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performed. The attacks can be so severe that they might interfere with everyday
activities and impair school performance of affected children, decreasing their quality of life [5].
Although the presence of this condition has been acknowledged since the early
1900s, the initial denition as a separate condition appeared in the ICHD second
edition in 2004 under the “Childhood Periodic Syndromes” section, as a precursor
of migraine headache [6, 7], followed by the Rome Classication of Functional
Gastrointestinal Disorders in 2006 [8]. The prevalence in school-aged children
(3–15 years old) is estimated between 1% and 4.5%, with a predominance of
females (3/2 female/male) [9], while the exact prevalence in adulthood remains
scarce [4].
There is a handful of extensive research about abdominal migraine and a signicant gap of knowledge regarding the pathophysiology, epidemiology, pathogenesis,
and management, which limits awareness and recognition of this condition [7]. In
this chapter, AM will be reviewed comprehensively in separate subsections in the
light of the latest scientic literature to emphasize this important but underdiagnosed condition.
7.2 Pathophysiology
Multiple hypotheses have been proposed to explain the pathophysiology of AM, but
none have been conclusively proven.
Most comprehensive explanation for functional gastrointestinal disorders
(FGIDs), emphasizes the strong connection between the enteric and central nervous
systems (CNS), which share a common embryonic origin. Individuals with FGIDs
have an increased sensitivity to nociceptive stimuli, inuenced by genetic, environmental, and psychosocial factors like early-life stressors, leading to visceral
hyperalgesia.
Proposed mechanisms for visceral hyperalgesia include increased sensitivity of
primary sensory and central spinal neurons, impaired inhibitory pain control, and a
dysfunctional stress response. These disruptions affect the gut–brain axis, resulting
in abnormal secretion of excitatory neurotransmitters such as serotonin, a key regulator of gastrointestinal (GI) motility, secretion, and sensation. The continuous communication between the brain and gut through neural and hormonal pathways may
contribute to changes in the CNS, causing symptoms like headaches. Additionally,
autonomic nervous system stimulation and heightened sympathetic activity may
explain associated symptoms like pallor.
Advanced imaging techniques, including functional MRI (magnetic resonance
imaging), have revealed abnormalities in visceral pain processing pathways in
FGID patients. Although the visceral hyperalgesia theory has not been specically
validated in abdominal migraine (AM) patients, it remains the most well-supported
explanation for FGIDs [10].
7 Episodic Syndromes That May BeAssociated withMigraine: Abdominal Migraine
63
Abnormal gut motility is another potential factor in the pathophysiology of
AM.It is thought that gastrointestinal distension and irregular contractions could
lead to functional abdominal pain, increasing the sensitivity to pain (hyperalgesia).
A study conducted in Sri Lanka between 2007 and 2012 assessed gastric motility
in 17 children with AM (ages 4–12) and compared them to healthy controls. The
ndings revealed signicantly slower gastric emptying rates and reduced antral
motility in the children with AM.Furthermore, a slower gastric emptying rate was
linked to longer pain episodes, while weaker antral contractions correlated with
more severe symptoms. These results suggest that disruptions in gastric motility
might contribute to the onset and progression of AM [10].
Patients with AM may experience altered gut permeability, as mucosal permeability serves as an indirect indicator of overall gut health. A 1995 study by Bentley
etal. examined gut mucosal permeability in 11 children diagnosed with AM, comparing them to healthy controls. The results showed a signicant increase in gut
permeability among AM patients.
Longitudinal follow-ups of three patients over 3years, with assessments conducted three times annually, revealed a correlation between permeability changes
and symptom severity. As symptoms improved, gut permeability decreased, and
vice versa. This observation may help explain why non-steroidal anti-inammatory
drugs (NSAIDs) are ineffective in AM management, as these drugs are known to
increase mucosal permeability.
Despite these ndings, no further research has been conducted to conrm this
hypothesis or explore its clinical relevance in treating AM.Additionally, this study
was conducted before formal diagnostic criteria for AM were established [11].
Dietary inuences may play a role in the development and severity of AM symptoms. Studies on cephalic migraines have shown a notably higher prevalence among
individuals with atopy and other allergic conditions, suggesting a possible link
between dietary allergens and migraine episodes. Similarly, in AM, specic food
allergens may trigger an immune response in the gut, leading to inammation and
symptom manifestation in predisposed individuals.
This theory is reinforced by the observation that some AM patients experience
symptom relief when following an oligoantigenic diet, which removes common
dietary triggers. The diet’s effectiveness suggests that food sensitivities or immunemediated reactions might contribute to AM.
While this connection is promising, further research is necessary to better understand the role of diet in AM and to develop targeted dietary interventions for affected
individuals [11–13].
In 1995, Bentley et al. studied IgE levels and positive radioallergosorbent
(RAST) test results in 14 patients with AM and a group of healthy individuals. Their
ndings showed no signicant differences in IgE levels or RAST test results
between the two groups. Additionally, skin prick tests did not identify any dietary
allergens in patients with AM.This suggests that AM may mainly cause a localized
immune response in the gut rather than affecting the whole immune system.
Laboratory studies have shown that enterocytes (intestinal cells) can express
Major Histocompatibility Complex (MHC) class II antigens and release certain
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chemical signals, which stimulate immune cells in the gut lining when exposed to
dietary antigens. More recent research highlights the mucosal immune system as a
key regulator of the gut–brain axis. Both the adaptive immune system (especially
T-cells) and the innate immune system (such as mucosal lymphoid cells, mast cells,
and mononuclear phagocytic cells) help maintain gut–brain balance. When this balance is disrupted, it has been linked to functional gastrointestinal disorders (FGIDs).
A similar immune system dysfunction is also involved in cephalic migraines.
Further studies on immune system changes in AM patients could help improve
understanding of the condition and lead to better treatment options [14–16].
Disruptions in neurotransmitter metabolism, resulting in an imbalance between
excitatory and inhibitory amino acids, have been widely investigated in cephalic
migraine. A comparable process may contribute to the development of AM [17, 18].
In the central nervous system (CNS), glutamic acid and aspartic acid act as key
excitatory neurotransmitters, while gamma-aminobutyric acid (GABA) plays a
major role as an inhibitory neurotransmitter.
Phenol sulfotransferase (PST) enzymes (S and P) are essential for metabolizing
catecholamines and other amine neurotransmitters. Studies indicate that individuals
with diet-induced migraines have signicantly reduced PST enzyme activity. This
decline results in the accumulation of inammatory neuropeptides and neurotransmitters, disrupting the balance between excitatory and inhibitory signals and affecting brain circuits associated with dopamine, serotonin, and norepinephrine. CNS
hyperexcitability is considered a crucial factor in cephalic migraine.
A range of factors—including genetic predisposition, environmental inuences,
dietary triggers, and psychosocial stress—can activate the trigeminovascular system, leading to the release of inammatory neuropeptides and neurotransmitters
like calcitonin gene-related peptide (CGRP), substance P, serotonin, and nitric
oxide, all of which contribute to migraine development. A similar mechanism
involving heightened excitatory amino acid activity may also play a role in AM.This
could potentially explain the effectiveness of certain treatments, such as valproate,
which enhances GABA levels in AM patients [19–21].
In 1995, Bentley etal. reviewed the platelet expression of the two PST isoenzymes (S and P) in 21 patients with AM, comparing them to normal subjects. No
signicant change in enzyme activity was noted between the two groups. However,
the level of enzyme activity in platelets might not accurately reect the levels in the
enteric nervous system. Further studies are needed to conrm this hypothesis [14].
7.2.1 Genetic andPsychosocial Factors inAMPathogenesis
Genetic mutations and polymorphisms, though not yet fully understood, play a role
in regulating ion channels, neurotransmitter metabolism, and mitochondrial function in the central nervous system (CNS), contributing to the development of
migraine headaches. There is also strong evidence suggesting a genetic predisposition to functional abdominal pain. A 2017 study indicated that Y2 receptor
7 Episodic Syndromes That May BeAssociated withMigraine: Abdominal Migraine
65
antagonism and YY gene deletion might be associated with visceral hypersensitivity. The link between genetics and AM is further supported by the fact that many
patients have a family history of migraines or chronic abdominal pain. However,
more research is needed to identify the specic genetic factors involved.
Psychosocial factors such as hormonal changes (menstrual cycle and pregnancy),
lifestyle, diet, anxiety, and chronic stress are known to inuence cephalic migraines.
Similarly, stress and anxiety have been associated with functional gastrointestinal
disorders (FGIDs). While the role of these factors in AM is not yet fully understood,
future research may provide more insights into their impact [22].
Other theories about the causes of FGIDs and cephalic migraine suggest that factors such as autonomic instability, problems with the hypothalamus–pituitary axis,
changes in the gut microbiome, small intestinal bacterial overgrowth, previous
infections with long-term effects, lactose intolerance, and abnormal mitochondrial
function may play a role. More research is needed to fully understand how these
factors contribute to cephalic migraine [22].
7.3 Case Presentation
A 9-year-old girl was referred to our pediatric clinic with a 6-month history of
recurrent severe abdominal pain. The pain was midline and periumbilical inlocation, described as dull and moderate-to-severe in intensity, lasting 8–12h per episode. Attacks occurred approximately twice monthly, often disrupting school
attendance.
Associated symptoms included nausea, reduced appetite, and noticeable pallor
during episodes. No headaches occurred during these attacks. Between episodes,
she was completely asymptomatic and had normal growth and development.
Her medical history was unremarkable. Family history revealed that her mother
had migraine without aura. Physical examination was normal.
Extensive investigations were performed by her primary physician before referral, including complete blood count, inammatory markers, celiac serology, liver
and renal function tests, abdominal ultrasound, and urinalysis—all of which
were normal.
Given the clinical history and symptom pattern, abdominal migraine was considered. The diagnosis was conrmed based on ICHD-3 criteria: ≥5 attacks of midline
abdominal pain lasting 2–72h with associated vasomotor symptoms and complete
return to baseline between attacks.
Management included education about the diagnosis, lifestyle modications
(regular meals and sleep hygiene), and identication of potential triggers (caffeinecontaining soft drinks and skipped meals). Due to attack frequency and severity,
prophylactic therapy with cyproheptadine was initiated at 0.25mg/kg/day. At follow- up after 3months, the patient reported a marked reduction in attack frequency
(one mild episode) and severity, with no signicant side effects from treatment.
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7.4 Clinical Characteristics andDiagnosis
Diagnosing abdominal migraine is challenging, as recurrent abdominal pain is common in childhood and can be caused by various systemic diseases, including gastrointestinal system disorders [23]. A correct clinical diagnosis is essential for
preventing patients from excess and unnecessary diagnostic interventions and treatments hence a detailed differential diagnosis is needed [4].
Currently, two separate sets of diagnostic criteria are proposed for AM: the
International Classication of Headache Disorders third edition (ICHD-3) criteria
[1] and the Rome Foundation, Rome-IV Functional GI Disorders criteria [24, 25].
Although both set of diagnostic criteria share some common points in terms of
abdominal pain and associated symptoms, there are certain variations regarding the
details.
Both criteria accept AM as a childhood disorder, and it is widely accepted that
AM resolves over time as the patient reaches adulthood and evolves into migraine
thus might be accepted as “a migraine precursor of childhood” [4, 26]. Contrary to
this belief, cases regarding patients with AM of adulthood are increasingly being
reported although the exact prevalence is still not known due to the lack of extensive
research and the under-recognition of this condition in adulthood [4].
According to the ICHD-3 criteria, AM is classied under the heading of “1.6
Episodic syndromes that may be associated with migraine” as a subheading with the
code 1.6.1.2 [1]. The main properties of AM are listed as, an idiopathic disorder
with recurrent attacks of moderate-to-severe abdominal pain coexisting with vasomotor symptoms, nausea, and vomiting that lasts for 2–72h. The patient should be
asymptomatic and completely normal between the episodes [1]. As a rule, headache
should not exist during these episodes.
The Rome-IV criteria have been published in 2016 [25] and has similar points to
that of ICHD-3 criteria [4]. The criteria can be summarized as follows: paroxysmal
episodes of intense periumbilical, midline, or diffuse abdominal pain lasting equal
to or more than 1h. Abdominal pain is very severe and interferes with normal everyday activities and these symptoms are not related with another medical condition.
There are some associated symptoms such as anorexia, nausea, vomiting, headache,
photophobia, or pallor. At least two of these symptoms should accompany to
abdominal pain and a minimum of two episodes in 6months are mandatory for
exact diagnosis [24].
The major differences between these two sets of criteria are in terms of pain
duration and the number of episodes to conrm the diagnosis. In addition, the obligatory “lack of headaches during the episodes” in ICHD-3 [4] is another important point.
These main differences can be summarized as follows:
1. Pain duration should be between 2 and 72h in ICHD-3 criteria whereas it was
stated as 1h or more in Rome-IV criteria.
2. Five attacks are mandatory for diagnosis in ICHD-3 whereas 2 episodes are
enough in Rome-IV criteria.
7 Episodic Syndromes That May BeAssociated withMigraine: Abdominal Migraine
67
3. Headache was dened as an associated symptom in Rome-IV whereas lack of
headache is obligatory for diagnosis in ICHD-3.
4. At least 6months of period is needed for diagnosis in Rome-IV but in ICHD-3
no time period was reported.
5. Gastrointestinal and renal diseases should be ruled out for diagnosis in ICHD-3
criteria but in Rome-IV it was reported as “other medical conditions” that should
be ruled out.
The nal diagnosis is made clinically and there are no certain biomarkers or
symptoms that point out to an exact diagnosis of AM in a child/adolescent. A
detailed anamnesis and a thorough systemic and neurological examination are the
hallmarks of diagnosis along with necessary diagnostic interventions. The questioning of dietary habits, the history of medical and neurological conditions, and triggers of the abdominal pain is essential. The most common triggers of AM are light
(bright or ickering), lack of sleep/poor sleep, fasting, traveling, stressful life events,
and certain dietary habits (citrus food, caffeine, cheese, chocolate, carbonated
drinks, colorings, and avorings) [5]. Once identied, avoiding these triggers can be
benecial in order to minimize the attacks [3].
The questioning of pain characterization and associated symptoms is important.
The localization of pain can be either periumbilical (65–80%) or diffuse (16%) and
the pain quality can be dull (60%) or colicky (22%) [9]. Some children can express
behavioral irritability before the attacks as a premonitory symptom [9, 27, 28]. The
average duration of episodes is between 1 and 17h and the patient can experience
2–20 attacks per month [5]. The child should be neurologically normal between the
attacks.
7.5 Differential Diagnosis
It is imperative that a detailed differential diagnosis including evaluation for secondary and treatable causes of recurrent abdominal pain is performed [9]. The following medical conditions should be investigated thoroughly before making AM
diagnosis in a child with recurrent abdominal pain [5].
• Gastrointestinal disorders (pancreatitis, small bowel obstruction, pseudo-
obstruction), acid peptic disease (esophagitis, gastritis, peptic ulcer disease),
eosinophilic diseases (esophagitis, gastritis, enteropathy), celiac disease, gall
bladder disease (choledochal cyst, cholelithiasis, cholecystitis), inammatory
bowel disease, pancreatitis, other functional abdominal pain disorders (func-
tional dyspepsia, irritable bowel syndrome, cyclic vomiting syndrome [CVS],
functional abdominal pain), lactose intolerance, chronic hepatitis
• Surgical causes (hernia, appendicitis, intussusception)
• Renal disorders (obstructive uropathy, urinary tract infections, nephrolithia-
sis, etc.)
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A. C. Atalar et al.
• Central nervous system disorders (intracranial hypertension, posterior fossa dis-
orders, hematoma or familial dysautonomia, cerebral venous sinüs thrombosis,
epilepsy)
• Endocrine disorders (diabetes, adrenal insufciency)
• Metabolic diseases (methylmalonic acidemia, acute intermittent porphyria, orni-
thine transcarbamylase deciency, lead poisoning, etc.)
The following investigations/interventions can be helpful to rule out the possible
alternative diagnoses when evaluating a patient with recurrent abdominal pain:
• Routine blood examinations (full blood count, erythrocyte sedimentation rate
[ESR], C-reactive protein [CRP], electrolytes, urea and creatinine, glucose lev-
els), liver and renal function tests, celiac antibodies
• Pregnancy test
• Urine and stool studies (microscopy, culture, and sensitivity, stool occult blood
and microscopy, etc.)
• Radiological studies (abdominal X-ray, pelvis and abdominal ultrasound
investigations)
• Brain magnetic resonance imaging
• Contrast study of upper gastrointestinal tract and small bowel
• Endoscopic interventions (esophagogastroduodenoscopy, colonoscopy, etc.) [5]
Cyclic vomiting syndrome (CVS) is another important migraine equivalent in
children, which can easily be confused with AM and should be differentiated. It is
characterized by episodic attacks of intense nausea and vomiting (at least ve
attacks), with predictably cyclical timing of episodes (periodic), and the child is
completely normal between attacks [1]. The major difference between these two
syndromes is that vomiting is the hallmark symptom in CVS but is less prominent
in AM.Vomiting is most intense at the start of the episode especially within the rst
hour, and gradually decreases at the following 4–8h [9]. CVS is a benign disorder
and can sometimes overlap with AM.
AM is often seen as an early indicator of cephalic migraine, even though most
patients eventually outgrow the condition. Main outcomes of a study by Dignan
etal. focused on whether abdominal migraine persisted or resolved and whether
participants had a past or present history of migraine headaches, based on
International Headache Society (IHS) criteria. Results showed that 31 cases (61%)
experienced a complete resolution of abdominal migraine. However, 70% of those
previously diagnosed with abdominal migraine had either current (52%) or past
(18%) migraines that met IHS criteria, compared to only 20% of the control
group [29].
However, 70% of these individuals later developed migraines, with or without
aura, compared to just 20% in the control group [30]. While AM can occasionally
persist into adulthood, further longitudinal research is necessary to better understand its long-term prognosis and progression from childhood into adulthood.
7 Episodic Syndromes That May BeAssociated withMigraine: Abdominal Migraine
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7.6 Management ofAbdominal Migraine
Different strategies may be used to treat abdominal migraine but double-blind,
placebo- controlled trials are still inadequate. Treatment of abdominal migraine is
very similar to all pediatric migraine patient prole although there are some details
to give attention to [31].
Management of abdominal migraine focuses on acute symptom relief, prophylaxis, lifestyle modications, and patient education. Before trying pharmacological
agents, it is very important to take developmental growth status, lifestyle characteristics, school work scheme, and accompanying activities into consideration [32].
7.7 The Following Strategies Are Essential
7.7.1 Acute Symptom Relief
Before pharmacological methods, ensuring adequate hydration and allowing the
patient to rest in a quiet, dark environment may help reduce symptom severity.
7.7.1.1 Pharmacological Treatment
First-line medications used in acute attacks include paracetamol/acetaminophen
(10–15mg/kg/dosage) and non-steroidal anti-inammatory drugs (NSAIDs), such
as ibuprofen (7.5–10mg/kg/dosage) for pain relief. In cases with nausea and vomiting, antiemetics (e.g., ondansetron) can be benecial but it is better to use them as
additives to other acute medications [33].
Triptans are being more widely used in all migraine patients as published data
increase our experience. Though primarily used for classic migraines, triptans (such
as sumatriptan) may help alleviate abdominal migraine episodes, especially in older
children and adults. Four important agents—Almotriptan (ages 12–17), Rizatriptan
(ages 6–17), Zolmitriptan nasal spray (ages 12–17), and Sumatriptan/Naproxen
combination (ages 12–17)—are available for pediatric age groups [34].
A 5HT-1F agonist Lasmiditan is a relatively new molecule with triptan-like
effect by decreasing Calcitonin Gene Releasing Peptide (CGRP) release from presynaptic vesicles [35].
Although there is limited knowledge about CGRP antagonists such as rimegepant, ubrogepant, and zavegepant among pediatric population, they may take part in
future treatment strategies of abdominal migraine.
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7.7.2 Prophylaxis ofAbdominal Migraine
For patients experiencing frequent or severe abdominal migraine episodes, prophylactic treatment is necessary to reduce occurrence and intensity. During deciding
pharmacological prophylaxis, it is also important to make lifestyle modications
such as:
Dietary Adjustments: Identifying and avoiding trigger foods (e.g., chocolate, caf-
feine, processed meats) can help prevent recurrent episodes [32]. There are also
some oral nutraceuticals such as Riboavin (50–400 mg/day), Vitamin D,
Magnesium (up to 9mg/kg/day as magnesium oxide), which are well tolerated
and shorten attacks and reduce symptom severity [36].
Regular Sleep Patterns: Establishing a consistent sleep schedule and ensuring suf-
cient rest play a crucial role in preventing migraine attacks. Melatonin (0.3mg/
kg) may be used to regulate sleep patterns.
Mind–body therapies such as cognitive-behavioral therapy (CBT), mindfulness
(MDT), and biofeedback (BFB) help patients cope with stressors that may trigger
migraine episodes. Published data suggest that they have minimal side effects in
adult patients but pediatric group data are still missing [31]. These methods can be
benecial in children and adolescents to help control physiological responses associated with migraines. Stress management techniques such as cognitive-behavioral
therapy (CBT), meditation, and relaxation exercises can be benecial in reducing
attack frequency [32].
Non-invasive neuromodulation techniques are non-invasive vagal nerve stimulator (nVNS), transcranial magnetic stimulator (TMS), remote electrical neuromodulation (REN), transcutaneous supraorbital electrostimulation, and external
trigeminal nerve stimulator (eTNS). Transcranial direct current stimulation (tDCS)
is also another inexpensive and portable method that shows some benecial effect
among adults. REN has FDA approval above 12years of age and eTNS has approval
above 8years of age, but there are no published data of these non-invasive methods
in abdominal migraine cohort.
7.7.2.1 Pharmacologic Prophylaxis
Classical and approved drugs for pediatric migraine can also be used for abdominal
migraine prophylaxis. Beta-blockers (propranolol, 2–4mg/kg/day) have been commonly used since many years but sometimes they are ineffective among severe
recurrent attacks [31].
Antiepileptic drugs, especially topiramate (1–10mg/kg/day) and valproic acid
(20–40mg/kg/day), have been found effective in preventing attacks. Tricyclic antidepressants, especially Amitriptyline, have shown efcacy in reducing the frequency of attacks, particularly in patients with comorbid anxiety or depression but
usually less preferred in pediatric age group.
7 Episodic Syndromes That May BeAssociated withMigraine: Abdominal Migraine
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Calcium channel blockers such as Verapamil are another option that may
help in preventing episodes. Serotonin modulators such as Cyproheptadine, an
antihistamine with serotonin-blocking properties, are particularly effective in
children [33].
CGRP monoclonal antibodies such as Erenumab, Fremenazumab, and
Galcanezumab are promising subcutaneous agents for migraine prophylaxis. An
intravenous CGRP monoclonal antibody eptinezumab is another potential agent for
pediatric age group although their placebo-controlled clinical trials have not been
concluded yet [36].
7.8 Conclusion
Abdominal migraine is a debilitating condition of both children and adults that
requires a comprehensive management approach. Since differential diagnosis is
based on clinical ndings and there is no biomarker or neuroimaging clue, it is very
important to consider a wide range of both gastrointestinal and pain syndromes
especially in pediatric age group. Treatment of this relatively rare condition resembles migraine treatment approach, including acute symptom relief and lifestyle
modications and prophylaxis. While pharmacologic interventions such as NSAIDs,
triptans, and antiemetics provide symptomatic relief, prophylactic treatments play a
crucial role in long-term management. Also, CGRP monoclonal antibodies are
promising relatively new agents in this particular syndrome. Additionally, nonpharmacologic approaches such as cognitive-behavioral therapy, stress management, and dietary modications signicantly contribute to reducing episode
frequency. Early diagnosis, patient education, and individualized treatment plans
are essential to improving quality of life for individuals suffering from abdominal
migraine. Ongoing research is necessary to further understand its pathophysiology
and develop more targeted treatment modalities.
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