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Abstract

Background

Abdominal migraine (AM) is a syndrome usually recognised in childhood. The syndrome is characterised by episodic attacks of severe abdominal pain and vasomotor symptoms, nausea and vomiting. It is a poorly understood disorder largely due to a limited recognition of this condition by the medical community. However, the publication of AM diagnostic guidelines by the International Headache Society a decade ago and the recognition of AM in the Rome Classification of functional gastrointestinal disorders have helped to legitimise this disorder and facilitate research.

Overview

AM is relatively common, affecting up to 4% of the paediatric population. Whilst AM is not believed to continue into adulthood for the majority of children, it has the propensity to develop into probable migraine and recurrent abdominal pain in adulthood. The pathophysiology of this condition remains unclear and as a result treatment for this condition is suboptimal with avoidance of triggers and prophylactic treatment currently recommended when an episode begins.

Conclusion

The recognition of AM by the IHS and the Rome Foundation should help facilitate future research into the pathophysiology of this debilitating condition and as a result better treatments for AM should emerge. Randomised controlled trials should be a priority.

Keywords

Abdominal migraine periodic syndrome headache

Introduction

In an editorial in 1991, Axon and colleagues posited the question: ‘Abdominal migraine: Does it exist?’ (1). They concluded that despite the difficulties in identifying objective criteria and the circumstantial evidence available, this is the correct diagnosis for a subset of patients who present with recurrent abdominal pain. Abdominal migraine (AM) is an episodic syndrome usually recognised in childhood, although adult cases are becoming increasingly identified. The syndrome is characterised by episodes of severe abdominal pain and vasomotor symptoms, nausea and vomiting (2,3). It is a poorly understood disorder largely due to a limited recognition of this condition by the medical community. However, the publication of AM diagnostic guidelines by the International Headache Society (IHS) (2) a decade ago and the recognition of AM in the Rome Classification (4) of functional gastrointestinal disorders have helped to legitimise this disorder. While research into AM is limited, the data which are available for the diagnosis, epidemiology, prognosis, pathogenesis and management of AM will be reviewed.

Diagnosis of AM

The term ‘abdominal migraine’ was first coined in 1922 to describe the experience of abdominal pain in the absence of headache (5). However, until relatively recently the existence of AM as a distinct disorder was seriously questioned and AM was often confused with other forms of recurrent abdominal pain (6). In 2004, the IHS published the International Classification of Headache Disorders (ICHD) and included abdominal migraine in section 1.3, childhood periodic syndromes that are commonly precursors to migraine (7). This recognition was based on evidence suggesting that episodic abdominal pain occurring in the absence of headache may be a probable migraine phenomenon.

A number of studies have demonstrated a common co-existence of abdominal pain and migraine headaches (8 –12). One prospective study of 136 children found the co-occurrence of stomach ache and headache increased from 4% of children at 4 years of age to 20% when they reached 10 years of age (10). AM and migraine headaches also share a number of other similarities. Abu-Arafeh and Russell (13) evaluated 1754 Aberdeen school-aged children; AM and migraine headaches had similar demographic characteristics including being more prevalent in girls than boys with both conditions beginning around a mean age of 7 years. Both AM and migraine headaches have been observed to have similar triggering factors including stress, tiredness and travel as well as relieving factors such as resting and eating. A family history of migraine is also common in children experiencing AM and migraine headaches (11). Both conditions are also associated with similar symptoms during attacks including anorexia, nausea, pallor, feeling unwell, limb pain and cyclic vomiting (9,13). Table 1 outlines precipitating factors for attacks of migraine and abdominal migraine from the Aberdeen series (13).

Table 1.

Precipitating factors of attacks of migraine and abdominal migraine (%) (13).

Precipitating factors of attacks of migraine and abdominal migraine (%)
	Migraine (n = 159)	Abdominal migraine (n = 58)
Stress	53 (33)	15 (26)
Tiredness	40 (25)	13 (22)
Travel	32 (20)	9 (16)
Bright light	31 (19)	0
Lack of sleep	30 (18)	3 (1.5)
Certain foods	23 (14)	5 (9)
Hot climate	23 (14)	1 (0.5)
Missing a meal	19 (12)	10 (17)

The ICHD formally defines AM as an idiopathic disorder seen mainly in children as recurrent attacks of moderate to severe midline abdominal pain, associated with vasomotor symptoms, nausea and vomiting, lasting 2–72 hours and with normality between episodes’ (14). These episodes do not involve headache and there are usually prolonged symptom-free periods between episodes. The pain is of moderate to severe intensity and associated with nausea and vomiting. The diagnostic criteria according to the ICHD are listed in Table 2.

Table 2.

International Classification of Headache Disorders (ICHD) diagnostic criteria – abdominal migraine (14).

ICHD diagnostic criteria – abdominal migraine
A. At least five attacks fulfilling criteria B–D
B. Attacks of abdominal pain lasting one to 72 hours (untreated or unsuccessfully treated)
C. Abdominal pain has all of the following characteristics:
1. midline location, periumbilical or poorly localised
2. dull or ‘just sore’ quality
3. moderate or severe intensity
D. During abdominal pain at least two of the following:
1. anorexia
2. nausea
3. vomiting
4. pallor
E. Not attributed to another disorder

AM has also been recognised by the gastroenterology community, and is included in the Rome Criteria for functional gastrointestinal disorders (4). The Rome Criteria specify that childhood AM is a separate nosological entity to chronic abdominal pain of childhood as its clinical presentation, treatment and prognosis is quite distinct to that of AM. The most recent Rome III Criteria for AM are similar to the IHS criteria and are outlined in Table 3.

Table 3.

Rome III Criteria for abdominal migraine.

Rome III Criteria. Abdominal migraine
Diagnostic criteria fulfilled in separate episodes twice within 12 months.
Must include all of the following:
1. Paroxysmal episodes of intense, acute periumbilical pain that lasts for one hour or more
2. Intervening periods of usual health lasting weeks to months
3. The pain interferes with normal activities
4. The pain is associated with two of the following:
a. Anorexia
b. Nausea
c. Vomiting
d. Headache
e. Photophobia
f. Pallor
5. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process considered that explains the subject's symptoms

Criteria fulfilled two or more times in the preceding three months.

Drossman DA, Corazziari E, Delvaux M, et al. Rome III: The functional gastrointestinal disorders. 3rd ed. McLean, VA: Degnon Associates, 2006.

The diagnosis of AM according to IHS or the Rome III Criteria is made only after the exclusion of other causes of periodic abdominal pain, which may include for example inflammatory bowel disease and disaccharide intolerance. Overlap of AM with other specific conditions including cyclic vomiting syndrome (CVS) (15) and irritable bowel syndrome (IBS) (16) has been reported. Helgeland et al. observed that IBS and AM co-exist in 33% of children presenting to paediatric outpatient clinics for recurrent abdominal pain (16) and both conditions are associated with migraine headache (17). However, while both IBS and AM lack accepted objective diagnostic biomarkers and rely on symptom-based diagnostic criteria, the Rome III Criteria for IBS require abdominal pain to be associated with bowel disturbances and requires the occurrence of symptoms for at least three months. AM should also be considered in the differential diagnosis of recurrent abdominal pain in adults, especially if there is a family history of migraine headaches (18). In the absence of any clear data suggesting an alternative case definition, the Rome III classification at present remains suitable.

Epidemiology

Epidemiological data are limited, but the prevalence of AM in the paediatric population has been found to range between 0.4% (19) and 4% (20). In a random population of 2165 Aberdeen school children, a total of 1754 children completed a questionnaire inquiring about symptoms consistent with migraine and AM (13). Of these 1754, 4.1% fulfilled the IHS guidelines for AM (13). The male-to-female ratio in this study was 1:1.6 for AM, with a peak age between 10.3 years and 11.5 years. Almost half of the boys with AM had a first-degree relative with migraine headache compared to 34% of girls (13). A lower prevalence of 1%, however, was reported in another school-based cross-sectional survey from Sri Lanka, although the age of the children in this study was older (between 12 and 16 years) (21).

Mortimer et al. (22) evaluated 1104 children registered with general practice and found the prevalence of AM with and without migrainous headache was 0.7% and 1.7%, respectively. The peak prevalence of AM without migrainous headache was between ages 5 and 7 years for both sexes. Similarly, in a cohort study (19) of 243 African American children with a mean age of 10.7 years visiting a general paediatric clinic for annual school physicals, the numbers of children fulfilling the Rome Criteria for AM were only 0.4% of patients.

Among tertiary centres, the prevalence of AM is higher. In a retrospective chart review of children aged 1 to 21 years referred to an academic paediatric gastroenterology practice with the clinical complaint of recurrent abdominal pain in the United States (US), 4.4% of these children met ICHD second edition (ICHD-2) criteria for AM, although another 11% had features of AM but lacked one of the specific criteria (20). A similar finding was found among 439 consecutive paediatric patients aged 4–18 years referred to the Pediatric Gastroenterology Department at a Medical University in Poland for evaluation of abdominal pain of at least two months' duration (23). They found 5% of children met Rome III criteria for AM. These findings have also been confirmed in a prospective study of 114 new patients presenting to a tertiary care children's medical centre with recurrent abdominal pain where 4.7% of children met Rome criteria for AM (24).

While AM is not traditionally considered a disorder of adulthood, a small cohort study (18) published in 2012 reviewing 13 patients with unexplained abdominal pain found that 10 of the 13 adult patients fulfilled both the ICHD and Rome III Criteria for AM. AM is probably uncommon in adults (25). Blau and MacGregor (26) surveyed 100 adult patients with migraine and found only one patient who had abdominal pains during attacks.

Migraine is associated with other gastrointestinal diseases that may be mislabelled as AM. For example, the prevalence of migraine is increased in coeliac disease (27) and may present with abdominal pain and IBS-like features. CVS is comorbid with migraine and abdominal pain (28).

Prognosis

Several authors have commented on the tendency for AM to transform into migraine headaches as the child matures (25,29,30). Lanzi et al. (30) showed a sequential timing of periodic symptoms with motion-sickness occurring at a mean age of onset of 2 years, followed by cyclic vomiting at age 3 and abdominal pain beginning around age 5 followed by paroxysmal vertigo at 7 years of age (30). These findings lend support for the concept that AM children may be experiencing a prodrome of migraine headache (30).

There are few data on the long-term prognosis of AM, although it is believed that AM does not continue into adulthood for the majority of children. Dignan et al. (25) evaluated 54 patients with a childhood history of AM and found that symptoms had resolved in 61% of cases, although almost one-third of patients experienced pain well into their late teens. A long-term follow-up study (29) followed 300 children with AM for 12 years. Of the 108 followed up, 37 (34%) achieved remission by 10 years, although no further remissions occurred after 18 years of age (29). However, prospective studies on whether children with AM continue to have this syndrome into adulthood are needed.

Pathogenesis

The biochemical and physiologic pathogenesis of AM is at best incompletely understood. A relationship has been established between mitochondrial disease (31), gene mutations and hypothalamic-pituitary-axis dysfunction (32) and other episodic functional gastrointestinal disorders of childhood; however, such associations have not been investigated in patients with a diagnosis of AM.

In childhood migraine, abnormalities have been identified using neurophysiologic testing (33,34). One study found significant differences in the fast wave activity in the visual evoked response to a red and white flash among children with clinically diagnosed AM compared with normal controls (33). Good, in a 1995 study (33), matched 18 children with CVS or AM with groups of children with classic migraine and normal controls (33). The children with migraine, AM and CVS had similar changes in visual evoked responses compared with the normal controls (33). Older children with AM exhibited less evidence of sharp wave activity in the visual evoked responses (33). No studies have been identified on the use of neurophysiologic testing in adults with AM. A combined electrophysiologic approach using measurements of visually provoked beta-activity, high-frequency photic following responses, and visually stimulated event-related potentials have also been found to have a diagnostic specificity for migraine in excess of 90% (33), highlighting the potential usefulness of this approach in the diagnosis of AM, although this needs confirmation.

Genetics play a role in migraine (heritability around 50%) and IBS (heritability 25%) based on twin studies of pain conditions, but whether AM is a genetic syndrome is unknown (35).

Management

There are no published data that provide an evidence base for the management of AM. As with other functional gastrointestinal disorders, the initial approach to management should focus on the exclusion of other abdominal pathology which may be surgical or medical in nature. Children with AM have no impairment of growth or development and are well between attacks. Alarm signs would include weight loss, right iliac fossa pain, poor growth, chronic diarrhoea or haematemesis. Systemic features such as fever or tachycardia would also represent alarm signs and warrant alternate investigations. In the absence of any localising signs, there does not appear to be any clear benefit in the routine use of endoscopy, pH impedance testing or upper abdominal ultrasonography in the assessment of either discrete episodes of abdominal pain or in the investigation of chronic abdominal pain, especially in children (36).

Essentially the approach to the treatment of AM should follow those general principles of acute and prophylactic treatments for childhood migraine but data confirming their effectiveness in AM are lacking.

Avoidance of triggers

Once identified, certain triggers such as bright light, poor sleep, travel and prolonged fasting should probably be avoided or minimised. For some children emotional stressors related to school or family activities may be a trigger and should be reduced or avoided (37). Biofeedback and counselling are thought to offer benefit if emotional stress is a trigger factor in the development of migraine in children (38), although there are no specific randomised trials assessing their effectiveness in AM.

The role of elimination diets is unclear. However, an immunoglobulin G (IgG)-based elimination diet appears promising in reducing migraine episodes in patients with suffering both with migraine and IBS symptoms (39). There is little other evidence that diet strongly influences the onset of migraine in children (40).

Abortive treatment of AM

There is a scarcity of treatment studies for AM and as such many of the recommendations given here have been extracted from existing paediatric migraine data and need to be properly tested in AM before it can be ascertained that they are effective in this disorder. Once AM is established, abortive treatment should commence with simple analgesia – either acetaminophen or a nonsteroidal anti-inflammatory drug (NSAID) such as ibuprofen (41) has been established to be a safe and effective initial intervention in migraine. Ibuprofen can be given at a dose of 10 mg/kg initially, repeated sixth hourly. Similarly, acetaminophen can be given at a dose of 15 mg/kg every six hours.

AM can be associated with nausea and vomiting. As an antiemetic, prochlorperazine and chlorpromazine are infrequently used in children because of the risk of extrapyramidal side effects (42). Nevertheless, a study in Milwaukee, US, (43) that randomised 62 children with paediatric migraine headaches to proclorperazine or ketorolac found that proclorperazine was safe and superior to the (NSAID). There are risks of acute dystonia associated with the use of metoclopramide in children (44). and its routine use is not recommended.

5HT_1a/1d agonists – triptans – have been shown to be effective in acute abortive treatment of migraine but a role in AM is unclear. Nasal sumatriptan is the most widely studied of this class, and nasal sumatriptan has the most consistent results (45). Almotriptan has also recently been studied in adolescents with migraine and shown to be effective (46). There were 866 adolescents included in this study and at two hours pain relief for all doses of almotriptan (66.7% for 25 mg up to 71.8% for 6.25 mg) was significantly higher than placebo (55.3%) (46). Sumatriptan was also observed to be effective in the treatment of AM according to a published case report (47), but no other data are available.

Prophylaxis

The pattern of AM is unpredictable; however, when it occurs, it is disabling for the patient, causing school absenteeism and emotional upset. When the episodes of AM become troublesome, prophylactic treatment is warranted. Treatment approaches include the use of beta blockers, cyproheptadine, tricyclic antidepressants, and there are a few scattered case studies of flunarizine (48).

Cyproheptadine is a serotonin and histamine antagonist and is useful for children younger than 6 years of age. It also has some calcium channel-blocking properties. One study found that of 12 children with AM treated with cyproheptadine, 50% experienced milder and less frequent symptoms (49). In comparison with amitriptyline and propranolol, cyproheptadine is almost as efficacious at a dose of around 0.3 mg/kg/day (49).

Older therapies such as beta blockers are used in paediatric migraine, although the data supporting their benefits are mixed (50). The side effects of beta blockers are well documented, and include depression, orthostatic hypertension and glucose intolerance. Of the very small evidence base for treatment for AM in children, a retrospective case series of 24 patients showed that of those who were treated with propranolol, 75% had an excellent response resulting in the cessation of symptoms (51). Dosage of propranolol for AM in the paediatric population should be no more than 3 mg/kg/day in four divided doses. It is contraindicated in those patients with moderate to severe asthma and should be used with caution in patients with depression.

Flunarizine is a calcium channel-blocking agent which was studied in 10 children with AM, using a mean dose of 7.5 mg/day (48). This study reported a 61% reduction in the frequency of symptoms and 51% reduction in the duration of attacks. The good side effect profile of this calcium channel-blocking agent and single-day dosing make it a viable alternative for the treatment of AM in children.

Pizotifen is one of the few drugs that have been shown to be efficacious in prevention of AM. In a double-blind cross-over trial of 14 children with AM treated with pizotifen and placebo, pizotifen was found to be superior to placebo in the prophylaxis of AM (52). Complete remission of abdominal attacks was also obtained during a four-month treatment period with pizotifen in a 23-year-old woman with late-onset IHS-defined AM but a placebo response cannot be excluded (53).

Conclusion

AM is a poorly understood episodic syndrome of childhood that has the propensity to develop into migrainous headache and recurrent abdominal pain in adulthood. Further studies of the epidemiology, pathogenesis and treatment are needed to better characterise and manage this chronic disorder. The recognition of AM by the IHS and the Rome Foundation should help facilitate future research into the pathophysiology of this debilitating condition, but at present avoidance of triggers and prophylactic treatment is recommended when an episode begins. Prophylactic treatment should be considered when frequency begins to affect school attendance and starts to cause sustained emotional upset.

Clinical implications

Paroxysmal episodes of intense, acute periumbilical pain that lasts for one hour or more.

Intervening periods of usual health lasting weeks to months.

The pain interferes with normal activities.

Footnotes

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

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