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Peripheral [[Nociceptor|nociceptors]] become more sensitive, which increases the amount of impulses that reach the [[Dorsal horn|spinal dorsal horn]]. [[Nociplastic pain|Central sensitization]] may result from an increase in the frequency and amplitude of peripheral signals that reach the [[Dorsal horn|spinal dorsal horn]]. An increase in presynaptic [[glutamate]] release causes [[Nociplastic pain|central sensitization]] by removing the [[magnesium]] ion block of the [[N-Methyl-D-aspartic acid|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 activation of other important enzymes.<ref name="Mechanisms and management" />
Peripheral [[Nociceptor|nociceptors]] become more sensitive, which increases the amount of impulses that reach the [[Dorsal horn|spinal dorsal horn]]. [[Nociplastic pain|Central sensitization]] may result from an increase in the frequency and amplitude of peripheral signals that reach the [[Dorsal horn|spinal dorsal horn]]. An increase in presynaptic [[glutamate]] release causes [[Nociplastic pain|central sensitization]] by removing the [[magnesium]] ion block of the [[N-Methyl-D-aspartic acid|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 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 [[Dorsal horn|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">{{cite journal | last=Wilder-Smith | first=C H | title=Brain functional magnetic resonance imaging of rectal pain and activation of endogenous inhibitory mechanisms in irritable bowel syndrome patient subgroups and healthy controls | journal=Gut | publisher=BMJ | volume=53 | issue=11 | date=2004-11-01 | issn=0017-5749 | doi=10.1136/gut.2003.028514 | pages=1595–1601}}</ref>

== Diagnosis ==
Since pain is the primary symptom of chronic functional abdominal pain, obtaining a complete medical history and conducting a comprehensive physical examination continue to be essential components of the diagnosing process.<ref name="Geriatric Gastroenterology">{{cite book | last=Drossman | first=Douglas A. | last2=Deutsch | first2=Jill K. | title=Geriatric Gastroenterology | chapter=Functional Abdominal Pain | publisher=Springer International Publishing | publication-place=Cham | date=2020 | isbn=978-3-319-90761-1 | doi=10.1007/978-3-319-90761-1_99-1 | page=1–12}}</ref> The chronic functional abdominal pain 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 chronic functional abdominal pain, 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 (symptom)|anorexia]]). If the physical examination yields negative results, no more diagnostic testing is necessary.<ref name="Current Gastroenterology">{{cite journal | last=Grover | first=Madhusudan | last2=Drossman | first2=Douglas A. | title=Functional Abdominal Pain | journal=Current Gastroenterology Reports | volume=12 | issue=5 | date=2010 | issn=1522-8037 | doi=10.1007/s11894-010-0125-0 | pages=391–398}}</ref>

The [[Rome process|Rome IV]] diagnostic criteria for chronic functional abdominal pain is as follows:<ref name="Rome">{{cite web | title=Rome IV Criteria | website=Rome Foundation | date=2023-03-06 | url=https://theromefoundation.org/rome-iv/rome-iv-criteria/ | access-date=2024-04-09}}</ref>

# Constant or almost constant [[abdominal pain]].<ref name="Rome"/>
# There is either no correlation or a very weak one between pain and physiological processes (e.g., eating, feces or [[Menstruation|menses]]).<ref name="Rome"/>{{efn|Some degree of gastrointestinal dysfunction may be present}}
# Some aspects of daily functioning are limited by pain.<ref name="Rome"/>{{efn|Daily function could include impairments in work, intimacy, social/leisure, family life, and caregiving for self or others}}
# Pain is not feigned.<ref name="Rome"/>
# No other medical illness or structural or functional gastrointestinal issue may account for the pain.<ref name="Rome"/>

To fit the [[Rome process|Rome IV]] diagnostic criteria for chronic functional abdominal pain 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 chronic functional abdominal pain, a number of other [[Functional gastrointestinal disorder|functional GI illnesses]] should be taken into account initially. [[Irritable bowel syndrome|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 gall bladder disease.<ref name="Current Gastroenterology" />

== Notes ==
{{notelist}}


== References ==
== References ==

Revision as of 23:48, 9 April 2024

Functional abdominal pain syndrome
Other namesCentrally mediated abdominal pain syndrome, functional abdominal pain syndrome
SpecialtyGastroenterology

Chronic functional abdominal pain (CFAP), centrally mediated abdominal pain syndrome (CMAP) or functional abdominal pain syndrome (FAPS) 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 chronic functional abdominal pain from other functional gastrointestinal illnesses, such as irritable bowel syndrome (IBS) and functional dyspepsia.[1]

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

Signs and symptoms

Chronic functional abdominal pain is characterized by frequent or chronic stomach pain and a reduction in everyday activity.[2] The pain is persistent, near-constant, or regularly reoccurring. The pain is not related to food intake or defecation.[1] Functional abdominal pain is usually periumbilical and is not accompanied by weight loss, vomiting, diarrhea, nocturnal symptoms, or slowed growth.[3] Typically, the level of abdominal pain in chronic functional abdominal pain seldom varies, with maximum pain being felt the majority of the time. Chronic functional abdominal pain 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.[1]

Causes

Chronic functional abdominal pain is a functional gastrointestinal disorder.[4] 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.[5]

Mechanism

The pain from chronic functional abdominal pain 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.[2]

Peripheral sensitization, also known as elevated ascending visceral afferent signaling, can happen following GI tract inflammation or damage.[6] For example, about one-third of individuals with IBS report that their symptoms started after an acute infection episode; this is a phenomena known as postinfectious IBS (PI-IBS).[7] PI-IBS has consistently been linked to the existence of a low-grade inflammatory infiltrate.[8] 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.[2] 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.[8] 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.[2]

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 activation of other important enzymes.[2]

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.[2] 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.[9]

Diagnosis

Since pain is the primary symptom of chronic functional abdominal pain, obtaining a complete medical history and conducting a comprehensive physical examination continue to be essential components of the diagnosing process.[10] The chronic functional abdominal pain 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.[2]

In a patient with chronic functional abdominal pain, 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.[2]

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.[11]

The Rome IV diagnostic criteria for chronic functional abdominal pain is as follows:[12]

  1. Constant or almost constant abdominal pain.[12]
  2. There is either no correlation or a very weak one between pain and physiological processes (e.g., eating, feces or menses).[12][a]
  3. Some aspects of daily functioning are limited by pain.[12][b]
  4. Pain is not feigned.[12]
  5. No other medical illness or structural or functional gastrointestinal issue may account for the pain.[12]

To fit the Rome IV diagnostic criteria for chronic functional abdominal pain 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.[12]

When diagnosing chronic functional abdominal pain, 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 gall bladder disease.[11]

Notes

  1. ^ Some degree of gastrointestinal dysfunction may be present
  2. ^ Daily function could include impairments in work, intimacy, social/leisure, family life, and caregiving for self or others

References

  1. ^ a b c Clouse, Ray E.; Mayer, Emeran A.; Aziz, Qasim; Drossman, Douglas A.; Dumitrascu, Dan L.; Mönnikes, Hubert; Naliboff, Bruce D. (2006). "Functional Abdominal Pain Syndrome". Gastroenterology. 130 (5). Elsevier BV: 1492–1497. doi:10.1053/j.gastro.2005.11.062. ISSN 0016-5085.
  2. ^ a b c d e f g h Farmer, Adam D; Aziz, Qasim (2014). "Mechanisms and management of functional abdominal pain". Journal of the Royal Society of Medicine. 107 (9). SAGE Publications: 347–354. doi:10.1177/0141076814540880. ISSN 0141-0768.
  3. ^ Sood, Manu R.; Kovacic, Katja (2017). "Functional Abdominal Pain". Pediatric Neurogastroenterology. Cham: Springer International Publishing. p. 411–422. doi:10.1007/978-3-319-43268-7_38. ISBN 978-3-319-43266-3.
  4. ^ Sperber, A. D.; Drossman, D. A. (2011). "Review article: the functional abdominal pain syndrome". Alimentary Pharmacology & Therapeutics. 33 (5): 514–524. doi:10.1111/j.1365-2036.2010.04561.x. ISSN 0269-2813.
  5. ^ Riddle, Mark S.; Shlim, David R.; Connor, Bradley A. (2019). "Persistent Gastrointestinal Symptoms in the Ill-Returning Traveler". Travel Medicine. Elsevier. p. 213–224. doi:10.1016/b978-0-323-54696-6.00021-5.
  6. ^ Aziz, Q.; Furlong, P.L.; Barlow, J.; Hobson, A.; Alani, S.; Bancewicz, J.; Ribbands, M.; Harding, G.F.A.; Thompson, D.G. (1995). "Topographic mapping of cortical potentials evoked by distension of the human proximal and distal oesophagus". Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section. 96 (3). Elsevier BV: 219–228. doi:10.1016/0168-5597(94)00297-r. ISSN 0168-5597.
  7. ^ Spiller, Robin; Lam, Ching (2012-07-31). "An Update on Post-infectious Irritable Bowel Syndrome: Role of Genetics, Immune Activation, Serotonin and Altered Microbiome". Journal of Neurogastroenterology and Motility. 18 (3). The Korean Society of Neurogastroenterology and Motility: 258–268. doi:10.5056/jnm.2012.18.3.258. ISSN 2093-0879.
  8. ^ a b Gwee, Kok-Ann (2001). "Postinfectious irritable bowel syndrome". Current Treatment Options in Gastroenterology. 4 (4). Springer Science and Business Media LLC: 287–291. doi:10.1007/s11938-001-0053-z. ISSN 1092-8472.
  9. ^ Wilder-Smith, C H (2004-11-01). "Brain functional magnetic resonance imaging of rectal pain and activation of endogenous inhibitory mechanisms in irritable bowel syndrome patient subgroups and healthy controls". Gut. 53 (11). BMJ: 1595–1601. doi:10.1136/gut.2003.028514. ISSN 0017-5749.
  10. ^ Drossman, Douglas A.; Deutsch, Jill K. (2020). "Functional Abdominal Pain". Geriatric Gastroenterology. Cham: Springer International Publishing. p. 1–12. doi:10.1007/978-3-319-90761-1_99-1. ISBN 978-3-319-90761-1.
  11. ^ a b Grover, Madhusudan; Drossman, Douglas A. (2010). "Functional Abdominal Pain". Current Gastroenterology Reports. 12 (5): 391–398. doi:10.1007/s11894-010-0125-0. ISSN 1522-8037.
  12. ^ a b c d e f g "Rome IV Criteria". Rome Foundation. 2023-03-06. Retrieved 2024-04-09.

Further reading

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