits colonic motility, wbereas stimulation of

the parasympathetic nervous system enhances motility

(11.12)

Two types of electrical activity are generated by

mus-cle cells of the colon, the slow waves and the

calcium-dependent spike potentials The slow waves are of

vari-able frequency (3-12 cycies/min) and amplitude

Mus-cle contraction is generated by the spike potentials,

which are rapid depolarizations that last a few

milli-seconds Spike potentials of short duration occur only

on the peak depolarization of the slow waves, suggesting

that these slow waves act as the pacemaker of the colon

(Fig 1)- Stretch, neural, and hormonal stimulation are

all able to generate spike potential activity (12 13)

Three main types of muscular contractions occur in

the colon Segmental contractions are nonpropulsive

events caused by spike activity of short duration (<5 s):

their main function is to retard the fecal stream

Pro-pulsive contractions occur in association with 15- to

30-s bursts of electrical activity, whereas mass

move-ments propagate over the entire colon after spike bursts

of about 30 s and may result in defecation

Adminis-tration of atropine decreases the frequency of the slow

wave-spike complexes (13) Control of the electrical

events in the colon, and, therefore, propulsion, appears

to be largely a function of the cholinergic system (13,

14), although noncholinergic excitatory nerves also

bave been identified in the human colon (12, 13)

For about 40 min after a meal is eaten, there is an

increase in colonic spike activity that is usually

associ-ated with propulsive contractions or mass movements

This gastrocolonic response is initiated by the fat

com-ponent of the meal (15) and is mediated in part by

cbolecystokinin although other gastrointestinal

pep-tides such as gastrin (16), neurotensin (17), and

sub-stance-P (18) may also play a role Secretin inhibits this

choleeystokinin-induced motor activity (19) This

gas-trocolonic response persists after vagotomy (20), and

seems to be mediated via the spinal cord, as it is absent

after thoracic cord transection (21) The response also

> Slow w»¥»

COLONIC PRESSURE

/ \

FIG I Transmcmbranc potential in the colon (top) and colonic motor activity {bottom) Spike potentials occur only on ihc peak

depolarization of the slow waves and produce myogcnic contractions which can be measured using pressure Iransduccr^.

SAGITTAL

SPMItlCT£ft

Kui 1 Sagittal views of the anorectum illustrating the important structural components Inset illustrates ihe anterior pull of the

ano-rectum and closure of the anal canal during simultaneous contraction

of the puborectalis muscle and external anal sphincter Adapted from Wald (23V

requires muscarinic and opioid receptors as it is blocked

by alropine and naloxone (22)

Anorectal anatomy

Tbe anal canal is an anteroposterior slit, 3 to 4 cm long, which is kept closed by the tonic activity of the smooth internal and striated external anal sphincter muscles The rectum is a compliant reservoir which at rest is kept at an approximately 90° angle to the anal canal by the tonic contraction of the puborectalis mus-cle (Fig 2) This musmus-cle is part of the pelvic floor, and forms a "sling" around the anorectal junction with its insertions attached anteriorly to the pubis (23)

The anal canal has a dense network of nerve fibers which can discriminate between solid, liquid, and gas (24, 25) This area is therefore felt to be important in the maintenance of continence The rectum possesses stretch receptors oniy (26)

Normal defecation

At the initiation of defecation, closure of the glottis and contraction of the abdominal wall muscles increase

June 1989 COLONIC AND ANORECTAL DYSFUNCTION IN MS 589 intraabdominal pressure, thus propelling feces forward

When the fecal bolus reaches the upper rectum, the

pelvic floor and puborectalis muscle relax

simultane-ously, resulting in straightening ofthe anorectal angle

Distension of the rectum by stool results in reflex

relaxation ofthe internal anal sphincter (RISR) and a

transient contraction of the external anal sphincter

When a critical pressure is reached in the rectum, the

external sphincter is inhibited and the fecal bolus

ex-pelled After cessation of straining, the pelvic floor

ascends, the anorectal angle is restored to normal, and

a rebound contraction of the external anal sphincter

occurs

The higher control of defecation is incompletely

understood There is evidence to suggest that a

defeca-tion center exists in the pons, which is under cortical

control (27 28) Other areas of the brain may also be

important: stimulation of the hypothalamus may

in-hibit or enhance colonic motility, depending on the

area stimulated (28) Another defecation center is

prob-ably present in the sacral cord In patients with high

spinal cord transection rectal sensation is lost, but

defecation can proceed in a regular fashion if an

appro-priate stimulus (e.g., digital stimulation) is applied to

the rectum This has been termed "automatic

defeca-tion," as it occurs without the influence of higher

cortical control In patients with low spinal injury, rapid

distension of the rectum does not produce a rectal

contraction as in normal individuals and patients with

high spinal cord injury Therefore, this contraction

presumably is mediated by a spinal reflex (29)

Colorectal dysfunction in multiple sclerosis

Studies of colonic dysfijnction in multiple sclerosis

were performed by Glick et al (30), who evaluated

seven men with severe spastic quadriparesis who also

were severely constipated and had bladder dysfunction

Somatosensory-evoked potentials, cystometrograms,

colonmetrograms and colonic motor and myoelectric

activity were carried out All seven patients exhibited

"hyperreflexic" or high pressure/volume

colonmetro-grams {Fig 3); the authors felt that these were analogous

to the hyperreflexic cystometrograms which were

pres-ent in most of these patipres-ents Colonic motor and

myo-electrical activity were also abnormal in all seven

pa-tients The baseline mean amplitude of colonic motor

activity in the multiple sclerosis patients was

signifi-cantly lower than in normal controls In addition,

pa-tients had no demonstrable postprandial increase in

colonic motility as was observed in the controls (Fig

4) All patients had abnormal cortical

somatosensory-evoked responses demonstrating lesions in the central

neural pathways Based on these results, the authors

proposed the existence of a "visceral neuropathy" as

the cause of severe constipation in this group of

pa-tients

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Fici 3 Colonomelrograms in which water is infused into Ihe rectum while intracolonic pressures are monitored continuously, A

normal colonometrogram {ahove) is compared with a hyperreflexic study in a patient wiih multiple sclerosis {hvlow) "C" denotes colonic contractions and "R" indicates respiratory excursions From Glick ei

al (30).

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Fi(i 4 Colonic myoelectrical spike potential frequency recorded from the rectosigmoid colon of seven patients wiih multiple sclerosis

and 11 control subjects From Glick et at (30).

Absence of the gastrocolonic response has also been seen in chronic idiopathic intestinal pseudoobstruction (31) and in diabetics who are severely constipated (32) The colonic muscle responds normally to the cholin-esterase inhibitor, neostigmine, in these patients, sug-gesting that the cholinergic postganglionic neurons are intact This response to neostigmine has not been in-vestigated in patients with multiple sclerosis Neverthe-less, it appears that all three groups of patients have a disorder ofthe neurohormonal control of colonic mo-tility Further assessment ofthe gastrocolonic response

in multiple sclerosis patients should include response

to neostigmine and evaluation of patients with consti-pation who are less disabled than Glick's subjects High pressure/volume colon metrograms have been reported in constipated subjects who have other neu-rological diseases (33) This response is thought to result from interruption of the normal cortical inhibition of colonic motor activity The net result may be a func-tional obstruction to the passage of colonic contents In contrast, low pressure/volume colonmetrograms have been reix)rted in patients with sacral cord and sacral

plexus lesions (33) and in multiple sclerosis patients

with demyelination ofthe conus medullaris (34) This

may result in a highly compliant rectum (megarectum)

which may lead to difficulty with defecation through

several mechanisms There may be failure ofthe rectum

to contract around the distending stool, or the ability

to perceive rectal distension may be impaired, resulting

in the accumulation of a large fecal bolus that is too

large or painful to expel (35)

Forty-eight percent of the constipated subjects with

multiple sclerosis in our survey population reported a

need to digitally manipulate the rectum to facilitate

defecation This may reflect poor expulsion effort due

to generalized muscle weakness or megarectum as

al-ready mentioned However, the possibility of a

func-tional obstruction to defecation also must be

consid-ered

In a recent study, Weber et al (36) evaluated 16

patients with multiple sclerosis and urinary bladder

dysfunction, using anorectal manometry, colonic

transit studies, and urodynamic testing Fifteen

de-scribed themselves as constipated, and six also

com-plained of fecal incontinence Prolonged colonic transit

was demonstrated in 14 patients, of whom seven had

left-sided delay only, whereas seven had a more

gener-alized slowing Five patients had decreased perception

of rectal sensation, and 10 exhibited manometric

cri-teria suggestive of so-called "outlet obstruction." These

criteria were defined as hypertonia in the upF>er anal

canal, with or without ultraslow waves greater than 20

cm H:O; the presence of an "overshoot" contraction

after the rectoanal inhibitory reflex (RISR); and RISR

absent or the amplitude insufficient Twelve patients

had a hyperreflexic urinary bladder on cystometrogram,

and detrusor urethral dyssnergia was seen in 14 cases

On the basis of these results, the authors suggest that

the prolonged colonic transit and anorectal dysfunction

are secondary to tbe neurological disorder, and

hypoth-esize the existence of "rectoanai dyssnergia" causing

problems of rectal evacuation in the same way that

detrusor urethral dyssnergia causes abnormal bladder

emptying

These findings need confirmation and further

clari-fication As the authors point out, the manometric

abnormalities seen in outlet obstruction are also seen

in other disorders (37) Second, compliance

measure-ments of the rectum were not performed This is an

important parameter to measure if abnormalities of

internal sphincter relaxation are to be interpreted

ac-curately Furthermore, it is possible that some of the

anorectal abnormalities described are a consequence,

rather than a cause, ofthe constipation These questions

notwithstanding, it is likely that neurogenic

abnormal-ities of colonic and/or anorectal function are the cause

of constipation and defecatory difficulty in this disease

Evaluation

When evaluating constipated patients with multiple sclerosis, one should establish the duration of consti-pation and its relationship to the onset and other man-ifestations ofthe disease Stool frequency alone may be

a poor parameter to follow, as laxative use and digital evacuation of the rectum are very common (3) The degree of straining and the presence or absence of a defecatory urge should be ascertained The presence of other medical conditions associated with constipation should be established A drug (Table 2) and diet history should be taken and the degree of immobility assessed Patients with genitourinary symptoms should be asked about fluid intake, since they commonly restrict fiuids

in order to avoid urinary incontinence: unfortunately, constipation often follows

In addition to a detailed physical examination, a rectal and pelvic examination should be done to look for prolapse, rectocele, fissures, and fecal impaction Resting anal tone and external sphincter pressures should be assessed digitally Puborectalis function can

be evaluated by hooking the examining finger poste-riorly onto the puborectalis "bar" and feeling the mus-cle contract when the patient squeezes and relax when asked to strain Initial investigation should include blood glucose, electrolytes, calcium, and thyroid func-tion tests if necessary Flexible sigmoidoscopy and bar-ium enema should be done to look for structural ab-normalities if discontinuation of ofFending drugs and/

or addition of fiber supplementation have not resolved the problem If easily remediable causes of constipation are not found, more specialized studies are indicated (38) Such studies have been found useful in patients with idiopathic constipation and are presumed to be useful in constipated patients with multiple sclerosis

If the complaint is decreased stool frequency, a co-lonic transit study using radiopaque markers may be helpful, and allows estimation of segmental and total colonic transit times Slow transit may have several patterns: transit may be slow through all segments

TABLE 2

Drugs That May Cause Constipation

Antacids (aluminum, calcium) Anticholinergics

Anticonvulsants Antidepressanls Antihypertensives Anti-Parkinsonian Bismulh compounds Laxatives (long-term) Muscle relaxants Diuretics Iron Opiates Psychotherapeutic drugs

June 1989 COLONIC AND ANORECTAL DYSFUNCTION IN MS 591 (colonic inertia); slow through the left colon only

(hind-gut dysfunction), or through the rectosigmoid only

(outlet obstruction or functional rectosigmoid

obstruc-tion) Anorectal manometry allows the evaluation of

internal and external sphincter pressures, internal

sphincter relaxation, rectal sensation, and rectal

com-pliance, as well as indirect assessment of defecatory

technique and effort on attempted expulsion of the

manometry apparatus (38, 39)

Defecography is a dynamic study of defecation (40)

which may be helpful in evaluating patients who have

difficulty with expulsion of stool Puborectalis

relaxa-tion, pelvic floor descent, and completeness of

evacua-tion of a "barium stool" can be assessed In addievacua-tion,

anatomic abnormalities that may interfere with

defe-cation, such as an intussusception or a rectocele, may

be revealed by this technique A recently described

modification of this technique (41) would be potentially

helpful in studying patients with multiple sclerosis It

employs a pressure-sensitive radiotelemetry capsule

which is placed in the rectum and permits assessment

of defecatory effort, a factor that is crucial for normal

defecation and that may be significantly impaired in

this population Abnormalities or lack of coordination

of puborectalis and external sphincter function can be

assessed by simultaneous needle electromyogram This

technique, although complicated, may provide the most

scientific means of assessing the complex problems with

defecation that exist in this population However, the

utility of defecography in evaluating patients with

con-stipation is uncertain at the present time

Colonic transit studies, anorectai manometry, and

defecography, therefore, may allow the separation of

patients into categories of constipation which may

re-quire different therapeutic approaches (Table 3)

Treatment

Treatment of constipation in patients with multiple

sclerosis should be undertaken with the recognition that

TABLE 3

Possible Mechanisms of Fecal Incontinence in Multiple Sclerosis

Mechanism

Sensory

Abnormal

Megarectum

Reservoir

Decreased compliance, ui^ency

Sphincteric

Anal sphincter

Puborectalis

Other

Immobility

Motivation

Fecal impaction with overflow

Reference 36

34, 35 60 30.33 10.36 Not studied

23

42 43

one may be treading a fine line between treating con-stipation and precipitating fecal incontinence (see be-low) Coexistence of constipation and fecal inconti-nence is common, as evidenced by our survey, which revealed that 70 (59%) constipated subjects had expe-rienced fecal incontinence at least once in the preceding

3 months Indeed, it is our experience that certain patients prefer to remain constipated so as to avoid soiling episodes, regarding this as the lesser of two evils However, treatment is important, in that a distended rectum may exacerbate bladder symptoms from a local pressure effect as well as by causing increased afferent impulses to the spinal cord (42) Constipation has also been reported to cause increased limb spasticity (42, 43)

In the absence of a clearly defined physiological abnormality, treatment is largely empirical An ade-quate fluid intake and high-fiber diet should be encour-aged Certain individuals may tolerate only small amounts of fiber initially, due to abdominal bloating, necessitating a very gradual increase in dosage over several weeks Exercise, preferably walking, should be encouraged; if this is not possible, wheelchair exercises

or swimming are alternatives (42, 43) Generally speak-ing, it is helpful to establish a regular schedule for defecation Patients should be encouraged to sit on the commode for 5 or 10 min after a chosen meal to take advantage ofthe gastrocolonic reflex, although this may

be absent in the most disabled patients (30) If these measures are unsuccessful, a glycerin suppository or, if ineffective, a bisacodyl suppository or an enema may

be given on a twice-per-week schedule Digital stimu-lation ofthe rectum may provoke defecation in subjects with intact sacral reflexes; rarely is manual disimpac-tion required Stimulant laxatives should be avoided if possible; not only are these agents potentially addictive, but they have been shown to damage the enteric nerv-ous system (44) Oral agents often loosen the stool and have an unpredictable onset of action, thus exposing susceptible individuals to fecal incontinence Stool soft-eners are widely used, but recent evidence suggests that some of these agents are ineffective (45)

For patients with colonic inertia, cholinergic agents such as bethanechol and neostigmine (46) may be tried, but experience with these agents in idiopathic consti-pation has been disappointing Cisapride, a new proki-netic agent which facilitates peripheral acetylcholine release, may be more helpful (47), although experience with this drug has been limited However, the use of these drugs in multiple sclerosis carries the risk of exacerbating genitourinary symptoms in patients with uninhibited bladders Alternatively, it is possible that anticholinergic drugs may be helpful in patients with constipation associated with hyper-reflexic colonome-trograms, just as they are helpful in managing patients

with hyper-reflexic cystometrograms This area needs

further investigation

Abnormalities of puborectalis function and rectoanal

dyssnergia, if they exist, may cause obstruction to

de-fecation Further evaluation of these issues is necessary

FECAL INCONTINENCE

Fecal incontinence occurred at least once in the

preceding 3 months in 51% of our survey population

(3) Fecal incontinence was common even in mildly

disabled subjects, increased with decreasing mobility,

and correlated strongly with the presence of

genitouri-nary symptoms This is not unexpected, since the

cor-ticospinal and reticulospinal tracts which serve motor,

sphincter, and bladder functions lie in close proximity

to each other and are frequent sites of demyelination

in this disease (48)

Normal anorectal continence mechanisms

At rest, the internal anal sphincter (IAS) contributes

up to 85% of the pressure in the anal canal (49) and

provides a passive barrier to leakage of stool

Stimula-tion of stretch receptors in the rectal wall by arrival of

stool causes a transient reflex relaxation ofthe IAS and

a phasic contraction of the external anal sphincter

(EAS) This contraction of the EAS is an important

continence mechanism Since it is present in spinal

cord-injured patients (50, 51) it has been termed a

reflex, although it is subject to modiflcation by cortical

input (52) The amplitude and duration of the phasic

EAS response increase with increasing rectal distension

up to a volume of approximately 150 ml (5!) or a

pressure of 50 mm Hg (53), at which point it is

inhib-ited If defecation is to be postponed, continence is

maintained by simultaneously increasing pressure in

the anal canal (by contracting the EAS) and narrowing

the anorectal angle (by contracting the puborectalis

muscle) The rectum stretches to accommodate the

stool, intrarectal pressure decreases, and the urge to

defecate subsides The requirements for normal

conti-nence therefore are the ability to sense the arrival of

stool in the rectum, the ability of the rectum to act as

a compliant reservoir, the effective contraction of the

EAS and puborectalis consciously and subconsciously,

and motivation to make the appropriate responses (23)

Synchrony of these events requires a normal intrinsic

and extrinsic nervous system, as well as uninterrupted

pathways to and from the cerebral cortex IAS resting

tone is dependent on input from the sympathetic (54)

and parasympathetic nervous systems (55), whereas

relaxation of the IAS is mediated via the myenteric

plexus and persists after section of the pelvic nerves

(55) cord transection (50), and high and low spinal

anesthesia (56) The nerve supply ofthe EAS is from

sacral nerves 2,3, and 4 via the pudendal nerve, whereas

that of the puborectalis arises from branches of Si and S4 which lie above the pelvic floor (57) Rectal sensation

is transmitted by parasympathetic flbers of S2, S3, and S4 (26) Bilateral damage to the nerve supply of the anorectum is probably required before fecal inconti-nence ensues (55), although incontiinconti-nence has been reported with unilateral paralysis of the puborectalis (57)

Normally, the muscles of the pelvic floor are kept in

a state of constant activity by a spinal reflex The afferent limb of this reflex is via the posterior columns ofthe spinal cord Evidence for this comes from EMG studies ofthe pelvic floor of patients with tabes dorsalis

No activity is seen in the pelvic floor muscles at rest, but voluntary effort produces a normal pattern of elec-trical activity indicating intact efferent pathways (51)

In multiple sclerosis, bilateral disease of the posterior columns is frequently present (48)

Fecal incontinence

There is a paucity of information available concern-ing this problem in multiple sclerosis; accordconcern-ingly, the proposed mechanisms are largely speculative (Table 4)

ln multiple sclerosis, resting anal pressures may be low Arrival of stool in the rectum may trigger IAS relaxation which is poorly antagonized by weak puborectalis and EAS musculature (36) Furthermore, in the presence of EAS denervation, relaxation ofthe IAS has been shown

to be more pronounced and of longer duration than normal, thereby adding lo the risk of incontinence (49 50) We have noted an inability of incontinent patients with multiple sclerosis to keep an inflated balloon in the rectum (unpublished observation) This has been previously reported in subjects with spinal cord tran-section (50, 51), and probably reflects impairment of striated muscle function

Abnormalities of rectal sensation reported in patients with multiple sclerosis (36) may predispose to inconti-nence as they do in other disorders (26 58 59) De-myelinating plaques in the sensory and motor pathways

TABLE 4

Po.isihle Mechanisms of Constipation in Multiple Sclerosis

Mechanism Abnormal colonic motiiity Colonic inertia Absent gastrocolonic reflux Laxative abuse

Anorectal dysfunction High rectal compliance Rectoanai dyssynergia Decreased sensation Others

Poor expulsion efTort Immobility

Drugs Inadequate fluid intake

Reference

36 30 44 34 36 36

June 1989 COLONIC AND ANORECTAL DYSFUNCTION IN MS 593

in patients with multiple sclerosis may result in loss of

or delay in perception of rectal distension with inability

to respond as quickly or as effectively as needed The

presence of a megarectum is also associated with

de-creased rectal sensation (60); it therefore is important

to measure rectal compliance so that the significance

of abnormal rectal sensation can be interpreted

appro-priately

Urgency of defecation is a frequent accompaniment

to incontinence in patients with multiple sclerosis (3,

61) This may be due, in part, to low colonic/rectal

compliance as demonstrated by colonometrogram in

patients with multiple sclerosis who have lesions ofthe

motor fibers of the brain or descending spinal tracts

(38) It has been suggested that this high pressure/

volume response to colonic filling is due to interruption

ofthe normal cortical inhibition of colonic motor

ac-tivity (30 33) In contrast, low pressure/volume

colon-ometrograms have been described in patients with

de-myelination of the conus meduUaris (34) These

pa-tients also have fecal incontinence, but it appears to be

primarily sphincteric in origin More manometric

stud-ies are needed to clarify these issues

Evaluation

When evaluating bowel dysfunction in a patient with

multiple sclerosis, it is helpful to establish the time of

onset of symptoms in relation to the initial diagnosis of

the disease, as well as an association, if any with the

appearance or worsening of urinary symptoms and long

tract signs The frequence of incontinence episodes, the

quantity and consistency of the stool, the presence of

urgency or lack of warning, and the impact of the

problem on the patient's social life should be assessed

Potential explanations of incontinence other than those

secondary to multiple sclerosis need to be explored,

such as history of anorectal surgery, multiple childbirths

(61, 62), back injuries, or a previous history of

consti-pation with severe straining (63) As consticonsti-pation

co-existed in 49% ofthe incontinent subjects in our survey,

it is important to take a history concerning laxative use;

these agents may predispose susceptible individuals to

soiling In addition, the possibility of fecal impaction

with overflow incontinence must be considered in

se-verely disabled patients who complain of soiling

On examination, signs of denervation such as atrophy

of gluteal muscles, diminished perianal sensation (S3,

S4, S5), and an absent anocutaneous reflex or anal

"wink" may be apparent Resting anal tone and external

sphincter pressures may be diminished After posterior

traction of the puborectalis or on withdrawal of the

examining finger, anal "gaping," a sign of neurogenic

sphincter denervation, may be seen (64) The presence

or absence of fecal impaction should also be noted

Patients who experience troublesome fecal

inconfi-nence may benefit from a detailed physiological

assess-ment Manometric assessment of sphincter pressures and rectal compliance measurement should be per-formed Single-fiber EMG (65) ofthe EAS and pubo-rectalis may reveal evidence of denervation but this test is available in only a few specialized centers A proctogram (66) is helpful in evaluating the anorecta! angle at rest and on straining Abnormalities of pelvic floor descent may also be assessed Paralysis of the puborectalis has been noted in other neurological dis-orders (67, 68), but it is not known if this occurs in multiple sclerosis

Treatment of fecal incontinence

As with incontinence due to other neurological dis-eases, treatment of fecal incontinence in multiple scle-rosis patients can be frustrating, and often is only partly successful Establishing a daily time for defecation and

a routine schedule of enemas or suppositories to keep the rectum empty may reduce the frequency of unex-pected soiling episodes If stools are loose, loperamide

or diphenoxylate may be helpful in improving stool consistency and reducing stool frequency Loperamide has been shown to improve anal sphincter pressures and rectal compliance in subjects with idiopathic fecal incontinence (69); its efficacy in patients with multiple sclerosis is unknown If frequent incontinence of solid stool occurs, stool frequency and bulk can be decreased

by reducing fiber in the diet The patient is given a weekly enema followed by a bisacodyl suppository to empty the colon in order to prevent fecal impaction There are no published trials of biofeedback therapy for fecal incontinence in patients with multiple scle-rosis Such treatment aims to coordinate EAS contrac-tion with rectal distension (simulating a stool in the rectum) using a three-balloon probe (70, 71) To be eligible, subjects must have the ability to contract the EAS and sense appropriate volumes of air when a balloon is distended in the rectum Previous studies of biofeedback in children with meningomyelocele (59) demonstrated that abnormal rectal sensation is a pre-dictor of therapeutic failure Accordingly, it is likely that only mildly disabled subjects would benefit from this treatment In addition, studies may be difficult to interpret, due to the waxing and waning of neurological signs and symptoms, characteristic of the disease

SUMMARY Bowel dysfunction in patients with multiple sclerosis

is common and to date has not been satisfactorily characterized The problem is somewhat diflRcuIt to analyze since constipation and fecal incontinence often coexist; furthermore, more than one causative neuro-logical lesion may be present, thus adding to the com-plexity of evaluating bowel dysfunction in this disease

In addition, the fluctuating pattern ofthe neurological

manifestations in multiple sclerosis may result in

symp-toms of bowel dysfunction that are acute, chronic, or

intermittent The higher prevalence of multiple sclerosis

in women further complicates the issue, as both

idi-opathic constipation and fecal incontinence are more

common in women than men

Comprehensive studies of colorectai function are

needed in multiple sclerosis patients with and without

bowel dysfunction in order to characterize more fully

the abnormalities that exist in this population In

ad-dition, the relationship between genitourinary and

an-orectal dysfunction in this disease needs further

clarifi-cation Hopefully, increasing our understanding ofthe

pathophysiology of bowel dysfunction in multiple

scle-rosis will lead to more effective therapeutic

interven-tions for this often socially disabling problem

ACKNOWLEDGMENT

The authors thank Mrs Loretta Malley for expert

secretarial assistance in the preparation of this

manu-script

Reprint requests; Arnold Wald M,D Gastroenterology Unit.

Monlefiorc Hospital, 3459 Fifth Avenue Pittsburgh PA 15213.

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