Fecal Incontinence Diagnosis and Treatment - part 9 ppsx

con-1/11 9%, p >0.10], had flatus incontinence [4/15 Table 4.Prevalence of persistent defect after anal sphincter repair EAS external anal sphincter, IAS internal anal sphincter... con-I

Overlapping Repair

The high rate of failed repair associated with the

end-to-end approximation suggests that it is an

ineffec-tive method of repairing torn anal sphincters

Inves-tigators have tried different repairs and various other

ancillary therapies to improve the surgical outcome

One frequently suggested approach was to abandon

the end-to-end approximation in favor of the

over-lapping repair Although obstetricians primarily use

the end-to-end approximation, some investigators

believe that this technique is inherently incapable of

repairing the torn anal sphincter because the

sphinc-ter muscle and capsule are just not strong enough to

hold the sutures in an end-to-end configuration In

contrast, colorectal surgeons generally favor the

overlapping repair This method, originally

described in the early 1970s by Sir Allen Park,

dis-tributes the tension on the sutures over a larger area

to reduce the likelihood that they will tear through

the sphincter muscle and capsule [24]

Two small case series seemed to suggest that the

overlapping repair has a lower failure rate than

end-to-end approximation [25, 26] Two British

investiga-tors used the overlapping technique to repair 32 anal

sphincters torn during vaginal delivery [25] After 20

weeks, the authors reported that their subjects had a

lower incontinence rate (40% vs 8%) and fewer

failed repairs (85% vs 15%) than historical controls

(repaired with end-to-end approximation) A

Swedish study found only one (3%) failed repair

among 30 cases of third- and fourth-degree perineal

lacerations that were repaired with the overlapping

technique at 24 months postpartum [26]

In contrast, data from controlled studies were less

encouraging A group of investigators from the

Dublin Maternity Hospital compared the end-to-end

and overlapping methods in a prospective study

One hundred and fifty-four women with third- or

fourth-degree perineal laceration were repaired witheither the end-to-end or overlapping method,depending on the obstetrician’s preference After 3months, the percent with a small persistent defect[47/84 (54%) vs 33/67 (49%)], a large persistentdefect [27/87 (31%) vs 24/67 (36%)], and a success-ful repair [13/87 (15%) vs 10/67 (15%)] were similarbetween the two methods [27] In addition, the twosurgical repairs were equally efficacious in preserv-ing anal continence, evidenced by the similar pro-portion that developed incontinence [36/67 (54%)

vs 46/87 (53%)] and the median incontinence score[Cleveland Clinic Florida Fecal Incontinence (CCF-FI) score: 1/20 (range: 0–5) vs 2/20 (range: 0–16)][28]

The same group of investigators subsequentlycompared the end-to-end and overlapping repairs in

a randomized controlled trial [29] Again, the portion that had a small persistent defect [50/57

pro-(88%) vs 42/55 (78%), p = 0.27], a large persistent defect [3/57 (5%) vs 3/57 (5%), p = 0.45], and a suc- cessful repair [4/57 (7%) vs 6/55 (11%), p = 0.70]

were similar between the two methods after 3months In addition, the two types of repair wereequally effective in preserving anal continence post-partum The proportion of patients who developed

anal incontinence [27/55 (49%) vs 33/57 (58%), p =

0.46] and the median incontinence score [modifiedWexner score: 0/20 (range: 0–13) vs 2/20 (range:

0–14), p = 0.20] [28] were also similar between the

two types of repair

Findings from the Dublin studies were later firmed by a small randomized controlled trial fromthe University of New Mexico [30] The latter studyalso found that the overlapping method is no moreeffective in repairing the torn anal sphincter or pre-serving continence than the end-to-end method Theproportions that had failed repair [4/15 (27%) vs

con-1/11 (9%), p >0.10], had flatus incontinence [4/15

Table 4.Prevalence of persistent defect after anal sphincter repair

EAS external anal sphincter, IAS internal anal sphincter

(27%) vs 3/11 (27%)], and had fecal incontinence

[1/15 (7%) vs 3/11 (27%)] were similar between the

end-to-end and the overlapping methods at 4

months

Interestingly, the New Mexico study was much

more successful in repairing the torn internal and

external anal sphincters using either the end-to-end

or the overlapping method than other studies,

including earlier data from the same investigators

[31] Eleven (73%) of 15 women in the end-to-end

group and 10 (91%) of 11 in the overlapping group

had intact external and internal anal sphincters at 4

months postpartum Findings from this study may

have been affected by its small sample size (n = 41),

problem with randomization, and the 37% of

sub-jects who did not return for follow-up

In 2006, a group of investigators from Great

Britain published a third randomized controlled trial

that compared the end-to-end with the overlapping

method [32] They found that the outcome was

simi-lar between the two methods at 3 and 6 months

post-partum However, after 1 year, more women in the

end-to-end group had developed anal incontinence

(0/27 vs 5/25, p = 0.009) and more severe

inconti-nence [median Wexner incontiinconti-nence score: 1/20

(range 0–9) vs 0/20 (range 0–5), p = 0.05] than

sub-jects in the overlapping group Although these

differ-ences were statistically significant, clinical

signifi-cance was less certain because the median Wexner

incontinence score was 1/20 for the end-to-end

repair and 0/20 for the overlapping repair Also, the

scores for all four components (mean life style,

cop-ing/behavior, depression/self-perception, and

embarrassment) of the Fecal Incontinence Quality of

Life (FIQOL) scale [33] were similar

The British study had another interesting

find-ing [32] More women whose torn anal sphincter

was repaired with the overlapping method

experi-enced improvement in their incontinence during

the study period [17/27 (63%) vs 9/25 (36%), p =

0.01], whereas more subjects that had end-to-end

approximation developed an exacerbation of

incontinence [0/27 vs 4/25 (16%), p = 0.01] This

finding is perplexing, as both repairs have been

shown in several studies to have a similar failure

rate at 3–4 months postpartum [29, 30, 32]

Although the exacerbation of incontinence may be

due to a difference in the 1-year outcome between

the two repairs, the improvement in incontinence

is difficult to explain because a failed repair is not

likely to heal itself A possible explanation is that

this study did not have a sufficient sample size,

which resulted in an unequal distribution of

sub-jects with flatus and fecal incontinence between the

overlapping and end-to-end repairs As about 11%

of flatus incontinence would resolve spontaneously

during the first 18 months postpartum but a lar percent of fecal incontinence would exacerbateduring the same period, the insufficient sample sizecould result in a discrepancy between the two sur-gical outcomes [34] However, the British study didnot compare the condition of the repaired analsphincters or differentiate between subjects withflatus and fecal incontinence or the extent ofimprovement and exacerbation of incontinenceafter 1 year Whether the observed differences weredue to a type I error or the two repair methods need

simi-to be further evaluated in a larger study remainsunclear

After reviewing the available data, one must clude that the overlapping technique is no moreeffective in repairing the torn anal sphincter or pre-serving continence postpartum than the end-to-endmethod

con-Internal Anal Sphincter

As all fourth-degree perineal lacerations and a icant number of third-degree tears involved theinternal anal sphincter, some investigators have pro-posed that obstetricians should specifically look for,and repair when present, a torn internal sphincter.The function of the internal anal sphincter is tomaintain a constant tone in the anal canal, andrepairing it would theoretically reduce the risk ofdeveloping passive incontinence

signif-Two British investigators attempted to identifyand repair torn internal anal sphincter in 27 cases ofthird-degree perineal laceration [25] After an aver-age follow-up of 20 (range: 7–34) weeks, only two(7%) women developed flatus incontinence Internalanal sphincter repair probably did not contribute tothis study outcome, as four (33%) of the 12 repairsfailed and eight (40%) of the 20 torn internal sphinc-ters were not identified despite the investigators’concerted effort

A group of Norwegian investigators also

attempt-ed to identify and repair torn internal anal sphinctersamong 30 cases of third- and fourth-degree perineallacerations [26] These investigators were unable toidentify one (6%) of the 18 torn internal sphincters,and two (12%) of the 17 repairs failed After a medi-

an follow-up of 34 (range: 12–63) months, fivepatients (17%) complained of flatus incontinence,and two (7%) had developed fecal incontinence Although findings from these two studies appearpromising, data from two small uncontrolled seriesare insufficient to determine whether repairing thetorn internal sphincter would help retain anal conti-nence after a third- or fourth-degree perineal lacera-tion

Consult a Specialist

Recently, several studies from Scandinavia reported

that obstetricians in their hospital were encouraged to

routinely consult a colorectal surgeon to repair

third-and fourth-degree perineal lacerations [35–37]

In a Norwegian study, two colorectal surgeons

repaired 30 cases of third- and fourth-degree perineal

lacerations using the overlapping method [36] After

24 months, one (3%) external sphincter and two (6%)

internal sphincter repairs failed In addition, they

also failed to identify one (3%) internal sphincter

tear In another small study, two British

urogynecol-ogists repaired 27 anal sphincters torn during vaginal

delivery [25] After 20 weeks, four (15%) of the 27

external sphincter and four (33%) of the 12 internal

sphincter repairs failed These investigators also

failed to identify eight (40%) of the 20 torn internal

anal sphincters Although these outcomes look very

favorable, findings from two small uncontrolled

series are insufficient to establish that colorectal

sur-geons or urogynecologists would have more success

than obstetricians in repairing third- and

fourth-degree perineal lacerations

Operating Room

In European countries, third- and fourth-degree

per-ineal lacerations are frequently repaired under

gen-eral or regional anesthesia in the operating room [1,

2, 7, 8, 10, 13, 14, 19–21, 23, 25–27, 29, 32] The

oper-ating room provides superior lighting, appropriate

equipment, and better exposure In addition, general

or regional anesthesia relaxes the patient and

sphinc-ter muscle tone This allows the operator to retrieve

the torn ends of the anal sphincter that had retracted

into its fibrous capsule and perform the repair

with-out tension Investigators found that anal sphincter

repair performed under such optimal conditions still

has a 54–91% failure rate (Table 4) [10, 18–21]

In contrast, anal sphincter tear in the United

States is frequently repaired in the birthing room

under local or regional anesthesia with less lighting

and exposure However, there are very little data

evaluating the outcome of repairs performed in the

birthing room Investigators from the University of

New Mexico were much more successful in repairing

torn internal and external anal sphincters in the

delivery room using either the end-to-end or the

overlapping method than their European

counter-parts [30] As previously noted, the New Mexico

study had only 41 patients, and 15 (37%) did not

return for follow-up Whether anal sphincter repair

performed in the operating room under regional or

general anesthesia has a better outcome than those

repaired in the birthing room needs to be objectivelyevaluated in a larger study

Bowel Confinement

Another approach that has been used to improve gical outcome is bowel confinement Many obstetri-cians routinely order a soft diet and a stool softenerfor women who had an anal sphincter repair, where-

sur-as others prefer a laxative or a constipating agent.These regimens are intended to lessen tension on thesutures during bowel movement and allow the tornends of the anal sphincter to heal together However,there are very little data that show whether bowelconfinement affects the outcome of anal sphincterrepair A study from Dublin randomized 105 patientswho had a third-degree perineal laceration to either 3days of codeine followed by 4 days of laxative or 7days of laxative [37] After 3 months, the medianincontinence score was similar between the twogroups [Wexner incontinence score: 1/20 (range:

0–8) vs 0/20 (range: 0–9), p = 0.096].

Current data show that the only available ment that would increase a woman’s chance of main-taining anal continence after sustaining a third- orfourth-degree perineal laceration is a successfulrepair However, there are no guidelines available tohelp obstetricians consistently perform a successfulrepair

treat-Childbirth after a Third-degree Tear

Third- and fourth-degree perineal lacerations occurthree to seven times more frequently among nulli-paras than multiparas [27, 38, 39] Consequently,many women who had an anal sphincter tear wouldwant to have more children Vaginal delivery after ananal sphincter tear has frequently been cited as amajor risk factor for developing a new and moresevere anal incontinence [8, 14, 21, 38] As we do notknow how to effectively repair a torn anal sphincter,and a significant number of failed repairs woulddevelop incontinence, obstetricians are naturallyreluctant to subject women who had a prior third- orfourth-degree perineal laceration to the stress ofanother vaginal birth In addition, about 7.5–10.5%

of women who had a prior third- or fourth-degreeperineal laceration would develop a recurrentsphincter tear during subsequent vaginal delivery.These findings have led some investigators to pro-pose that women with a prior third- or fourth-degreetear should have elective cesarean for all subsequentbirths [40] However, there are very few studies thatobjectively evaluate the effect of vaginal delivery or

elective cesarean on the anal function of these

women

Current data have not clearly delineated the effect

of vaginal delivery on the anal function of women

who had already sustained a third-degree sphincter

tear A prospective study from Sweden followed 34

primiparas who had a prior third-degree perineal

laceration and two who had a prior fourth-degree

anal sphincter tear [8] Among the nine subjects who

had no subsequent delivery after the anal sphincter

tear, 44% were incontinent at 9 months and at 5 years

postpartum In contrast, the prevalence of anal

incontinence among 27 subjects with at least one

additional vaginal delivery had increased from 44%

at 9 months to 56% at 5 years (p = 0.009).

A second Swedish study prospectively followed for

10 years 23 women who had a third-degree perineal

laceration [14] Four women had at least two

addi-tional vaginal deliveries, 13 had one subsequent

vagi-nal birth, and six had no additiovagi-nal birth The only

difference among the three groups was that women

with two or more additional vaginal deliveries had

more severe flatus incontinence, whereas the severity

of fecal incontinence was similar

A group of Danish investigators followed 72

women who had a third-degree perineal laceration

for 2–4 years Four (24%) of the 17 women who had a

subsequent vaginal delivery after the anal sphincter

tear developed new or more severe flatus

inconti-nence Eight (15%) of 55 with no additional birth

developed flatus incontinence and nine (16%)

sus-tained fecal incontinence [38]

In contrast to the previous two findings, this study

suggests that subsequent vaginal delivery has a

pro-tective effect on the anal function of women who had

a prior third-degree perineal laceration However,

findings from all three studies may have been

affect-ed by their small sample size, inclusion of subjects

with superficial and partial third- and fourth-degree

tears, and those that had subsequent cesarean

deliv-ery

Findings from retrospective studies also vary as to

whether vaginal birth after a third-degree perineal

laceration is associated with a higher or lower rate of

anal incontinence A Swiss study found that women

with no additional delivery after a third-degree

per-ineal laceration experienced anal incontinence more

frequently than those who had one or at least two

subsequent vaginal births [10/49 (20%) vs 4/60 (7%)

vs 1/20 (5%), p = 0.03) [41] In contrast, a group of

Scandinavian investigators found that the prevalence

of anal incontinence was higher among women who

had a vaginal birth after sustaining a third-degree

perineal laceration than those who had no further

delivery [24/43 (56%) vs 23/67 (34%), risk ratio (RR)

= 1.6, 95% confidence interval (CI): 1.1–2.5] [21] A

probable reason for this discrepancy is that bothstudies included women of different parity who sus-tained either a partial or complete anal sphincter lac-eration with and without extensions into the analmucosa, and the possible inclusion of women withrecurrent sphincter tear or cesarean during subse-quent deliveries [21, 35, 41–47] All of these factorshave been shown to affect anal continence and, con-sequently, may have altered the study outcome

A third retrospective study from East CarolinaUniversity included only women who sustained acomplete third-degree perineal laceration duringtheir first childbirth and did not have cesarean,repeat anal sphincter tear, or operative vaginal deliv-ery during subsequent births [48] Among womenwho had 0, 1, and at least 2 additional vaginal deliv-eries after the sphincter tear, the prevalence of analincontinence [11/65 (17%), 11/67 (16%), and 12/40

(30%), p = 0.179] and the severity of incontinence

(mean Pescatori score: 3.2±1.4, 3.5±1.1, and 3.2±1.4,

p = 0.846) [49] were similar In addition, the

propor-tion that had severe incontinence, defined as having

a Pescatori score of 5 or 6 points out of a maximum

of 6 and that the incontinence had a severe effect onthe subject’s daily activities and quality of life, were

also similar (2/65, 1/67, and 2/40, p = 0.811)

Howev-er, this retrospective study probably did not have ficient sample size to detect the observed difference.Also, it did not use a validated system to grade incon-tinence severity or to measure the effect of inconti-nence on quality of life These data suggest that theeffect of subsequent vaginal birth on the anal func-tion of women who had a prior third-degree perineallaceration has not been established

suf-Childbirth after a Fourth-degree Tear

There are very few studies evaluating the effect ofvaginal birth on women’s anal function after afourth-degree perineal laceration However, findingsfrom available studies are fairly consistent A Swissstudy reported that women who had one or at leasttwo vaginal deliveries after a fourth-degree perineallaceration developed fecal incontinence more fre-quently than those who had no subsequent birth

[7/25 (28%) vs 2/9 (22%) vs 0/14, p = 0.04] [41].

Although the prevalence of anal incontinence wassimilar [20/52 (38%) vs 14/60 (23%) vs 10/36 (28%),

p = 0.208], the East Carolina study found that women

who had at least two additional vaginal deliveriesafter a fourth-degree sphincter tear developed severeincontinence more frequently than those who had no

or one subsequent delivery [4/36 (11%) vs 0 vs 0, p

= 0.002] [50] Thus, existing data suggest that vaginaldelivery after a fourth-degree perineal laceration

probably increases the prevalence and/or severity of

anal incontinence

Elective Cesarean after an Anal Sphincter Tear

Although elective cesarean for all births after a

third-or fourth-degree perineal laceration has been widely

advocated as the method to prevent the occurrence

of a new or more severe incontinence, there is very

little evidence to support the effectiveness of this

prophylactic measure Elective cesarean has a rather

limited protective effect on the anal function The

International Randomized Term Breech Trial found

that at 3 months postpartum, only mild flatus

incon-tinence was more prevalent among the planned

vagi-nal delivery than the planned cesarean group (33/58

vs 20/61, p = 0.008) [51] The prevalence of flatus

incontinence (66/616 vs 59/606, p = 0.64), severe

fla-tus incontinence (1/61 vs 2/58, p = 0.481), fecal

incontinence (5/619 vs 9/607, p = 0.29), and mild

fecal incontinence (2/4 vs 7/9, p = 0.353) were

simi-lar between the two groups The reason for this

limit-ed protective effect is that anal incontinence that

develops during childbirth occurs primarily during

antepartum [52, 53] Whether elective cesarean

would prevent the occurrence of a new and/or more

severe incontinence during subsequent childbirth

among women who had a prior anal sphincter tear

has not been studied

Conclusion

Third- and fourth-degree perineal lacerations are

major complications of vaginal birth Repair of the

torn anal sphincter frequently fails, which

predispos-es thpredispos-ese women to develop incontinence At the prpredispos-es-

pres-ent time, there is no available method that can

consis-tently repair the torn sphincter and restore its

func-tion To achieve the best possible outcome, current

evidence suggests that third- and fourth-degree

per-ineal lacerations probably should be repaired in the

operating room under general or regional anesthesia,

preferably by someone with expertise in this area

Elective cesarean for all births has been widely

advocated as the prophylactic method to prevent the

occurrence of a new or more severe incontinence

among women who had a prior third- or

fourth-degree perineal laceration Although vaginal delivery

after a fourth-degree perineal laceration has been

associated with a higher prevalence and more severe

incontinence, the effect of subsequent vaginal birth

on the anal function of women who had a prior

third-degree perineal laceration has not been established

In addition, whether elective cesarean would protect

the anal function of women who had a prior third- orfourth-degree perineal laceration during subsequentchildbirth also has not been established Consequent-

ly, there is no evidence to suggest that elective

cesare-an would prevent the occurrence of a new or moresevere incontinence during childbirth among womenwho had a prior third- or fourth-degree perineal lac-eration

References

1 Haadem K, Gudmundsson S (1997) Can women with intraprtum rupture of anal sphincter still suffer after- effects two decades later Acta Obstet Gynecol Scand 76:601–603

2 Jander C, Lyrenas S (2001) Third and fourth degree perineal tears Predictor factors in a referral hospital Acta Obstet Gynecol Scand 80:229–234

3 O’Leary JL, O’Leary JA (1965) The complete

episioto-my Analysis of 1224 complete lacerations, tomies, and episiproctomies Obstet Gynecol 25:235–240

sphinctero-4 Sieber EH, Kroon JD (1962) Morbidity in the third degree laceration Obstet Gynecol 19:677–680

5 Cunningham FG, Leveno KJ, Bloom SL et al (eds) (2005) Williams Obstetrics, 22nd edn McGraw-Hill, New York

6 Gabbe SG, Niebyl JR, Simposn JL (eds) (2002) rics, normal and problem pregnancies, 4th edn Churchill Livingston, Philadelphia

Obstet-7 Zetterstrom J, Lopez A, Anzen B et al (1999) Anal sphincter tears at vaginal delivery: Risk factors and clinical outcome of primary repair Obstet Gynecol 94:21–28

8 Pollack J, Nordenstam J, Brismar S et al (2004) Anal incontinence after vaginal delivery: A five year prospective cohort study Obstet Gynecol 104: 1397–1402

9 Crawford LA, Quint EH, Pearl ML (1993) Incontinence following rupture of the anal sphincter during deliv- ery Obstet Gynecol 82:527–531

10 Borello-France D, Burgio KL, Richter HE et al (2006) Fecal and urinary incontinence in primiparous women Obstet Gynecol 108:863–872

11 Nygaard IE, Rao SSC, Dawson JD (1997) Anal nence after anal sphincter disruption: A 30-year retro- spective study Obstet Gynecol 89:896–901

inconti-12 Faltin DL, Otero M, Petignat P et al (2006) Women’s health 18 years after rupture of the anal sphincter dur- ing childbirth: I Fecal incontinence Am J Obstet Gynecol 194:1255–1259

13 Wagenius J, Laurin J (2003) Clinical symptoms after anal sphincter rupture: A retrospective study Acta Obstet Gynecol Scand 82:246–250

14 Fornell EU, Matthiesen L, Sjodhl R et al (2005) ric anal sphincter injury ten years after: subjective and objective long term effects BJOG 112:312–316

Obstet-15 Parks AG, Swash M, Urich H (1977) Sphincter vation in anorectal incontinence and rectal prolapse Gut 18:656–665

dener-16 Bartolo DEC, Jarratt JA, Read MG et al (1983) The role

of partial denervation of the puborectalis in

idiopath-ic fecal incontinence Br J Surg 70:664–667

17 Kiff ES, Swash M (1984) Slowed conduction in the

pudendal nerves in idiopathic fecal incontinence Br J

Surg 71:614–616

18 Sultan AH, Kamm MA, Hudson CN et al (1994) Third

degree obstetric anal sphincter tears: risk factors and

outcome of primary repair BMJ 308:887–891

19 Nielsen MB, Hauge C, Rasmussen OO et al (1992) Anal

endosonographic findings in the follow-up of primary

sutured sphincteric ruptures Br J Surg 79:104–106

20 Gjessing H, Backe B, Sahlin Y (1998) Third degree

obstetric tears: outcome after primary repair Acta

Obstet Gynecol Scand 77:736–740

21 Poen AC, Felt-Bersma RJF, Strijers RLM et al (1998)

Third-degree obstetric perineal tear: long term clinical

and functional results after primary repair Br J Surg

85:1433–1438

22 Belmonte-Montes C, Hagerman G, Vega-Yepez PA et

al (2001) Anal sphincter injury after vaginal delivery in

primiparous females Dis Colon Rectum 44:1244–1248

23 Norderval S, Oian P, Revhaug A et al (2005) Anal

incontinence after obstetric sphincter tears: Outcome

of anatomic primary repair Dis Colon Rectum

48:1055–1061

24 Parks AG, McPartlin JF (1971) Late repairs of injuries

of the anal sphincter Proc R Soc Med 64:1187–1189

25 Sultan AH, Monga AK, Kumar D et al (1999) Primary

repair of obstetric anal sphincter rupture using the

overlap technique BJOG 106:318–323

26 Kairaluoma MV, Raivio P, Aarnio MT et al (2004)

Immediate repair of obstetric anal sphincter rupture:

Medium-term outcome of the overlap technique Dis

Colon Rectum 47:1358–1363

27 Fitzpatrick M, Fynes M, Cassidy M et al (2000)

Prospective study of the influence of parity and

oper-ative technique on the outcome of primary anal

sphincter repair following obstetric injury Eur J

Obstet Gynecol Reprod Biol 89:159–163

28 Jorge J, Wexner SD (1993) Etiology and management

of fecal incontinence Dis Colon Rectum 36:77–79

29 Fitzpatrick M, Behan M, O’Connell PR et al (2000) A

randomized clinical trial comparing primary overlap

with approximation repair of third-degree obstetric

tears Am J Obstet Gynecol 183:1220–1224

30 Garcia V, Rogers R, Kim SS et al (2005) Primary repair

of obstetric anal sphincter laceration: A randomized

trail of two surgical techniques Am J Obstet Gynecol

192:1697–1701

31 Kammerer-Doak DN, Wesol AB, Rogers RG et al

(1999) A prospective cohort study of women after

pri-mary repair of obstetric anal sphincter laceration Am

J Obstet Gynecol 181:1317–1323

32 Fernando RJ, Sultan AH, Kettle C et al (2006) Repair

techniques for obstetric anal sphincter injury Obstet

Gynecol 107:1261–1268

33 Rockwood TH, Church JM, Fleshman JW et al (2000)

Fecal incontinence quality of life scale: quality of life

instrument for patients with fecal incontinence Dis

Colon Rectum 43:9–16

34 Nazir M, Stien R, Carlsen E et al (2003) Early

evalua-tion of bowel symptoms after primary repair of

obstet-ric perineal rupture is misleading An observational

cohort study Dis Colon rectum 46:1245–1250

35 Norderval S, Nsubuga D, Bjelke C et al (2004) Anal incontinence after obstetric sphincter tears: incidence

in a Norwegian county Acta Obstet Gynecol Scand 83:989–994

36 Kairaluoma MV, Raivio P, Aarnio MT et al (2004) Immediate repair of obstetric anal sphincter rupture: Medium-term outcome of the overlap technique Dis Colon Rectum 47:1358–1363

37 Mahony R, Behan M, O’Herlihy C et al (2004) domized, clinical trial of bowel confinement vs laxa- tive use after primary repair of a third-degree obstet- ric anal sphincter tear Dis Colon Rectum 47:12–17

Ran-38 Tetzschner T, Sorenson M, Gunnar L et al (1996) Anal and urinary incontinence in women with obstetric anal sphincter rupture BJOG 103:1034–1040

39 Spydalaug A, Trogstad LIS, Skrondal A et al (2005) rent risk of anal sphincter laceration among women with vaginal deliveries Obstet Gynecol 105:307–313

Recur-40 McKenna DS, Ester JB, Fischer JR (2003) Elective cesarean delivery for women with a previous anal sphincter rupture Am J Obstet Gynecol 189:1251–1256

41 Sangalli MR, Floris L, Faltin D et al (2000) Anal tinence in women with third or fourth degree perineal tears and subsequent vaginal deliveries Aust N Z J Obstet Gynecol 3:244–248

incon-42 Ryhammer AM, Bek KM, Laurberg S (1995) Multiple vaginal deliveries increase the risk of permanent incontinence of flatus and urine in normal pre- menopausal women Dis Colon Rectum 38:1206–1209

43 Nichols CM, Lamb EH, Ramakrishnan V (2005) ferences in outcome after third- versus fourth-degree perineal laceration repair: A prospective study Am J Obstet Gynecol 193:530–536

Dif-44 Fynes M, Donnelly VS, O’Connell PR et al (1998) Cesarean delivery and anal sphincter injury Obstet Gynecol 92:496–500

45 Peleg D, Kennedy CM, Merrill D et al (1999) Risk of repetition of a severe perineal laceration Obstet Gynecol 93:1021–1024

46 Payne TN, Carey JC, Rayburn WF (1999) Prior

third-or fourth-degree perineal tears and recurrence risks Inter J Gynecol Obstet 64:55–57

47 Sorensen M, Tetzschner T, Rasmussen OO et al (1993) Sphincter rupture in childbirth Br J Surg 80:392–394

48 Sze EHM (2005) Anal incontinence among women with one versus two complete third-degree perineal lacerations Inter J Gynecol Obstet 90:213–217

49 Pescatori M, Anastasio G, Bottini C et al (1992) New grading and scoring for anal incontinence Dis Colon Rectum 35:482–487

50 Sze EHM (2005) Prevalence and severity of anal tinence in women with and without additional vaginal deliveries after a fourth-degree perineal laceration Dis Colon Rectum 48:66–68

incon-51 Hannah ME, Hannah WJ, Hodnett ED et al (2002) comes at 3 months after planned cesarean versus planned vaginal delivery for breech presentation at term JAMA 287:1822–1831

Out-52 Chaliha C, Kalia V, Stanton SL et al (1999) Antenatal prediction of postpartum urinary and fecal inconti- nence Obstet Gynecol 94:689–694

53 Chaliha C, Sultan AH, Bland JM et al (2001) Anal tion: Effect of pregnancy and delivery Am J Obstet Gynecol 185:427–432

Fecal incontinence, according to the most used

defi-nition, is the “involuntary loss of the stool or soiling

at a socially inappropriate time or place” [1] It is an

important health issue that strongly affects patient

quality of life and restricts their social activities It is

a common problem, with prevalence ranging from

2.2% to 15% in the community and up to 40% in

nursing homes [2] The prevalence of fecal

inconti-nence in neurological patients is higher than in the

general population Many neurological disorders are

associated with fecal incontinence, and this chapter

is a review of the current clinical knowledge

regard-ing the pathogenesis and clinical findregard-ings When

considering the possible effects of central and

peripheral neurological lesions on fecal continence, it

is important to keep in mind that continence

depends on intact neural pathways and normal

func-tion of the cerebral, spinal, and cauda equina centers,

and peripheral nerves It should be remembered,

however, that signs, symptoms, and gastrointestinal

dysfunction may differ from expectations by virtue

of incomplete neuronal lesions, coexisting

involve-ment of supraspinal or spinal centers, or damage to

the distal parts of the autonomic or somatic

innerva-tion of the pelvic floor sphincter muscles

Functional Anatomy and Physiology

Fecal continence is a complex function that requires

coordinated responses in the pelvic floor sphincter

muscles and abdominal and anorectal muscles

Con-sequently, fecal incontinence occurs when the

nor-mal anatomy or physiology of the anorectal unit is

disrupted In most cases, different

pathophysiologi-cal mechanisms are involved in the pathogenesis of

fecal incontinence, resulting in multifactorial

etiolo-gy [3] Physiological interaction of rectal motility and

sensation with the tonic activity of smooth and

stri-ated muscle is complex and incompletely

under-stood Neural control of the colon can be separated

into the intrinsic and the extrinsic colonic nervoussystems

The intrinsic enteric system (ENS) consists ofnerve-cell bodies and endings that are locatedbetween the circular and the longitudinal musclecoats The ENS is comprised of an outer myenteric orAuerbach’s plexus that regulates smooth-muscleactivity and an inner submucosal Meissner’s plexusthat influences the absorptive and secretory func-tions of the enteric mucosa The ENS can function inisolation, without input from the brain or spinalcord

The extrinsic system innervates the gut and acts as

a modulator of visceral activity through sympathetic,parasympathetic, and somatic functions The sympa-thetic inhibitory innervation of the gastrointestinaltract works by noradrenergic neurons on the entericnerves and originates in the thoracolumbar spinalcord (T5–L2) The sympathetic fibers, leaving thespinal cord, pass through the paravertebral ganglia torelay in the celiac and mesenteric ganglia, terminat-ing with postganglionic fibers on the enteric system.Sympathetic activity generally hyperpolarizessmooth-muscle cells, thereby reducing colorectalmotility Parasympathetic outflow to the colon isdivided into cranial (vagus nerve fibers) and sacraldivisions The vagus nerve innervates the foregut andmidgut, and the pelvic nerves innervate the descend-ing and sigmoid colons and the anorectum Parasym-pathetic activity inducing depolarization of smoothmuscle increases the overall activity of the gastroin-testinal tract by promoting peristalsis and increasingcolorectal motility

The internal anal sphincter (IAS), regulated by thesympathetic nerves, provides most of the resting analpressure and during voluntary squeeze is reinforced

by the tonic activity of the external anal sphincter(EAS) Fecal continence requires the ability to main-tain resting IAS tone and EAS contraction inresponse to increased intra-abdominal pressure, rec-tal distension, and rectal contraction The IAS iscomposed of smooth muscle arranged in inner circu-lar and outer longitudinal layers The EAS is com-

Neurogenic Fecal Incontinence

Giuseppe Pelliccioni, Osvaldo Scarpino

31

posed of striated voluntary muscle closely related to

the puborectalis (PR) muscle The PR muscle

origi-nates at the pubis, wraps around the junction of the

lower rectum and the anal canal, and plays an

impor-tant role in fecal continence and in physiological

defecation Relaxation of the PR is, in fact, necessary

for normal bowel emptying

Although the colon and the pelvic floor sphincter

muscles are peripherally innervated by the

autonom-ic nervous system, voluntary cortautonom-ical control is an

essential feature of their physiological behavior

Whereas clinical information is defined in relation to

the cortical control of the bladder, much less is

known about cerebral determinants of bowel

func-tion The medial prefrontal area and the anterior

cin-gulate gyrus seem to represent two of the most

important cortical centers that modulate bowel

func-tion, mediating voluntary control through spinal

pathways In particular, frontal-lobe lesions of the

inferior and medial surfaces are associated with fecal

and urinary incontinence [4]

The EAS is innervated by axons of the somatic

neurons originating from the anterior horns of the

S2–S4 spinal cord (Onuf’s nucleus) via the pudendal

nerves Its course through the pelvic floor makes the

pudendal nerve vulnerable to stretch injury,

particu-larly during vaginal delivery

Normal functions related to the pelvic organs,

such as urination, defecation, and ejaculation,

involves coordination between the different organ

systems [5] Experimental studies shown that

disten-sion of urinary bladder both inhibits colonic

contrac-tions and produces simultaneous contraction of the

anal sphincter [6, 7] The reverse also occurs: the

uri-nary system is inhibited during defecation Neural

mechanisms underlying the interactions between the

various pelvic organs are likely mediated by both the

peripheral and central nervous systems It is

hypoth-esized that there must be some sort of

visceroviscer-al convergence within the centrvisceroviscer-al nervous system

(CNS), both in the spinal cord itself and

supraspinal-ly

Sensory perception from pelvic floor, anal canal,

and rectal wall plays an essential role in defecation

and in maintaining fecal continence The afferent

pathway involved in the perception of rectal filling,

the preliminary event of defecation, is poorly

under-stood Rectal sensitivity arises from

mechanorecep-tors situated in the superficial and deep layers of the

rectal wall and from the stimulation of nerve endings

at the anal transitional zone [8, 9] Recent animal

models confirmed the presence of intraganglionic

laminar nerve ending receptors specialized for

mechanical distension in the myenteric plexus of the

rectal wall [10] The superficial receptors travel to the

autonomic presacral ganglia, whereas the deep

receptors project to the lumbar cord Rectal sion is most likely transmitted along the S2–S4parasympathetic pathway When this innervation isabsent (i.e., in paraplegics or traumatic sacrallesions), rectal filling is perceived as a minor sensa-tion of discomfort

disten-Pelvic nerves are the main sensory pathways fromthe rectum; some sensory information is also con-veyed in the sympathetic hypogastric nerves to thethoracolumbar spinal cord Sensory informationfrom the anal canal, perineum, and urethra is carriedalmost exclusively by the pudendal nerves Pudendalnerve block induces, in fact, a loss of sensation ingenital perianal skin and EAS weakness but does notaffect rectal sensation [11]

Little is known about the cortical processing ofanorectal sensation The differences between rectaland anal sensation relate both to the differences inperipheral innervation and cortical representation.Unlike somatic sensation strongly represented in theprimary somatosensory cortex, visceral sensation isprimarily represented in the secondary somatosen-sory cortex Furthermore, other cortical areas, such

as prefrontal cortex and paralimbic and limbic areas(in particular, anterior insular cortex, amygdala, andcingulated cortex) contribute to the affective andcognitive components of rectal sensation [12, 13]

Fecal Incontinence in Disease Mainly Affecting the Brain

Loss of control of the ascending and descendingpathways induced by lesions in the CNS may presentwith urinary and fecal incontinence Any supraspinallesion of brain, brainstem, and spinal cord rostral tothe sacral Onuf’s nucleus–including cerebrovasculardisease, hydrocephalus, intrinsic or extrinsic tumors,traumatic head injury, multiple sclerosis, Parkin-son’s disease (PD) and other neurodegenerative dis-eases, and spinal cord injury (SCI)–may affect void-ing and fecal continence

Furthermore, in most patients with neurologicaldisease, colorectal dysfunction is frequently caused

by a combination of lesions of the central or eral nervous systems, altered dietary habits, immo-bility, or use of different drugs The effects of fecalincontinence in nonneurological and in neurologicalpatients are very severe and are associated with areluctance to leave home [14] Kamm pointed outthat fecal incontinence is, in fact, a more commonreason than dementia for seeking placement in anursing home [15] However, Andrew and Nathanstated that in patients with bladder and bowel distur-bances as a result of frontal-lobe lesions, defecationwas affected much less often than micturition [4] A

periph-particular type of fecal incontinence consisting of an

inappropriate context more than an involuntary

emptying of the bowel is described in frontotemporal

dementia or in vascular or traumatic frontal

encephalopathy A mixed pattern of urgency and

involuntary emptying of the bowel and bladder in

inappropriate context can occur in multifocal

vascu-lar or inflammatory disorders

Stroke and Cerebrovascular Disease

Fecal incontinence is a common complication after

stroke and affects about 30–40% of patients in the

acute phase and 11% at 3 and 12 months [16–18] The

occurrence of bowel and urinary symptoms is related

to the size of vascular lesion; in particular, fecal

incontinence is associated with the severity of the

stroke [18] Large ischemic frontoparietotemporal

lesions can induce a higher incidence of urinary and

bowel symptoms than can frontal injury alone In the

Copenhagen Stroke Study, patients with fecal

incon-tinence in the first week after stroke were

significant-ly more frequentsignificant-ly women and more often had a

his-tory of former stroke comorbidity of other disabling

diseases than patients without fecal incontinence

[18] The same study reported that lesions in patients

with fecal incontinence were significantly more often

due to a hemorrhage, were larger in size, and more

often involved the cerebral cortex than those in

patients without fecal incontinence Patients with

fecal incontinence also had significantly lower scores

on the initial Barthel Index and Scandinavian Stroke

Scale (SSS) [19]

Age, diabetes mellitus, severity of stroke (initial

SSS score and diameter of lesion) and comorbidity of

other disabling disease are significant risk factors for

fecal incontinence [18] Urinary and fecal

inconti-nence appear to be a powerful indicator for poor

prognosis in ischemic stroke [20] Patients who

develop fecal incontinence have a higher risk of

death within 6 months compared with those who

remain continent; furthermore, severe disability and

institutionalization frequently occur among stroke

survivors [18, 21–23] Fecal incontinence is also

linked with mortality Harari et al have shown that

36% of patients with initial fecal incontinence

com-pared with 4% of continent patients had died at 3

months after stroke and 20% of 3-month survivors

with fecal incontinence versus 8% of those continent

at 3 months had died by 1 year [16]

Functional urinary and bowel disorders can result

from a large cortical hemispheric lesion that

inter-rupts the central, frontally dependent pathways for

urinary and bowel storage and voiding [24] In the

acute phase of the illness, 30–40% of large ischemic

stroke patients develop fecal incontinence within 2weeks; however, this symptom tends to improvealong with neurological signs After a 6-month fol-low-up, between 3% and 9% of patients remainincontinent [25]

Harari et al [16] have also provided some tion of the impact of fecal incontinence on otheradverse outcomes Incontinent patients were morelikely to be in long-term care (28% vs 6%) and toreceive district nurse services (20% vs 11%) thancontinent patients at 3 months This suggests thatfecal incontinence in stroke survivors may increasethe risk of institutionalization and the need for nurs-ing support in the community It is presumed thatincontinence is a predicting factor for poor progno-sis for different reasons: the same lesion might causeneurogenic bowel and bladder dysfunction in addi-tion to cognitive or motor impairment; moreover,fecal and urinary incontinence may induce markedpsychological problems that hamper functionalrecovery

indica-Parkinson’s Disease and Parkinsonian Syndromes

The majority of patients with PD or parkinsoniansyndromes–in particular, multiple system atrophy(MSA)–complains of gastrointestinal and pelvicorgan dysfunction Stocchi et al [26] reported a simi-lar occurrence of altered bowel frequency and defe-cation in PD and MSA patients Gastrointestinalsymptoms in PD include gastroparesis and constipa-tion as a result of decreased bowel movement fre-quency and defecation difficulty In all patients, thesedisorders became manifest or worsened after theonset of neurologic symptoms The most striking fea-tures of bowel dysfunction in PD patients were con-stipation and difficulty in expulsion [27] The preva-lence of constipation in PD patients is high: morethan 50% suffer from moderate to severe constipa-tion [27, 28] PD patients are reported to have pro-longed colorectal transit time and paradoxical con-traction of the PR muscle on defecation [29, 30] Dif-ficulty in defecation is a very common symptom in

PD, occurring in 67–94% of patients; constipation ispresent in 29–77% of patients compared with 13% ofage-matched controls [31] Singaram et al [32] re-ported a reduction of dopamine-containing neurons

in immunostaining of biopsied submucosa andcolonic musculature and the presence of Levy bodies

in the myenteric plexus of the colon These findingssuggest that prolonged transit time and constipation

in PD patients may depend not only on central butalso on peripheral dopamine reduction in the colon.The most frequent anorectal manometric findings

by Stocchi et al [26] in MSA patients were low

rest-ing anal pressure, reduced voluntary anal

contractil-ity, and a paradoxical anal contraction or insufficient

anal relaxation during straining; the same

impair-ments have been reported by Edwards et al in PD

patients [28] Abnormal straining is an important

cause of constipation in both PD and MSA patients

and frequently is involved in the pathogenesis of

out-let-type constipation Therefore, anorectal

mano-metric variables do not differentiate PD from MSA

patients

Sakakibara et al [27] reported that fecal

inconti-nence in PD patients commonly occurred together

with urinary incontinence, but there was no

signifi-cant relation between sexual dysfunction and bladder

or bowel dysfunction Although much less common

than constipation, fecal incontinence may also occur

in MSA patients, which does not seem to be related

with the presence of voiding dysfunction and, in

par-ticular, urinary incontinence A low resting anal tone

is not a typical finding in MSA and PD patients, and

only some patients have marked sphincter hypotonia

involved in facilitating fecal incontinence [26]

Fecal Incontinence in Spinal Cord Disease

Multiple Sclerosis, Myelopathies, and Spinal Cord Injury

Multiple sclerosis (MS) is a progressive neurologic

disease that results from multiple demyelinating

lesions within the CNS and that shows a variety of

clinical presentations and courses determined by the

location and number of the same lesions Bladder

and bowel dysfunction is the third most important

discomfort in MS patients after spasticity and fatigue

[33, 34] Genitourinary dysfunctions in MS patients

frequently occur due to the spinal involvement, with

an incidence of 78% [35–38] Bowel-related disorders

in MS patients are very common The prevalence of

bowel dysfunction, fecal incontinence, and/or

consti-pation is reported to be between 52% and 66%

[39–41] Hinds et al [42] found that 51% of 280 MS

patients experienced fecal incontinence; it occurred

at least weekly in 25% The authors also

demonstrat-ed a strong correlation between fecal incontinence

and the duration of MS and degree of disability [42]

Conversely, Chia et al [39] found no correlation

between the presence of bowel dysfunction and

dis-ease duration, patients’ age, Disability Status Scale,

and Kurtzke score

The discrepancy in these studies may be explained

with the variety of underlying central and peripheral

pathogenesis of fecal incontinence in MS patients

MS leads to fecal incontinence by medullary

dysfunc-tion and in particular by conus medullaris lesions,

causing weakness and denervation of the pelvic floor

striated sphincter muscles [43] Changes in bowelfunction among MS patients are in many ways simi-lar to those described for SCI patients However, due

to the multiple lesions within the CNS, many patientshave a combination of supraconal and conal lesions.Loss of voluntary control of the EAS muscle may alsooccur as a consequence of MS plaques affecting thecentral pelvic floor motor control pathway Glick et

al [44] suggest that fecal incontinence can also occur

by alteration of colonic motility with the generation

of high intracolonic pressures due to reduction orinterruption of the normal cortical inhibition ofcolonic motor activity Most studies have also shownthat anorectal sensibility [45], anal squeeze pressure[45–48], and anal resting pressure are reduced in MSpatients The rectal wall is also hyperirritable withreduced compliance, and all these issues may result

in fecal incontinence [45, 49, 50]

Bowel and anorectal dysfunction resulting in fecalincontinence and severe constipation are commoncomplications of SCI [51–56] Bowel dysfunctionsand in particular fecal incontinence are the mostimportant factor affecting not only acute rehabilita-tion treatment following SCI but also both long-termquality of life [57, 58] and chronic treatment forbowel care [59, 60] Immediately after acute SCI,patients are in spinal shock, and all sensory percep-tions, motor functions, and reflex activity below thelevel of the spinal cord lesion are lost or reduced.Spinal shock with temporary loss of spinal reflexeslasts for a variable period of time Krogh et al report-

ed that in most patients, spinal shock affects the tum for less than 4 weeks [61] Colorectal problemscan be a cause of morbidity immediately after SCI,and these problems become more frequent withincreasing time after injury [57]

rec-Between 27% and 90% of SCI patients complain ofsymptoms of neurogenic bowel dysfunctions due tothe lack of nervous control [51, 62] Two types ofcolon dysfunctions and complications may arise,depending on the level of the spinal injury: uppermotor neuron bowel (UMNB) dysfunctions andlower motor neuron bowel (LMNB) dysfunctions[63–65] UMNB dysfunction results from a spinalcord lesion above the conus medullaris, whereasLMNB or areflexic bowel results from a lesion affect-ing the parasympathetic cell bodies in the conusmedullaris and the cauda equina [63] The main dif-ferences between the two clinical pictures consist ofthe presence of spinal-cord-mediated reflex peristal-sis and the functional integrity of the pudendal nerve

in UMNB, whereas in LMNB, no

spinal-cord-mediat-ed reflex peristalsis occurs, and there is slow stoolpropulsion Due to the complete or incomplete EASmuscle denervation on electromyography (EMG)examination, there is increased risk for fecal inconti-

nence The levator ani muscles lack tone, reducing

the rectal angle and causing the lumen of the rectum

to open [66] The EAS and pelvic muscles are flaccid,

and there is no reflex response to increased

intra-abdominal pressure The loss of parasympathetic

control and reflex innervation of the IAS means a

further reduction in resting anal tone and leads to

fecal incontinence [55] Only the myenteric plexus

coordinates colonic segmental peristalsis, and a

dryer stool and rounder stool shape can occur In

UMNB or hyperreflexic bowel, voluntary EAS muscle

control is discontinued; however, connections

between the spinal cord and the colon remain intact,

with the presence of reflex coordination and stool

propulsion There is increased colonic wall and anal

tone The EAS muscle remains tight, thereby

retain-ing stool and inducretain-ing constipation and fecal

reten-tion [63, 67]

The majority of SCI patients, 42–95%, suffer from

constipation, and two thirds need to induce

defeca-tion by digital stimuladefeca-tion of the anal canal or rectum

or to empty their rectum digitally [51, 53, 68]

Pat-terns of gut dysmotility have been described for

dif-ferent levels and degrees of SCI Rajendra et al

demonstrated that lesions above T1 result in delayed

mouth-to-caecum time, but lesions below this level

show normal transit times to the caecum and

markedly delayed transit times beyond the ileocaecal

valve [69] Keshavarzian et al [70] showed a slowed

transit throughout the whole colon in patients with

spinal cord lesions above the lumbar region, a delay

in part due to loss of colonic compliance The lack

of compliance leads to functional obstruction,

increased transit times, abdominal distension,

bloat-ing, and discomfort [55] Regarding the frequency of

defecation, Yim et al revealed that patients with

UMNB emptied their bowels about three times a

week, whereas LMNB patients did so about twice a

day, with a high risk of fecal incontinence due to lax

EAS muscle mechanism [64] To avoid incontinence,

the LMNB group tended to perform their bowel care

program about twice a day, but despite this frequent

care program, they experienced fecal incontinence

2.61 times per month This suggests that CNS

modu-lates and regumodu-lates colonic motility and that loss of

the descending inhibitory pathway from CNS

pro-duces an increased colonic activity and decreased

compliance [71]

The most common cause of neuropathic bowel in

children is myelodysplasia, in particular spina bifida,

that results in both constipation and fecal

inconti-nence Lie et al found that bowel dysfunctions are

present in approximately 78% of children aged 4–18

years with spina bifida, and lack of bowel control is

found to be as stressful as bladder dysfunction and

more stressful than impairment of motor function

[72] Typical changes in myelodysplasia include poorvoluntary sphincter function and poor anorectal sen-sibility Left-colon motility is usually disturbed,whereas IAS tone is normal or near normal At leasthalf of the patients with myelodysplasia suffer fromfecal incontinence, and 90% need assistance to main-tain bowel function [72] The majority of patientswith spina bifida also may have hydrocephalus thatresults in intellectual deficits potentially contributing

to fecal incontinence In a series of 109 adults withmyelodysplasia, Malone et al [73] found that 55%had regular fecal soiling The type of bowel dysfunc-tion is dependent on the myelodysplasia level Inhigh-thoracic or thoracolumbar-meningomyelocele

is relatively rare, the colonic transit time is very slow,voluntary sphincter function and rectal sensibilityare missing, and patients are prone to fecal loading[74] In most patients, the myelomeningocele is lum-bosacral or sacral, resulting in a lesion of the conusmedullaris or cauda equina Patients with lum-bosacral lesions show slow left-colonic transit time,resulting in pellet-like stools evacuated with the help

of the gastrocolic reflex; fecal loading is uncommon.The main functional problem in these patients is theautomatic event of bowel emptying, and careful tim-ing of rectal stimulation can induce bowel emptyingwith some degree of voluntary control Manypatients with sacral lesions usually are ambulant withnormal mobility and have some, but never normal,anorectal sensation and voluntary sphincter activity.Agnarsson et al found that in children with lum-bosacral or sacral myelomeningocele, rectal compli-ance is normal [75] Patients with spina bifida anddamage to the S2–S4 sacral roots present reducedresting and squeeze pressure in the anal canal thatinduce fecal incontinence [76] In addition, patientswith spina bifida may also develop a tethered cordsyndrome, which is associated with a worse bowelfunction that does not seem to improve after surgery[77]

Cauda Equina and Lumbosacral Plexus Disorders

Lumbar and sacral nerve roots arise from the conusmedullaris, the terminal part of spinal cord, forming

a nerve bundle within the spinal canal called thecauda equina The destinations for these roots are thelumbar and sacral plexuses, leaving the cauda equina

at their specific neural foramina Because of the ferential growth of the vertebral column comparedwith the spinal cord, the conus medullaris is located

dif-at the L1 level Acute injuries to cauda equina aremostly caused by sudden central disk herniation or,with minor frequency, by trauma, vertebral collapsedue to metastatic infiltration, or extradural

hematoma Extrinsic tumors, including metastases,

usually present with pain before neurological signs

develop

The incidence and prevalence of cauda equina

lesions are not known, but it is estimated that they

constitute from 1% to 5% of spinal pathology [78]

Cauda equina compression is an acute emergency

that may develop as a sudden major disk prolapse in

a patient with a long history of sciatica or of previous

lumbar or sacral laminectomy, sometimes

postoper-atively following disk excision with hemorrhage at

the operative site The disk usually involved is L4–L5,

but herniations at other levels can occur, inducing a

similar syndrome The clinical picture is

character-ized by weakness and sensory loss in the lower limbs,

buttocks, and perineum, usually with marked

impairment of bladder, bowel, erectile, and

ejacula-tory function Symptoms and signs vary depending

on the nerve roots involved, the size and position of

the disk herniated, and the dimension of the spinal

canal The patient complains usually a loss of

sensa-tion and burning pain in the perineum, with a

char-acteristic “saddle” distribution, weakness of hip

extension and abduction with sparing of hip flexion

and quadriceps movement, a patulous anal

sphinc-ter, and loss of the anal wink and bulbocavernosus

reflexes A marked impairment of the normal

sensa-tion of filling of the bladder and anorectum is also

present, resulting in retention of feces and urine,

with overflow and defecation and micturition

inabil-ity Anal motor response to coughing and anal

squeeze response to volitional activity are absent

Lumbosacral computed tomography (CT) scanning

and particularly magnetic resonance imaging (MRI)

are the urgent diagnostic imaging techniques of

choice to define acute cauda equina syndrome and to

perform early decompression surgery The disk, in

this case, should be urgently removed surgically

within 48 h for a good outcome [79] Delays of

sur-gical treatment lessen the chance of good recovery of

bowel, bladder, and sexual function

Fecal Incontinence in Peripheral Neuropathies

Many patients affected by “idiopathic” fecal

inconti-nence have evidence of either a neurogenic or

mus-cular injury, and some patients remain truly

idio-pathic without clear identifiable cause for sphincteric

dysfunction The peripheral nervous system is

divid-ed into the somatic and autonomic portions with

sensory and motor nerve fibers Autonomic nerve

fibers normally supply the gastrointestinal, bladder,

sexual, and cardiovascular functions Neuropathies

can be functionally selective so that sensory, motor,

or autonomic function can be involved separately or

in various combinations Disease process consists ofgeneralized polyneuropathies, with symmetric distri-bution on the two sides of the body, or focal and mul-tifocal neuropathies in which involvement is local-ized Focal and multifocal neuropathies involving thenerves of the pelvis and the polyneuropathies withautonomic impairment commonly induce bowel,bladder, and sexual dysfunction

Diabetes mellitus is the most common cause ofpolyneuropathy in developed countries Diabeticneuropathy is a chronic symmetrical sensorimotorpolyneuropathy that usually begins after years ofhyperglycemia and is frequently associated withautonomic neuropathy and bowel, bladder, and sex-ual dysfunction Severe diabetic autonomic neuropa-thy (DAN) is almost always associated with insulin-dependent diabetes Symptoms of autonomicinvolvement include impairment of sweating and ofvascular reflexes, constipation, nocturnal diarrheaand fecal incontinence, atonic bladder, sexual impo-tence, and occasionally postural hypotension Thepathogenetic mechanism of the constipation isuncertain, but autonomic neuropathy causingparasympathetic denervation is likely to be implicat-

ed Diarrhea typically occurs at night or after meals,

is a more troublesome complication of diabetes, andmay be an isolated symptom of autonomic dysfunc-tion It is usually chronic, but it is intermittent andalternates with bouts of constipation or normalbowel movements Reduced resting anal toneinduced by sympathetic autonomic neuropathy andloss of rectal sensation may play a role in the noctur-nal fecal incontinence [80] The upper gastrointesti-nal tract symptoms that consist of heartburn, dys-phagia, and bloating may sometimes occur in diabet-

ic patients in addition to bowel dysfunctions Neuropathy due to deposition of amyloid–a pro-teinaceous substance in different tissues and in par-ticular in peripheral nerve–can occur in patients withbenign plasma-cell dyscrasia or in multiple myelo-

ma, Waldenstrom’s macroglobulinemia, or Hodgkin’s lymphoma [81] The neuropathy is of thesmall-fiber type, with a predominant loss of pain andtemperature sensation early in the course of the ill-ness and a later involvement of motor functions andsensory modalities subserved by large myelinatedfibers Autonomic involvement is another early char-acteristic of amyloidotic neuropathy Anhidrosis,loss of papillary light reflexes, vasomotor paralysiswith orthostatic hypotension, and alternating diar-rhea and constipation are frequent in the course ofthe illness Amyloidosis can also present withreduced urinary flow and infrequent voiding withreduced bladder contractility and an increasedpostvoiding urine volume Uncoordinated contrac-tions of the small bowel have been demonstrated in

non-patients affected by familiar amyloidotic neuropathy,

mainly resulting in diarrhea, but sometimes

consti-pation may alternate with diarrhea Diarrhea and

steatorrhea are prominent in primary amyloidosis

Constipation or, occasionally, paralytic ileus and

bladder dysfunction with urine retention occurs in

20–30% of patients affected by Guillain-Barré

syn-drome [82] This inflammatory disease occurs in all

ages and both genders A mild respiratory or

gas-trointestinal infection, surgical procedure, or viral

exanthemas precede the symptoms by 1–3 weeks in

70–80% of patients The major clinical manifestation

is weakness of proximal and distal muscles of the

limbs, trunk, and intercostals, and neck muscles,

which evolves symmetrically over a period of several

days The weakness can progress to total motor

paralysis, with death from respiratory failure The

hyperactivity or hypoactivity of sympathetic and

parasympathetic fibers can induce severe

distur-bances of autonomic function Sinus tachycardia and

less often bradycardia with cardiac arrhythmias,

fluc-tuating hypertension and hypotension, loss of

sweat-ing ability, or facial flushsweat-ing are frequent in the

course of the disease

Vitamin B12 deficiency may arise from inadequate

oral intake, deficiency of intrinsic factors, various

malabsorption disorders, resection of the stomach,

or terminal ileum, inducing various neurological

symptoms including peripheral neuropathy,

myelopathy, altered mental status, and optic

neu-ropathy [83] Subacute combined degeneration of the

spinal cord and distal peripheral neuropathy are the

main neurological consequences of vitamin B12

defi-ciency Most patients with pernicious anemia and

neurological dysfunction show, therefore, a mixed

myelopathic or neuropathic clinical picture

Sym-metrical numbness and paraesthesia of lower limbs

and gait ataxia are the commonest presenting

com-plaints Weakness is sometimes found but is always

accompanied by sensory lower-limb abnormalities

A small number of patients have symptoms of

auto-nomic dysfunction with fecal and urinary

inconti-nence

Fecal Incontinence in Myopathies

Anal sphincter function in myopathies has been

investigated infrequently In myotonic dystrophy,

most patients suffer from diarrhea and abdominal

cramps Different studies showed widespread

abnor-malities of gastrointestinal motility in myotonic

dys-trophy, involving the esophagus and small and large

intestines [84–87] Dysphagia is a prominent

symp-tom in myotonic dystrophy patients, with a reported

prevalence of 25–85% in different series Impaired

pharyngeal contraction, myotonia of the tongue andpharynx, gastric and small-bowel dilation, mega-colon, and abnormal anal sphincter contractionshave been reported [88–90] Abercrombie et al illus-trated degeneration of smooth-muscle cells andfibrosis in the IAS and loss of striated muscle fibers

in the EAS and puborectalis muscles [91] EMG dataconfirm EAS involvement, with reduced numbers ofmotor units, myotonia, and myopathic features with-out neurogenic lesions Digital and manometricanorectal examination show poor resting tone andlow squeeze pressure in the anal canal and reducedrectal compliance

Constipation and diarrhea are frequent in mostmuscular dystrophies; these clinical features havebeen particularly investigated in Duchenne’s dystro-phy, where colonic transit time is commonlyincreased [92] Altered motility of the small and largeintestines has been described in other muscular dys-trophies [93] Atrophy and fibrosis of the intestinalsmooth muscles possibly reflect the diffuse muscle-dystrophic process Chronic constipation fromimmobility is believed to contribute to bowel dys-functions, which include abdominal pain, distension,and vomiting Acute gastric dilation, gastric perfora-tion, and, rarely, peritonitis may occur [94]

Dysfunction of the smooth muscles at several els of the gastrointestinal tract in myasthenia gravis

lev-is well known, and about 33% of patients complain ofsignificant fatigable dysphagia [95, 96] Masticationand swallowing difficulties worsen as a meal pro-gresses, in particular at the end of the day Myasthe-nia gravis can also present with a clinical picture offecal and urinary incontinence [97]

Neurophysiologic Investigations

Neurophysiological examination of patients withfecal incontinence usually follows surgical and clini-cal evaluation and, almost always, other endoscopic,manometric, ultrasound, and MRI investigationsable to diagnose the most important causes of fecalincontinence [98] These different investigations canidentify focal morphological lesions to the IAS andEAS muscle [99–101], location of neoplastic lesions[102], capacity and compliance of the rectum, reflexactivity, reduced sensation of the anorectum, andIAS and EAS muscle dysfunctions [103]

With the advent of neurophysiological techniquesavailable to evaluate anorectal disorders, a moredetailed understanding of the neurogenic pathophys-iological mechanisms underlying fecal incontinence

is evolving Clinical history and neurological nation should be performed to propose a diagnosis ofneurogenic bowel dysfunction and to plan further

exami-electrophysiological tests [98, 104] Although clinical

neurophysiologic investigations and concentric

nee-dle EMG are performed worldwide, their application

to pelvic floor disorders is limited to a few centers

No consensus statement for a standardized approach

to anorectal neurogenic disorders has been reached,

and the role of different tests has not yet been clearly

defined Extensive neurophysiological investigations

should be performed in any patient with anorectal

disorders of suspected central or peripheral

neuro-genic etiology These tests include concentric needle

EMG of different pelvic floor muscles, measurement

of sacral reflex latency (pudendoanal and

bulbocav-ernosus reflex) induced by electrical stimulation,

pudendal somatosensory-evoked potentials (SEP)

after electrical stimulation of the anal canal, and

motor-evoked potentials (MEP) from EAS muscles

by transcranial and lumbosacral magnetic

stimula-tion

A short clinical assessment should precede the

neurophysiological tests, along with a history of the

patient’s complaints Usually the main symptoms

described are pain variably located in the low back

and perineal and sacral areas, paresthesias, leg

weak-ness, erectile dysfunction, and bladder and bowel

disturbances Scoring systems for symptoms of fecal

incontinence are used and have been validated

against the severity of the bowel disorder [105] The

Cleveland Clinic Florida Fecal Incontinence (CCF-FI)

scoring system is one of the most recognized method

for quantifying the degree of symptoms in patients

undergoing neurological sphincter assessment [106]

A clinical neurological examination is performed

with special attention to the status of the lower limbs

and the perineal and buttock areas, particularly

look-ing for signs of pyramidal and peripheral nervous

system lesions [107] Examination usually includes

anal sphincter tone, strength in the S1–S2 innervated

muscles (gastrocnemius, gluteal muscles), sensation

extending from the soles of the feet to the perianal

area, and presence of anal and bulbocavernous

reflexes Anal reflex is induced by pricking or

scratching the perianal skin area, whereas

bulbocav-ernosus reflex is evoked by a nonpainful clitoral or

gland squeeze [108, 109] Clinically elicited reflexes

may be extinguished by mild or severe nerve lesions,

whereas the same reflexes can be recorded

neuro-physiologically, though with a prolonged latency and

reduced amplitude, also in almost complete nerve

lesions [110]

Concentric needle EMG is the most important

neurophysiologic test in the evaluation of patients

with suspected neurogenic etiology of bowel

dys-function [107] EMG assessment for the pelvic floor

and EAS muscle is mainly indicated to determine: (1)

the presence of pathological spontaneous activity,

fibrillation potentials and positive sharp waves, anddenervation of muscle fibers, (2) presence of muscle-fiber reinnervation [111–114], (3) normal mild con-tinuous tonic contraction in the EAS and puborectal-

is muscles [115] and adequate contraction or ation during squeeze or straining, and (4) recruit-ment pattern and motor-unit–potential (MUP) wave-form [116] The most important parameters in theanalysis of MUP are amplitude, duration, area, num-ber of phases and turns, and firing rate that can beautomatically evaluated by advanced EMG systemsprovided with special software analysis

relax-Examination of the EAS muscle holds the centralposition in Podnar’s and Vodusek’s algorithm forelectrodiagnostic evaluation of the sacral nervoussystem [104] With the patient in a comfortable later-

al position with knees and hips flexed, after

ground-ed electrically at the thigh, a standard concentric dle EMG electrode is inserted into the subcutaneousportion of the EAS muscle to a depth of 3–5 mmunder the mucosa, 1 cm from the anal orifice [66,

nee-104, 117, 118] Both left and right halves of the cutaneous EAS muscle must be examined separately,starting on the side with the clinical evidence ofsphincter dysfunction (episiotomy scar tissue, patu-lous anus) If partial or complete atrophy of the sub-cutaneous EAS muscle is appreciated, a concentricneedle electrode can be introduced 1- to 3-cm deeperthrough the skin to evaluate spontaneous activity,recruitment pattern, and functional contractilecapacity of the deeper EAS and 4- to 5-cm deeper forexamination of the PR muscle In the presence offibrosis, there is a loss of contractile capacity of pelvicfloor muscles, and consequently, no spontaneousactivity or MUP is recognized When the needleadvances in the EAS muscle, continuous firing oflow-threshold MUP is normally appreciated, andduring a brief period of relaxation, the presence ofspontaneous activity, fibrillation, or jasper potentialscan be recorded EMG recordings from the EAS wereperformed at rest and during squeezing, coughing,and straining that simulates rectal evacuation Inhealthy subjects, squeeze and cough increase theMUP recruitment pattern, whereas strain decreases

sub-or inhibits MUP firing Needle examination of thebulbocavernosus muscles is indicated when no EMGsignals are recorded in the subcutaneous or deeperEAS muscles [119]

Sacral reflexes evaluate the functional status of theafferent neural fibers of the clitoris or penis, theS2–S4 sacral intraspinal segments, and the efferentpathways to EAS and bulbocavernosus muscles [108,

110, 120] The central circuit at the spinal level iscomplex and probably involves many sacralinterneurons These sacral reflexes, named puden-doanal reflex and bulbocavernosus reflex, reveal, in

fact, two components with different thresholds at the

electrical stimulation: a first component with a

short-er latency, probably oligosynaptic, and a second

component with a longer latency, typical for a

poly-synaptic response A latency delay of these reflexes

may be of localizing neurological value Only the

largest myelinated, fastest fibers convey the

neuro-physiological signals traveling in the afferent limb of

these reflexes Many disorders of bowel and

anorec-tal function are the result of unmyelinated fiber

dys-function; therefore, conduction in these fibers is not

tested by these procedures [121]

Scalp recording of pudendal SEP is a method for

evaluating the afferent sensory pathway and is used

in investigating central and peripheral neurological

diseases Cortical responses can be evoked by

mechanical stimulation (balloon distension of the

rectum) [122] or by electrical stimulation of the

rec-tosigmoid colon [123], the rectum [122, 124, 125],

and the anal canal [126] All these anatomical

struc-tures are innervated by the inferior branches of the

pudendal nerve Pudendal SEP are recorded by

sur-face electrodes placed on the scalp 2-cm behind the

vertex over the cortical representation of the pelvic

region A first positive peak can be recorded in

nor-mal subjects at about 42 ms using a stimulus

inten-sity of two to four times the sensory threshold Later

negative and positive peaks show a large variability

in amplitude between individuals

Transcranial magnetic stimulation (TMS) is a

neu-rophysiological technique that permits activation of

the cortical motor areas without causing patient

dis-comfort; therefore, it is widely used to study the

cen-tral motor pathways in normal subjects [127] and

neurological patients [128] TMS is also applied to

study the corticospinal pathway to the EAS muscle

[129–131] The EAS MEP after TMS have a mean

latency of about 27 ms in the resting state and 23 ms

during facilitation, a functional condition of mild

contraction of the pelvic floor muscles The intensity

of TMS necessary to obtain an MEP in the EAS

mus-cle is much higher than the intensity to elicit an MEP

in the limbs This fact can be explained by the

corti-cal representation of the anogenital area that is locorti-cal-

local-ized deep within the motor strip in the

interhemi-spheric fissure The magnetic stimulation applied

over the lower lumbar spine is known to activate the

lumbosacral ventral roots at their exit from the

verte-bral canal [132] Latency of the motor response is

approximately 6 ms [131] Corticospinal

abnormali-ties detected by this method in patients with

neuro-genic bladder and bowel disorders have been

report-ed [133–137]

The different types of MEP abnormalities, i.e.,

responses with decreased amplitude or delayed

latency, may imply the axonal or demyelinative

impairment underlying the different clinical logical conditions TMS might improve the under-standing of different pelvic floor dysfunctions; how-ever, a rigorous electrophysiological technique andstandardized methods will be required

patho-The inferior rectal branches of the pudendalnerve can be electrophysiologically evaluated bymeasuring pudendal nerve terminal motor latency(PNTML), which is the technique most often usedfor neurologic assessment in patients with idiopath-

ic neurogenic anorectal incontinence [118] ThePNTML technique was first described in 1984 by Kiffand Swash [138, 139] PNTML is determined byrecording anal sphincter motor potential evoked bystimulation of the pudendal nerve with a special sur-face electrode assembly fixed to a gloved index fin-ger (St Mark’s electrode) near the ischial spinethrough the rectal wall The test owes its popularity

to different studies showing abnormal latencies invarious clinical situations [140–146] More recently,however, the PNTML clinical value has been ques-tioned, and two consensus statements, uroneurolog-ical and gastroenterological, did not propose thistest for evaluating patients with bladder and boweldysfunction [119, 147] In particular, the AmericanGastroenterological Association (AGA) medicalposition statement concluded that PNTML cannot

be recommended for evaluating patients with fecalincontinence because: (1) PNTML has a poor corre-lation with clinical symptoms and histologic find-ings, (2) the technique does not discriminatebetween muscle weakness caused by pudendal nerveinjury and muscle injury in patients with fecalincontinence, (3) there is a lack of test sensitivityand specificity for detecting EAS muscle weakness,(4) it is considered to be an operator-dependenttechnique, and (5) the test does not predict surgicaloutcome [147]

Conclusions

Fecal incontinence affects both genders and all agegroups and is a common symptom in patients withseveral different neurological diseases It often influ-ences their quality of life and induces a devastatingeffect on their social activities Knowledge of the neu-ronal mechanisms underlying colorectal and analsphincter function is useful in evaluating the differ-ent impairments occurring in each neurological dis-order

In patients with suspected neurogenic bowel orders and in particular those with fecal inconti-nence, electrodiagnostic techniques should be con-sidered in planning diagnostic workup, treatment,and management

4 Andrew J, Nathan PW (1964) Lesions on the anterior

frontal lobes and disturbances of micturition and

defaecation Brain 87:233–262

5 Kaddumi EG, Hubscher CH (2006) Convergence of

multiple pelvic organ inputs in the rat rostral medulla.

J Physiol 572:393–405

6 Bouvier M, Grimaud JC (1984) Neuronally mediated

interactions between urinary bladder and internal anal

sphincter motility in the cat J Physiol 346:461–469

7 Bouvier M, Grimaud JC, Abysique A (1990) Effects of

stimulation of vesical afferents on colonic motility in

cats Gastroenterology 98:1148–1154

8 Duthie HL, Gairns FW (1960) Sensory nerve-endings

and sensation in the anal region of man Br J Surg

47:585–595

9 Rogers J (1992) Testing for and the role of anal and

rectal sensation Baillieres Clin Gastroenterol

6:179–191

10 Lynn PA, Olsson C, Zagorodnyuk V et al (2003) Rectal

intraganglionic laminar endings are transduction sites

of extrinsic mechanoreceptors in the guinea pig

rec-tum Gastroenterology 125:786–794

11 Frenckner B, Euler CV (1975) Influence of pudendal

block on the function of the anal sphincters Gut

16:482–489

12 Hobday DI, Aziz Q, Thacker N et al (2001) A study of

the cortical processing of ano-rectal sensation using

functional MRI Brain 124:361–368

13 Grundy D, Al-Chaer ED, Aziz Q et al (2006)

Funda-mentals of neurogastroenterology: basic science

Gas-troenterology 130:1391–1411

14 Norton C (1996) Faecal incontinence in adults 1:

Prevalence and causes Br J Nurs 5:1366–1368,

1370–1374

15 Kamm MA (1998) Faecal incontinence BMJ

316:528–532

16 Harari D, Coshall C, Rudd AG, Wolfe CD (2003)

New-onset fecal incontinence after stroke: prevalence,

nat-ural history, risk factors, and impact Stroke

34:144–150

17 Baztan JJ, Domenech JR, Gonzalez M (2003)

New-onset fecal incontinence after stroke: risk factor or

consequence of poor outcomes after rehabilitation?

Stroke 34:e101–102

18 Nakayama H, Jorgensen HS, Pedersen PM et al (1997)

Prevalence and risk factors of incontinence after

stroke The Copenhagen Stroke Study Stroke 28:58–62

19 Scandinavian Stroke Study Group (1985) Multicenter

trial of hemodilution in ischemic stroke-background

and study protocol Stroke 16:885–890

20 Wade DT, Hewer RL (1985) Outlook after an acute

stroke: urinary incontinence and loss of consciousness

compared in 532 patients Q J Med 56:601–608

21 Ween JE, Alexander MP, D’Esposito M, Roberts M

(1996) Incontinence after stroke in a rehabilitation

setting: outcome associations and predictive factors Neurology 47:659–663

22 Patel M, Coshall C, Rudd AG, Wolfe CD (2001)

Natur-al history and effects on 2-year outcomes of urinary incontinence after stroke Stroke 32:122–127

23 Taub NA, Wolfe CD, Richardson E, Burney PG (1994) Predicting the disability of first-time stroke sufferers

at 1 year 12-month follow-up of a population-based cohort in southeast England Stroke 25:352–357

24 Gelber DA, Good DC, Laven LJ, Verhulst SJ (1993) Causes of urinary incontinence after acute hemispher-

ic stroke Stroke 24:378–382

25 Robain G, Chennevelle JM, Petit F, Piera JB (2002) [Incidence of constipation after recent vascular hemi- plegia: a prospective cohort of 152 patients] Rev Neu- rol 158:589–592

26 Stocchi F, Badiali D, Vacca L et al (2000) Anorectal function in multiple system atrophy and Parkinson’s disease Mov Disord 15:71–76

27 Sakakibara R, Shinotoh H, Uchiyama T et al (2001) Questionnaire-based assessment of pelvic organ dys- function in Parkinson’s disease Auton Neurosci 92:76–85

28 Edwards LL, Quigley EM, Harned RK et al (1994) Characterization of swallowing and defecation in Parkinson’s disease Am J Gastroenterol 89:15–25

29 Mathers SE, Kempster PA, Swash M, Lees AJ (1988) Constipation and paradoxical puborectalis contrac- tion in anismus and Parkinson’s disease: a dystonic phenomenon? J Neurol Neurosurg Psychiatry 51:1503–1507

30 Edwards LL, Quigley EM, Harned RK et al (1993) catory function in Parkinson’s disease: response to apomorphine Ann Neurol 33:490–493

Defe-31 Edwards LL, Quigley EM, Pfeiffer RF (1992) testinal dysfunction in Parkinson’s disease: frequency and pathophysiology Neurology 42:726–732

Gastroin-32 Singaram C, Ashraf W, Gaumnitz EA et al (1995) Dopaminergic defect of enteric nervous system in Parkinson’s disease patients with chronic constipa- tion Lancet 346:861–864

33 Bauer HJ, Firnhaber W, Winkler W (1965) Prognostic Criteria In Multiple Sclerosis Ann N Y Acad Sci 122:542–551

34 Crayton H, Heyman RA, Rossman HS (2004) A modal approach to managing the symptoms of multi- ple sclerosis Neurology 63:S12–18

multi-35 Miller H, Simpson CA, Yeates WK (1965) Bladder function In Multiple Sclerosis Br Med J 5445:1265–1269

Dys-36 Andersen JT, Bradley WE (1976) Abnormalities of detrusor and sphincter function in multiple sclerosis.

Br J Urol 48:193–198

37 Blaivas JG, Bhimani G, Labib KB (1979) Vesicourethral dysfunction in multiple sclerosis J Urol 122:342–347

38 Bennett N, O’Leary M, Patel AS et al (2004) Can

high-er doses of oxybutynin improve efficacy in neurogenic bladder? J Urol 171:749–751

39 Chia YW, Fowler CJ, Kamm MA et al (1995) lence of bowel dysfunction in patients with multiple sclerosis and bladder dysfunction J Neurol 242:105–108

Preva-40 Bakke A, Myhr KM, Gronning M, Nyland H (1996)

Bladder, bowel and sexual dysfunction in patients with

multiple sclerosis-a cohort study Scand J Urol

Nephrol Suppl 179:61–66

41 Rosenblum D, Saffir M (1998) The natural history of

multiple sclerosis and its diagnosis Phys Med Rehabil

Clin N Am 9:537–549

42 Hinds JP, Eidelman BH, Wald A (1990) Prevalence of

bowel dysfunction in multiple sclerosis A population

survey Gastroenterology 98:1538–1542

43 Swash M, Snooks SJ, Chalmers DH (1987) Parity as a

factor in incontinence in multiple sclerosis Arch

Neu-rol 44:504–508

44 Glick ME, Meshkinpour H, Haldeman S et al (1982)

Colonic dysfunction in multiple sclerosis

Gastroen-terology 83:1002–1007

45 Waldron DJ, Horgan PG, Patel FR et al (1993) Multiple

sclerosis: assessment of colonic and anorectal function

in the presence of faecal incontinence Int J Colorectal

Dis 8:220–224

46 Sorensen M, Lorentzen M, Petersen J, Christiansen J

(1991) Anorectal dysfunction in patients with urologic

disturbance due to multiple sclerosis Dis Colon

Rec-tum 34:136–139

47 Jameson JS, Rogers J, Chia YW et al (1994) Pelvic floor

function in multiple sclerosis Gut 35:388–390

48 Nordenbo AM, Andersen JR, Andersen JT (1996)

Dis-turbances of ano-rectal function in multiple sclerosis.

J Neurol 243:445–451

49 Weber J, Grise P, Roquebert M et al (1987) Radiopaque

markers transit and anorectal manometry in 16

patients with multiple sclerosis and urinary bladder

dysfunction Dis Colon Rectum 30:95–100

50 Haldeman S, Glick M, Bhatia NN et al (1982)

Colo-nometry, cystometry, and evoked potentials in

multi-ple sclerosis Arch Neurol 39:698–701

51 Glickman S, Kamm MA (1996) Bowel dysfunction in

spinal-cord-injury patients Lancet 347:1651–1653

52 Krogh K, Mosdal C, Laurberg S (2000) Gastrointestinal

and segmental colonic transit times in patients with

acute and chronic spinal cord lesions Spinal Cord

38:615–621

53 Krogh K, Nielsen J, Djurhuus JC et al (1997) Colorectal

function in patients with spinal cord lesions Dis

Colon Rectum 40:1233–1239

54 Lynch AC, Anthony A, Dobbs BR, Frizelle FA (2000)

Anorectal physiology following spinal cord injury.

Spinal Cord 38:573–580

55 Lynch AC, Antony A, Dobbs BR, Frizelle FA (2001)

Bowel dysfunction following spinal cord injury Spinal

Cord 39:193–203

56 Lynch AC, Wong C, Anthony A et al (2000) Bowel

dys-function following spinal cord injury: a description of

bowel function in a spinal cord-injured population

and comparison with age and gender matched

con-trols Spinal Cord 38:717–723

57 Stone JM, Nino-Murcia M, Wolfe VA, Perkash I (1990)

Chronic gastrointestinal problems in spinal cord

injury patients: a prospective analysis Am J

Gastroen-terol 85:1114–1119

58 Randell N, Lynch AC, Anthony A et al (2001) Does a

colostomy alter quality of life in patients with spinal

cord injury? A controlled study Spinal Cord

39:279–282

59 Stone JM, Wolfe VA, Nino-Murcia M, Perkash I (1990) Colostomy as treatment for complications of spinal cord injury Arch Phys Med Rehabil 71:514–518

60 Kelly SR, Shashidharan M, Borwell B et al (1999) The role of intestinal stoma in patients with spinal cord injury Spinal Cord 37:211–214

61 Krogh K, Mosdal C, Gregersen H, Laurberg S (2002) Rectal wall properties in patients with acute and chronic spinal cord lesions Dis Colon Rectum 45:641–649

62 Kirk PM, King RB, Temple R et al (1997) Long-term follow-up of bowel management after spinal cord injury SCI Nurs 14:56–63

63 Stiens SA, Bergman SB, Goetz LL (1997) Neurogenic bowel dysfunction after spinal cord injury: clinical evaluation and rehabilitative management Arch Phys Med Rehabil 78:S86–102

64 Yim SY, Yoon SH, Lee IY et al (2001) A comparison of bowel care patterns in patients with spinal cord injury: upper motor neuron bowel vs lower motor neuron bowel Spinal Cord 39:204–207

65 Benevento BT, Sipski ML (2002) Neurogenic bladder, neurogenic bowel, and sexual dysfunction in people with spinal cord injury Phys Ther 82:601–612

66 Bartolo DC, Jarratt JA, Read NW (1983) The use of conventional electromyography to assess external sphincter neuropathy in man J Neurol Neurosurg Psychiatry 46:1115–1118

67 Staas WE Jr, Nemunaitis G (1989) Management of reflex sweating in spinal cord injured patients Arch Phys Med Rehabil 70:544–546

68 De Looze D, Van Laere M, De Muynck M et al (1998) Constipation and other chronic gastrointestinal prob- lems in spinal cord injury patients Spinal Cord 36:63–66

69 Rajendran SK, Reiser JR, Bauman W et al (1992) trointestinal transit after spinal cord injury: effect of cisapride Am J Gastroenterol 87:1614–1617

Gas-70 Keshavarzian A, Barnes WE, Bruninga K et al (1995) Delayed colonic transit in spinal cord-injured patients measured by indium-111 Amberlite scintigraphy Am

J Gastroenterol 90:1295–1300

71 Glick ME, Meshkinpour H, Haldeman S et al (1984) Colonic dysfunction in patients with thoracic spinal cord injury Gastroenterology 86:287–294

72 Lie HR, Lagergren J, Rasmussen F et al (1991) Bowel and bladder control of children with myelomeningo- cele: a Nordic study Dev Med Child Neurol 33:1053–1061

73 Malone PS, Wheeler RA, Williams JE (1994) nence in patients with spina bifida: long term results Arch Dis Child 70:107–110

Conti-74 Rintala RJ (2002) Fecal incontinence in anorectal formations, neuropathy, and miscellaneous condi- tions Semin Pediatr Surg 11:75–82

mal-75 Agnarsson U, Warde C, McCarthy G et al (1993) Anorectal function of children with neurological prob- lems I: Spina bifida Dev Med Child Neurol 35:893–902

76 Arhan P, Faverdin C, Devroede G et al (1984) tal motility after surgery for spina bifida Dis Colon Rectum 27:159–163

Anorec-77 Levitt MA, Patel M, Rodriguez G et al (1997) The