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Gastroenterol Rep. 2007 ; 1(2): 56–65.

All Roads Lead to Rome: Update on Rome III Criteria and New
Treatment Options
David Q. Shih, MD1,2 and Lola Y. Kwan, MD1
1Cedars-Sinai Inflammatory Bowel Disease Center, Los Angeles, California, Los Angeles

2Department of Medicine, Division of Digestive Diseases, University of California, Los Angeles

Abstract
The recently published Rome III criteria reflect current understanding of functional
gastrointestinal disorders. These criteria include definitions of these conditions and their
pathophysiologic subtypes and offer guidelines for their management. At the 2006 Annual
Scientific Meeting of the American College of Gastroenterology, a panel of experts discussed
these criteria as they pertain to irritable bowel syndrome, functional dyspepsia, and chronic
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constipation. This article reviews the panel’s findings, highlights the differences between the
Rome II and III criteria, and summarizes best treatment options currently available to practitioners
and their patients.

Functional gastrointestinal (GI) disorders, such as irritable bowel syndrome (IBS),

functional dyspepsia, and chronic constipation, pose an extensive healthcare burden and
negatively affect quality of life. The total cost of caring for an IBS patient may reach
thousands of dollars; in fact, symptoms of IBS are second only to the common cold for
causing work absenteeism. 1 Similarly, patients and their insurers spend considerable
amounts of money for the diagnosis and treatment of chronic constipation, an uncomfortable
and distressing condition for which few satisfactory therapies are available.2,3

Over the past 15 years, the evolving definition of functional bowel disorders has been driven
by advanced understanding of symptom patterns. Currently, functional GI disorders are
classified into six major domains according to anatomical distribution, from the esophagus
to anorectum. These disorders are believed to be caused by disturbed motor and sensory
function, altered immune function and inflammation, and dysregulation of the central and
enteric nervous systems. Consensus-based definitions spearheaded by the Rome committee
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for various functional GI disorders were launched in May of this year during Digestive
Disease Week 2006.

During the annual scientific meeting of the American College of Gastroenterology, held in
Las Vegas, Nevada, October 20–25, 2006, a panel of experts reviewed the Rome III criteria
and their recommended therapeutic interventions. Participants included Nicholas J. Talley,
MD, PhD, FACG, Professor of Medicine at the Mayo Clinic College of Medicine,
Rochester; Minnesota; Charlene M. Prather, MD, MPH, Associate Professor of Internal
Medicine at St. Louis University, Missouri; and Satish S.C. Rao, MD, PhD, FACG,
Professor of Internal Medicine and Director of Neurogastroenterology and GI Motility at the
University of Iowa Hospital and Clinic, Iowa City.

Irritable Bowel Syndrome

Irritable bowel syndrome affects about 10%–20% of adolescents and adults; it
predominantly occurs in females. 4,5 As with other functional GI disorders, treating the
symptoms of IBS is expensive in terms of dollars and patient discomfort and anguish.6,7
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Rome III Criteria for IBS

Irritable bowel syndrome is characterized by abdominal pain or discomfort associated with
disturbed defecation or a change in bowel habit (Table 1).8 Based upon bowel patterns at a
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particular point in time, the disorder may be categorized further into four groups (Table 2).8
An individual with symptoms that do not correlate with either diarrhea- or constipation-
predominant IBS is categorized as having either mixed IBS (meeting criteria for both
diarrhea- and constipation-predominant IBS) or unsubtyped IBS (insufficient abnormality of
stool consistency to meet any of the three types). Alarming symptoms may suggest
involvement of structural or biochemical abnormalities, yet such findings are not required as
exclusionary criteria for the condition’s diagnosis.8

Historically, variations in patient and physician perception have made the diagnosis of
“constipation” and “diarrhea” difficult. For example, straining to defecate may occur with
soft or watery stools; on the other hand, the stool may be solid, yet defecation is frequent.9
Stool form reflects intestinal transit time, and the Rome committee recommends use of the
Bristol Stool Form Scale to classify patients into the four IBS subtypes (Figure 1).8–10 This
scale considers constipation to be related to IBS types 1 and 2 and diarrhea to be linked with
IBS types 6 and 7.8,10

Pathophysiology
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Mechanisms that explain the presence of visceral hypersensitivity and GI motor disturbances
in IBS are emerging. Some recent studies point to postinfectious changes, inflammation,
bacterial overgrowth, and neurotransmitter alteration as potential mechanisms of IBS.

Postinfectious and Inflammatory IBS—IBS may follow a bout of bacterial gastritis.

For example, Marshall and others11 reported a higher incidence of IBS among individuals
exposed to municipal water contamination than among controls (27.5% vs 10.1%,
respectively; P < 0.01). Furthermore, the incidence of IBS was even higher among
individuals with clinically documented gastroenteritis than among controls (36.2% vs
10.1%; P < 0.01). Mearin et al12 found that the relative risk of developing IBS after
Salmonella gastroenteritis increased by eightfold over the subsequent year, thereby
supporting the role of postinfectious gastroenteritis in the development of IBS.

Some IBS patients also have subtle gut mucosal inflammation and immune activation. For
example, an increase in mast cells, neutrophils, natural killer cells, eosinophils, and
intraepithelial lymphocytes has been recorded among individuals with documented
postinfectious and non-postinfectious IBS when compared with controls.13,14 Such
increased immune activation also is manifested as a shift toward inflammatory cytokine
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profiles with an abnormal interleukin (IL)-10/IL-12 ratio and an increased level of IL-1β.
15,16

Bacterial Overgrowth—The GI motor disturbances seen in IBS may lead to qualitative or

quantitative changes in bacterial flora that promote bacterial overgrowth and increase
bacterial fermentation/gas. This production of excess gas induces such symptoms as
abdominal discomfort and bloating.17

The association between bacterial overgrowth and IBS is supported by studies showing
improved IBS symptoms after antibiotic treatment. For example, a recent double-blind,
randomized, placebo-controlled study by Pimentel et al18 assigned participants meeting the
Rome I IBS criteria to receive either 400 mg of rifaximin three times daily for 10 days or
placebo. The rifaximin-treated patients achieved a significant global IBS symptom
improvement (36%) when compared with the placebo group (21%).

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Promising evidence supports the role of bacterial overgrowth in IBS and eradication of such
colonies for management of the disorder. However, the expert panel warned physicians to
accept this approach cautiously, noting that more work to confirm these observations is
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needed.

Neurotransmitter Alteration and IBS—Alterations in neurotransmitters may lead to

visceral hypersensitivity and GI motor disturbances. In particular, serotonin, or 5-
hydroxytryptamine (5-HT), and its effects on the GI system are the subject of active
research. Biologically, alterations in the levels or sensing mechanism of serotonin may lead
to IBS, since this neurotransmitter is a major regulator of the peristaltic reflex and sensory
relays in the gut.19

Two studies support this claim. Whereas Dunlop’s team20 reported that the release of
serotonin fell among patients with constipation-predominant IBS and rose in individuals
with the diarrhea-predominant form of the disorder, Coates et al21 showed that IBS patients
exhibited lower levels of gut mucosal serotonin and serotonin reuptake transporter than did
controls.

Updates in IBS Treatment

Initial IBS management includes education, reassurance, and investigation of psychosocial
issues.21
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Helping Patients Help Themselves—In a randomized study, Robinson’s team22 found

that introducing a self-help guidebook to IBS patients resulted in a 60% reduction in their
primary-care consultations (P < 0.001) and a drop in their perceived symptom severity (P <
0.001) when compared with controls.

The expert panel recommended the following resources for IBS patients:
• http://www.acg.gi.org/patientinfo/ibsrelief
• http://www.iffgd.org
• http://www.aboutibs.org
• http://www.med.unc.edu/medicine/fgidc

Pharmacologic Therapy—Drug therapy mainly targets IBS symptoms. The types of

drugs available are divided into three main categories (Figure 2).23

Fiber supplements: According to anecdotal reports, some patients with diarrhea experience
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a firming of stools after using fiber supplements; however, some studies showed no clear
benefit with use of these products.24–26 When prescribing a fiber supplement to patients
with diarrhea, start at a low dose and progressively titrate the dose up as tolerated to
minimize the bloating that patients frequently experience.

Loperamide: Loperamide is a µ-opioid-receptor agonist that reduces intestinal secretion,

slows colonic transit, and increases resting anal sphincter tone.27 When compared with
placebo, loperamide reduces diarrhea in IBS patients with this predominant symptom.25,26

Opioid-receptor activation reduces visceral pain via peripheral (spinal afferents) and central
mechanisms; however, loperamide has not been shown to alter abdominal pain or other IBS
symptoms when compared with placebo.25,26

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Alosetron: 5-HT plays an important role in visceral sensitivity, gut absorption/secretion,

and motility.19 The 5-HT type 3 (5-HT3) receptor antagonists may be useful in reducing
colonic transit time and in treating diarrhea.
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There is convincing evidence that a drug in this class, alosetron, may delay colonic transit
time.28,29 A meta-analysis of randomized trials showed that alosetron is effective against
diarrhea-predominant IBS.30 However, because of its suspected side effects (eg, ischemic
colitis, colonic ischemia), this drug is only approved for restricted use.31,32 Recently, a
meta-analysis showed that the incidence of ischemic colitis related to use of the drug is low
(1.1 per 1,000 patient-years of alosetron use) and is rarely associated with long-term
sequelae or serious morbidity.33

Functional Dyspepsia
Functional dyspepsia is a clinical syndrome characterized by chronic or recurrent upper
abdominal pain or discomfort having no identifiable cause.34 This disorder is not a
monosymptomatic entity; several predominant symptoms may be present, including
epigastric pain (22%), abdominal fullness (24%), bloating (15%), vomiting (3%), belching
(8%), early satiety (12%), nausea (10%), and heartburn (6%).35 These predominant
symptoms change over time, making functional dyspepsia difficult to define and classify.34
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Rome III Criteria for Functional Dyspepsia

After reviewing available evidence, the Rome committee proposed updated diagnostic
criteria for functional dyspepsia. As shown in Table 3,34 the Rome III criteria definition of
functional dyspepsia includes at least one of the following: bothersome postprandial
fullness, early satiation, epigastric pain, and epigastric burning; patients also must have no
evidence of structural disease that would likely explain their symptoms, including upper
endoscopic findings. The patient must meet the criteria for 3 months and must begin
experiencing symptoms for at least 6 months before diagnosis.34

Functional dyspepsia may be divided into postprandial distress syndrome (characterized by

postprandial fullness and/or early satiation) and epigastric pain syndrome (characterized by
epigastric pain). Dyspepsia is considered to be a continuum of various gastric complaints;
thus, a diagnosis of functional dyspepsia does not preclude the inclusion of gastroesophageal
reflux disease (GERD) and/or IBS in its symptom complex.34

Updates in Treatment of Functional Dyspepsia

Initial management of functional dyspepsia includes reassurance, education, smoking
cessation, consumption of several small and low-fat meals each day, and avoidance of
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coffee, alcohol, and nonsteroidal anti-inflammatory agents; however, no evidence exists that
these interventions are effective.36 Other treatment modalities include psychotherapy,
cognitive-behavioral therapy, and hypnotherapy; although a few studies have shown benefit
of psychological therapy in functional dyspepsia,37 additional studies must be done to
establish its efficacy.

Medical treatment options for functional dyspepsia remain limited, and available studies do
not address the newly defined subgroups of epigastric pain syndrome and postprandial
distress syndrome. In addition, up to 60% of patients respond to placebo, which further
limits tests of pharmaceutical effectiveness in this patient population.38

Gastric Acid Suppression and Helicobacter pylori Eradication—Several lines of

compelling evidence point to gastric acid suppression as the first-line drug therapy for
functional dyspepsia. A Cochrane systematic review39 showed histamine-2 (H2)-receptor

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antagonists and proton-pump inhibitors to be superior to placebo in managing the disorder.

Another meta-analysis of controlled, randomized trials40 both confirmed this finding and
showed acid suppression to be cost-effective in treating functional dyspepsia. The benefit of
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acid suppression against functional dyspepsia may be related to unrecognized GERD or

nonerosive reflux disease.40–42

Eradication of H pylori also appears to help treat functional dyspepsia. Another Cochrane
systematic review43 concluded that H pylori eradication therapy has a statistically
significant effect in treating H pylori-positive, nonulcer dyspepsia, and an economic model
suggested that H pylori eradication also may be cost-effective. Thus, H pylori eradication is
recommended for functional dyspepsia.

Antidepressants—Few studies have investigated the effectiveness of antidepressants

against functional dyspepsia. A small, randomized, crossover trial of seven patients showed
that 50 mg of amitriptyline increased tolerance to aversive visceral sensations when
compared with placebo administration.44

Despite the limited data, treatment with tricyclic antidepressants (eg,10–25 mg of

imipramine or desipramine at night) or a selective serotonin reuptake inhibitor (eg, 10 mg of
escitalopram or 20 mg of sertraline in the morning) is recommended after standard therapy
with a proton-pump inhibitor or H pylori eradication fails.45
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Prokinetic Agents—Prokinetic agents, such as metoclopramide, domperidone, and

cisapride, reduce symptoms of functional dyspepsia. These drugs have proven more
effective than has placebo against the disorder, especially in patients presenting with
predominant symptoms of fullness, bloating, or nausea.39,46

However, patients must be monitored closely when using these agents. For example,
metoclopramide must be used cautiously in the elderly because of undesired side effects (eg,
tardive dyskinesia).47 Domperidone is not available in the United States because of its risk
of cardiotoxicity48; cisapride was withdrawn from the US market because it caused QT-
interval prolongation and rare cases of fatal arrhythmia.49

5-HT Agonists/Antagonists—The 5-HT pathway is important to visceral sensitivity, so

its alteration may treat functional dyspepsia effectively.27 One randomized, controlled trial
showed that alosetron caused significantly greater reductions in the severity and frequency
of functional dyspepsia symptoms than did placebo (P < 0.001).50

Because a link between alosetron and ischemic colitis was suggested, the drug is not used
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for functional dyspepsia; however, no causal relationship between the two has been
established.51 However, a recent meta-analysis concluded that alosetron use is rarely
associated with serious morbidity and is associated with a low incidence of ischemic colitis
(1.1 cases per 1,000 patient-years of alosetron use).33

Chronic Constipation and Functional Anorectal Disorders

There have been advances in the understanding of symptom patterns of chronic constipation
and functional anorectal disorders, and updated criteria have been based on new scientific
evidence. These criteria are designed to enhance clinical recognition and develop better
scientific understanding of these disorders and to standardize their management.

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Rome III Criteria for Functional Constipation

Functional constipation presents as persistently difficult, infrequent, and seemingly
incomplete defecation that does not fulfill the IBS criteria. The subjective and objective
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criteria for functional constipation are summarized in Table 4.8

A comparison of the Rome II criteria and the Rome III criteria shows two main changes.
First, the more recent criteria are consistent with those for other functional bowel disorders,
as the frequency of bowel movements now is > 25% instead of ≥ 25%. Second, the newer
criteria permit laxative-induced loose stools when treating functional constipation, because
studies using Rome II criteria yielded a lower prevalence of the disorder than did those using
Rome I.52

Functional Anorectal Disorders

Functional anorectal disorders include fecal incontinence, anorectal pain, and disorders of
defecation; they are defined by specific symptoms, as shown in Table 5.53

Rome III Criteria for Functional Fecal Incontinence—Functional fecal incontinence

is defined as uncontrolled leakage of fecal material for at least 3 months in an individual
over 4 years of age (Table 6).53 Because it is unclear when the passage of flatus is
abnormal, leakage of flatus alone should not be considered a symptom of fecal incontinence.
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In general, the spectrum of functional incontinence is broader than that of fecal

incontinence. According to the Rome III criteria, functional fecal incontinence may be
associated with such organic disorders as dementia, multiple sclerosis, and Crohn’s disease,
because the relationship between structural disturbances and the disorder is unclear and
asymptomatic patients may have small anal sphincter defects. However, if anal sphincter
electromyography demonstrates abnormal innervation (eg, pudendal neuropathy), organic
diseases that may lead to denervation/ reinnervation changes (eg, dementia, multiple
sclerosis, and diabetes) are excluded as the cause of incontinence.53

Chronic Proctalgia—Chronic proctalgia and proctalgia fugax are the two functional
anorectal pain disorders. Chronic proctalgia may be broken down into levator ani syndrome
(tenderness during posterior traction on the puborectalis muscle) or unspecified anorectal
pain, depending upon the presence or absence of puborectalis tenderness during digital rectal
examination (Table 7).53 The distinction between these two types is emphasized by
modified nomenclature featured in the Rome III criteria.

Proctalgia Fugax—Proctalgia fugax is distinguished from chronic proctalgia by the

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duration, frequency, and character of the pain. This disorder is manifested as a sudden,
severe pain in the anal area that lasts several seconds to minutes and then disappears
completely (Table 8).8

For research purposes, the diagnostic criteria for proctalgia fugax must be fulfilled for 3
months or more. However, in clinical practice, its diagnosis, evaluation, and treatment may
take place before 3 months pass.53

Functional Defecation Disorders

Functional defecation disorders are defined as paradoxical contraction or inadequate
relaxation of the pelvic floor muscles along with fulfillment of the Rome III criteria for
functional constipation (Table 9).53 This anorectal disorder may be broken down further as
either dyssynergic defecation (inappropriate pelvic floor contraction or sphincter relaxation
with adequate propulsive forces during attempted defecation) or inadequate defecatory

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propulsion (inadequate propulsive forces during attempted defecation with or without

dyssynergic defecation).
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According to both the Rome II and Rome III criteria, the diagnosis for functional defecation
disorders requires both abnormal diagnostic test results and the presence of defecation
symptoms53; a list of symptoms alone does not distinguish patients with functional
defecatory disorders from those with functional constipation. Further, the diagnostic criteria
for dyssynergia also are the same for both maladies. However, studies using balloon
expulsion and rectal barium evacuation showed that inadequate rectal propulsive force
causes impaired evacuation54,55; thus, the revised criteria highlight the possibility that
functional defecation disorders may be caused by inadequate propulsive forces.

Updates in Treatment of Chronic Constipation and Functional Anorectal Disorders

As illustrated in Figure 3,56 a pathophysiologic approach to managing chronic constipation
is recommended. Classes of medications marketed to manage chronic constipation include
bulking agents, osmotic and stimulatory laxatives, stool softeners, lubricants, and newer
receptor-based therapies (eg, tegaserod, lubiprostone, and alvimopan). However, patients
with dyssynergic defecation may benefit more from biophysical therapies than from
pharmacotherapy.

The literature shows no clear benefit when chronically constipated patients used bulking
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agents (eg, psyllium, calcium polycarbophil, methylcellulose, bran, aloe vera),24 stimulant
laxatives (eg, bisacodyl, senna),57 or stool softeners (eg, docusate sodium, docusate
calcium).57,58 However, several high-quality, placebo-controlled, randomized trials have
shown osmotic laxatives (eg, polyethylene glycol solutions) and lactulose to be effective in
this population.57,59,60

Serotonin-Receptor Agonists/Antagonists—Approximately 90% of serotonin is

found within the enterochromaffin cells of the GI tract.61 When 5-HT interacts with 5-HT3
and 5-HT type 4 (5-HT4) receptors, it promotes peristalsis and modulates fluid content of the
stool and visceral sensation via 5-HT4 receptors.62 Such findings resulted in the
development of 5-HT4 receptor agonists.

Tegaserod, a partial 5-HT4 receptor agonist, was approved by the US Food and Drug
Administration (FDA) for long-term treatment of chronic idiopathic constipation in men and
women younger than 65 years of age. Kamm and others63 performed a placebo-controlled,
randomized clinical trial that compared placebo with 2 mg and 6 mg of tegaserod given
twice daily to patients with chronic constipation (defined as fewer than three complete
spontaneous bowel movements per week). At 4 weeks, a significantly greater number of
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spontaneous bowel movements were noted among patients receiving 2 mg (41.4%) or 6 mg

(43.2%) of tegaserod twice daily than among the placebo group (25.1%; P < 0.0001). These
results were confirmed by a similarly designed, international, multi-center study.63 The
high-quality designs of such trials and reproducibility of the findings led to tegaserod
receiving a “grade A” recommendation for treatment of chronic constipation from two
systematic reviews.57,58

Chloride-Channel Activators—Chloride channels are located on the apical surfaces of

the gut mucosal epithelial cells. As negatively charged chloride ions enter the intestinal
lumen through these channels, so do sodium ions and water passively to maintain isoelectric
neutrality.64

Lubiprostone, a bicyclic fatty acid, is the first chloride-channel activator to be approved by

the FDA. In a randomized clinical trial that compared placebo with 24 µg of lubiprostone

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given twice daily to patients with chronic constipation for up to 4 weeks, Johanson’s team65
found the drug to effectively increase the number of spontaneous bowel movements,
decrease straining, and improve stool consistency when compared with placebo (P < 0.002
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for all outcome measurements). Johanson et al66 also showed that lubiprostone improved
abdominal bloating, discomfort, and severity of constipation when compared with baseline
examination for up to 24 weeks (P < 0.001).

Adverse effects associated with lubiprostone therapy included nausea, diarrhea, headache,
and abdominal pain.

Peripheral µ-Opioid Antagonists—Another class of medications being tested against

chronic constipation, peripheral µ-opioid antagonists may be particularly useful in managing
opioid-induced constipation. In initial physiologic studies, a drug in this class, alvimopan,
accelerated whole gut transit time and reversed the constipating and gut-slowing effects of
codeine phosphate when compared with placebo at 24 and 48 hours (P < 0.05).67

Biofeedback Therapies—Functional defecation disorders also may be managed by

pelvic floor training or biofeedback therapies.68–71 Chiarioni and others72 recently
reported that biofeedback sessions were more effective than were continuous polyethylene
glycol for treating pelvic floor dyssynergia (80% vs 22% improvement, respectively; P <
0.001), noting that the benefits of biofeedback persisted for at least 2 years. Furthermore,
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this method also produced greater reductions in straining, sensations of incomplete

evacuation and anorectal blockage, use of enemas and suppositories, and abdominal pain (P
< 0.01 for all parameters). The superiority of biofeedback therapy to alternative treatments
for patients with pelvic floor dyssynergia-type constipation also was confirmed by two other
randomized controlled trials.73,74

Conclusion
The symptoms of functional bowel disorders vary and may include both GI and
extraintestinal complaints. Alarm symptoms suggest the possibility of structural disease, but
they do not exclude a diagnosis of functional bowel disorder. Thus, the patient’s diagnosis
should be based on a symptom complex that fulfills the accepted Rome criteria.

Over the past 15 years, the definition of functional bowel disorder has evolved with
advances in the understanding of symptom patterns; currently, this knowledge is reflected in
the Rome III criteria. Historically, management of functional bowel disorders has been
frustrating; today, however, it is possible to design effective therapies using a
pathophysiologic approach.
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The cure of functional bowel disorders ultimately requires scrutiny of basic research results
to better understand the underlying pathogenesis. With time, evidence-based therapy will
help us to specifically target these physical conditions—and not just their symptoms.

Biographies
Dr. Shih is a Gastroenterology Fellow at Cedars-Sinai Inflammatory Bowel Disease Center
and the University of California, Los Angeles.

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Dr. Kwan is a Resident in Internal Medicine at Cedars-Sinai Medical Center, Los Angeles,
California.

Acknowledgments
Dr. Shih is supported by a gastroenterology training grant (T32 DK07180-30) from the National Institutes of Health
and by the Specialty Training and Advanced Research (STAR) Program at the University of California, Los
Angeles.
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randomized controlled trial. Gastroenterology. 2005; 128:A268.
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dyssynergia-type constipation. Am J Gastroenterol. 2005; 100:S335.
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Figure 1.
Bristol Stool Form Scale. Adapted from Lewis and Heaton.10

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Figure 2.
Pharmacologic therapy for irritable bowel syndrome. PEG = polyethylene glycol. Adapted
from Prather.23
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Figure 3.
Pathophysiology-based treatment for chronic constipation. IBS-C = constipation-
predominant irritable bowel syndrome; PEG = polyethylene glycol. Adapted from Rao.56
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Table 1

Rome III Diagnostic Criteria* for Irritable Bowel Syndrome

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Recurrent abdominal pain or discomfort† more than 3 days per month over the previous 3 months associated with two or more of the following:
• Improvement with defecation
• Onset associated with a change in frequency of stool
• Onset associated with a change in form or appearance of stool

*
Symptom onset greater than 6 months prior to the diagnosis, with the above criteria fulfilled for the past 3 months
†
Discomfort means an uncomfortable sensation not described as pain

Adapted from Longstreth et al8

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Table 2
Irritable Bowel Syndrome (IBS) Subtypes by Predominant Stool Pattern
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1 IBS with constipation (IBS-C): hard or lumpy stool* with at least 25%, and loose or watery stool† with less than 25%, of bowel
movements‡
2 IBS with diarrhea (IBS-D): loose or watery stool† with at least 25%,and hard or lumpy stool* with less than 25%, of bowel
movements‡
3 Mixed IBS (IBS-M): hard or lumpy stool* with at least 25%, and loose or watery stool† with at least 25%, of bowel movements‡
4 Unsubtyped IBS: insufficient abnormality of stool consistency to meet criteria for IBS-C, -D, or -M‡

*
Bristol Stool Form Scale 1–2
†
Bristol Stool Form Scale 6–7
‡
In the absence of antidiarrheals or laxatives

Adapted from Longstreth et al8

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Table 3
Rome III Diagnostic Criteria for Functional Dyspepsia
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Symptom onset greater than 6 months prior to the diagnosis, with the following criteria fulfilled for the past 3 months:
• No structural disease by upper endoscopy to explain the symptoms
• At least one of the following symptoms:
a. Bothersome postprandial fullness
b. Early satiation
c. Epigastric pain
d. Epigastric burning

Postprandial Distress Syndrome

At least one of the following:
• Bothersome postprandial fullness after ordinary sized meals occurring at least several times a week
• Early satiation that prevents finishing a regular meal at least several times a week

Epigastric Pain Syndrome

Must include all of the following:
• Epigastric pain or burning at least once a week
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• Intermittent pain
• Not generalized or localized to other abdominal or chest regions
• Not relieved by defecation or passage of flatus
• Not related to gallbladder or sphincter of Oddi disorders

Adapted from Tack et al34

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Table 4
Rome III Diagnostic Criteria for Functional Constipation
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Symptom onset more than 6 months prior to the diagnosis, with the following criteria fulfilled for the past 3 months:
• Loose stools rarely present without the use of laxatives
• Insufficient criteria met to establish a diagnosis of irritable bowel syndrome
• Two or more of the following criteria must be met:
a. Less than three bowel movements per week
b. Manual maneuvers necessary to facilitate defecation more than 25% of the time.
c. Hard or lumpy stools more than 25% of the time
d. Sensation of incomplete evacuation more than 25% of the time
e. Sensation of anorectal obstruction more than 25%of the time
f. Straining with defecation more than 25% of the time.

Adapted from Longstreth et al8

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Table 5
Functional Anorectal Disorders
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Functional fecal incontinence

Functional anorectal pain
• Chronic proctalgia
a. Levator ani syndrome
b. Unspecified functional anorectal pain
• Proctalgia fugax

Functional defecation disorders

• Dyssynergic defecation
• Inadequate defecatory propulsion

Adapted from Bharucha et al53

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Table 6
Rome III Diagnostic Criteria for Functional Fecal Incontinence
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Recurrent uncontrolled passage of fecal material in a patient at least 4 years of age and more than one of the following:
• Abnormal functioning of normally innervated and structurally intact muscles
• Minor abnormalities of sphincter structure and/or innervation
• Normal or disordered bowel habits: fecal retention or diarrhea
• Psychological causes

Symptoms must persist for over 3 months

Exclusion of all of the following:
• Abnormal innervation caused by lesion(s) within the brain (eg, dementia), spinal cord or sacral nerve roots or mixed lesions (eg,
multiple sclerosis), or generalized peripheral or autonomic neuropathy (eg, diabetes)
• Anal sphincter abnormalities associated with a multisystem disease (eg, scleroderma)
• Structural or neurogenic abnormalities believed to be the primary cause of fecal incontinence

Adapted from Bharucha et al53

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Table 7
Rome III Diagnostic Criteria for Chronic Proctalgia
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Symptom onset more than 6 months prior to the diagnosis, with all of the following criteria fulfilled for the past 3 months:
• Chronic or recurrent rectal pain or aching
• Episode lasting for longer than 20 minutes
• Exclusion of other causes of rectal pain, including ischemia, inflammatory bowel disease, cryptitis, intramuscular abscess and
fissure, hemorrhoids, prostatitis, and coccygodynia

Levator Ani Syndrome

Fulfilled criteria for chronic proctalgia and tenderness during posterior traction on the puborectalis
Unspecified Functional Anorectal Pain
Fulfilled criteria for chronic proctalgia but no tenderness during posterior traction on the puborectalis

Adapted from Bharucha et al53

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Table 8
Rome III Diagnostic Criteria for Proctalgia Fugax
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Must include all of the following criteria:

• Recurrent anal or lower rectum pain episodes
• Episodes last from seconds to minutes
• No anorectal pain between episodes

For research purposes: criteria must be fulfilled for 3 months

Clinical practice: diagnosis and evaluation may be made before 3 months

Adapted from Longstreth et al8

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Table 9
Rome III Diagnostic Criteria for Functional Defecation Disorders
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Symptom onset more than 6 months prior to the diagnosis, with all of the following criteria fulfilled for the past 3 months:
• Diagnostic criteria for functional constipation fulfilled
• Must have at least two of the following:
a. Evidence of impaired evacuation based on balloon expulsion test or imaging
b. Inappropriate contraction of pelvic floor muscles or < 20% relaxation of basal resting sphincter pressure by manometry,
imaging, or electromyography
c. Inadequate propulsive forces assessed by manometry or imaging

Dyssynergic Defecation
Inappropriate contraction of the pelvic floor or less than 20% relaxation of basal resting sphincter pressure with adequate propulsive forces
during attempted defecation
Inadequate Defecatory Propulsion
Inadequate propulsive forces or less than 20% relaxation of the anal sphincter during attempted defecation.

Adapted from Bharucha et al53

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