Functional abdominal pain syndrome

Template:Infobox medical condition (new) Functional abdominal pain syndrome (FAPS), chronic functional abdominal pain (CFAP), or centrally mediated abdominal pain syndrome (CMAP) is a pain syndrome of the abdomen, that has been present for at least six months, is not well connected to gastrointestinal function, and is accompanied by some loss of everyday activities. The discomfort is persistent, near-constant, or regularly reoccurring. The absence of symptom association with food intake or defecation distinguishes functional abdominal pain syndrome from other functional gastrointestinal illnesses, such as irritable bowel syndrome (IBS) and functional dyspepsia.<ref name="Functional Abdominal Pain Syndrome">Template:Cite journal</ref>

Functional abdominal pain syndrome is a functional gastrointestinal disorder meaning that it is not associated with any organic or structural pathology. Theories on the mechanisms behind functional abdominal pain syndrome include changes in descending modulation, central sensitization of the spinal dorsal horn, peripheral enhancement of the visceral pain afferent signal, and, central amplification.

The diagnosis of functional abdominal pain syndrome is made based on clinical features and diagnostic criteria. A thorough clinical history must be taken to accurately diagnose functional abdominal pain syndrome. Diagnostic testing to rule out organic disorders should only be done when alarm features are present. Differential diagnosis of functional abdominal pain syndrome includes a variety of other functional gastrointestinal disorders.

There is no well-established treatment for functional abdominal pain syndrome. General measures such as a positive physician-patient relationship are beneficial. Antidepressants are often used to treat other functional gastrointestinal disorders and may be helpful in treating functional abdominal pain syndrome. Psychological interventions including various forms of therapy can also be helpful. While the exact presence of functional abdominal pain syndrome is unknown studies show that it affects between 0.5% and 2% of North Americans. Functional abdominal pain syndrome is more common in women than men and usually occurs in the fourth decade of life.

Signs and symptoms

Functional abdominal pain syndrome is characterized by frequent or chronic stomach pain and a reduction in everyday activity.<ref name="Mechanisms and management">Template:Cite journal</ref> The pain is persistent, near-constant, or regularly reoccurring. The pain is not related to food intake or defecation.<ref name="Functional Abdominal Pain Syndrome"/> Functional abdominal pain is usually periumbilical and is not accompanied by weight loss, vomiting, diarrhea, nocturnal symptoms, or slowed growth.<ref name="Pediatric Neurogastroenterology">Template:Cite book</ref> Typically, the level of abdominal pain in functional abdominal pain syndrome seldom varies, with maximum pain being felt the majority of the time. functional abdominal pain syndrome is frequently coupled with a proclivity to experience and report additional somatic symptoms of discomfort, such as chronic pain believed to be connected to the gynecological or urinary systems.<ref name="Functional Abdominal Pain Syndrome"/>

Causes

Functional abdominal pain syndrome is a functional gastrointestinal disorder.<ref name="Review article">Template:Cite journal</ref> Functional gastrointestinal disorders (FGD) are common medical conditions characterized by recurrent and persistent gastrointestinal symptoms caused by improper functioning of the enteric system in the absence of any identifiable organic or structural pathology, such as ulcers, inflammation, tumors or masses.<ref name="Riddle Shlim Connor 2019 pp. 213–224">Template:Cite book</ref>

Mechanism

The pain from functional abdominal pain syndrome is thought to be caused by changes in descending modulation, central sensitization of the spinal dorsal horn, peripheral enhancement of the visceral pain afferent signal, and, lastly, central amplification.<ref name="Mechanisms and management"/>

Peripheral sensitization, also known as elevated ascending visceral afferent signalling, can happen following GI tract inflammation or damage.<ref name="Topographic mapping">Template:Cite journal</ref> For example, about one-third of individuals with IBS report that their symptoms started after an acute infection episode; this is a phenomenon known as postinfectious IBS (PI-IBS).<ref name="Post-infectious">Template:Cite journal</ref> PI-IBS has consistently been linked to the existence of a low-grade inflammatory infiltrate.<ref name="Postinfectious">Template:Cite journal</ref> According to theory, this inflammatory infiltration results in increased sensitivity and field of peripheral receptors, the latter of which causes hyperalgesia by recruiting and activating nociceptors that were previously silent.<ref name="Mechanisms and management" /> Furthermore, it was discovered that the best indicators of who would develop PI-IBS were stress, as measured by traumatic life events, and a neurotic personality features.<ref name="Postinfectious"/> These convergent lines of data support the hypothesis that inflammation and/or injury in a psychologically predisposed person may cause visceral afferents to become peripherally sensitized, increasing the amount of nociceptive information that ascends to the spinal dorsal horn.<ref name="Mechanisms and management" />

Peripheral nociceptors become more sensitive, which increases the amount of impulses that reach the spinal dorsal horn. Central sensitization may result from an increase in the frequency and amplitude of peripheral signals that reach the spinal dorsal horn. An increase in presynaptic glutamate release causes central sensitization by removing the magnesium ion block of the N-methyl-d-aspartate (NMDA) receptor. The end result is an overall increase in dorsal horn neuron responsiveness, which frequently lasts longer than the initial shock when combined with the activation of other important enzymes.<ref name="Mechanisms and management" />

The anterior cingulate cortex is home to the majority of the central descending modulatory systems. These modulatory systems allow afferent signals from the periphery to be gated, which allows for the amplification or even restriction of the signal. They interface with the spinal dorsal horn.<ref name="Mechanisms and management" /> The pro-nociceptive condition that characterizes many chronic visceral pain syndromes is thought to be mostly caused by anomalies in the descending pain modulatory system.<ref name="functional magnetic resonance">Template:Cite journal</ref>

Diagnosis

Since pain is the primary symptom of functional abdominal pain syndrome, obtaining a complete medical history and conducting a comprehensive physical examination continue to be essential components of the diagnosing process.<ref name="Geriatric Gastroenterology">Template:Cite book</ref> The functional abdominal pain syndrome patient should be asked to provide a thorough history that thoroughly examines the timeline of pain occurrences, especially in connection with surgery, infection, or traumatic life events.<ref name="Mechanisms and management" />

In a patient with functional abdominal pain syndrome, the clinical examination should be normal by definition. Nonetheless, as a starting point, it is important to look closely for the existence of abdominal scars from prior operations or investigations. Similarly, Carnett's sign, which involves palpating a sore spot both before and after the patient tenses their abdominal wall, could be helpful.<ref name="Mechanisms and management" />

Diagnostic testing to rule out organic disease should not be done frequently in the absence of alarm signs, similar to other functional GI problems (ie, unexplained weight loss, bloody bowel movements, abdominal mass, anorexia). If the physical examination yields negative results, no more diagnostic testing is necessary.<ref name="Current Gastroenterology">Template:Cite journal</ref>

The Rome IV diagnostic criteria for functional abdominal pain syndrome is as follows:<ref name="Rome">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

1. Constant or almost constant abdominal pain.<ref name="Rome"/>
2. There is either no correlation or a very weak one between pain and physiological processes (e.g., eating, feces or menses).<ref name="Rome"/>Template:Efn
3. Some aspects of daily functioning are limited by pain.<ref name="Rome"/>Template:Efn
4. Pain is not feigned.<ref name="Rome"/>
5. No other medical illness or structural or functional gastrointestinal issue may account for the pain.<ref name="Rome"/>

To fit the Rome IV diagnostic criteria for functional abdominal pain syndrome the patient must fit all of the above criteria and the criteria must be met over the past three months, with the onset of symptoms occurring at least six months before diagnosis.<ref name="Rome"/>

When diagnosing functional abdominal pain syndrome, a number of other functional GI illnesses should be taken into account initially. IBS may be taken into consideration if the pain is accompanied by changes in bowel motions (frequent, loose stools or harder, infrequent stools). Functional gall bladder disease or sphincter of Oddi dysfunction should be considered if the pain is significant, occurs at different intervals (not daily), and is located in the right upper quadrant or epigastrium. Consider functional dyspepsia if the discomfort is in the epigastrium and does not meet the criteria for functional gallbladder disease.<ref name="Current Gastroenterology" />

Treatment

There is no definite agreement on how to best manage functional abdominal pain syndrome in adults. As a result, the majority of currently employed therapies are founded on data and firsthand knowledge from other functional bowel diseases and chronic pain syndromes. It is helpful to categorize therapy modalities into three groups: psychological interventions, pharmaceutical therapies, and general measures.<ref name="Mechanisms and management" />

The doctor-patient interaction is essential to the management of a patient with functional abdominal pain syndrome and to a successful outcome. A crucial component of treatment is, in particular, validating a patient's symptoms in a caring, interdisciplinary setting. In the framework of routine outpatient reviews, the patient and the doctor should also decide on and establish realistic treatment goals.<ref name="Mechanisms and management" />

Antidepressants, especially low-dose tricyclic antidepressants (TCAs), have been shown to be beneficial in the treatment of functional gastrointestinal disorders and chronic pain.<ref name="Jackson O'Malley Tomkins Balden 2000 pp. 65–72">Template:Cite journal</ref> They may also be helpful in the treatment of functional abdominal pain syndrome due to their dual effects of direct pain management and antidepressant properties.<ref name="Functional Abdominal Pain Syndrome" />

Trials utilizing tricyclic antidepressants have generally outperformed those using selective serotonin-reuptake inhibitors in other chronic pain disorders.<ref name="Fishbain Cutler Rosomoff Rosomoff 1998 pp. 503–509">Template:Cite journal</ref> Venlafaxine and duloxetine are two examples of more recent medications with combined serotonin and norepinephrine reuptake inhibitors (SNRIs), which have been shown to reduce pain in some somatic pain disorders and may be helpful in functional abdominal pain syndrome.<ref name="Briley 2004 pp. S21–S25">Template:Cite journal</ref> Patients with co-occurring anxiety and depression may benefit from both SNRIs and selective serotonin-reuptake inhibitors (SSRIs). The majority of analgesics, such as aspirin and nonsteroidal anti-inflammatory medications, don't really help much, maybe because they mostly have peripheral effects.<ref name="Functional Abdominal Pain Syndrome" /> Because of the risk of addiction and narcotic bowel syndrome, narcotic analgesics should be avoided.<ref name="SANDGREN 1984 p. 331">Template:Cite journal</ref>

There hasn't been a study explicitly looking at adult functional abdominal pain syndrome and psychological therapy. Studies on non-gastrointestinal pain diseases and other painful functional gastrointestinal illnesses, however, point to the potential benefit of psychological therapies.<ref name="Functional Abdominal Pain Syndrome" /> Stress management, hypnosis,<ref name="Whorwell Prior Colgan 1987 pp. 423–425">Template:Cite journal</ref> dynamic or interpersonal psychotherapy,<ref name="Creed Fernandes Guthrie Palmer 2003 pp. 303–317">Template:Cite journal</ref><ref name="Guthrie Creed Dawson Tomenson 1993 pp. 315–321">Template:Cite journal</ref> and cognitive behavioral therapy are among the interventions that may prove advantageous.<ref name="CBT">Template:Cite journal</ref><ref name="Keefe Dunsmore Burnett 1992 pp. 528–536">Template:Cite journal</ref> The most effective way to manage impairment resulting from refractory chronic pain may be to refer patients to pain treatment clinics for multidisciplinary treatment programs.<ref name="Kames Rapkin Naliboff Afifi 1990 pp. 41–46">Template:Cite journal</ref> While the previously discussed psychological treatments have demonstrated improvements in mood, coping, quality of life, and health care costs, their effect on specific visceral or somatic symptoms is less clear, indicating that their most effective application may be in conjunction with symptomatic treatment.<ref name="CBT"/><ref name="Heymann-Monnikes Arnold Florin Herda 2000 pp. 981–994">Template:Cite journal</ref>

Epidemiology

Due to a lack of data and methodological challenges in distinguishing functional abdominal pain syndrome from other more prevalent functional gastrointestinal diseases like IBS and functional dyspepsia, the epidemiology of the disease is not fully understood. Nonetheless, compared to functional dyspepsia or IBS, functional abdominal pain syndrome is generally thought to be a less frequent.<ref name="Functional Abdominal Pain Syndrome" /> The stated prevalence rates in North America are between 0.5% and 2%, and they are consistent with reports from other nations.<ref name="Koloski Talley Boyce 2002 pp. 2290–2299">Template:Cite journal</ref><ref name="KWAN BAO CHAKKAPHAK CHANG 2003 pp. 796–802">Template:Cite journal</ref><ref name="Thompson 2000 pp. 78–82">Template:Cite journal</ref> The condition affects women more frequently than men (3:2), with a peak in prevalence occurring in the fourth decade of life.<ref name="Drossman Li Andruzzi Temple 1993 pp. 1569–1580">Template:Cite journal</ref><ref name="Bharucha Camilleri 2001 pp. 517–529">Template:Cite journal</ref>

Further reading

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External links

• Yale Medicine
• The Children's Hospital of Philadelphia