Pediatric Abdominal Migraine

By Douglas Mendez, MD, MSc. *

The term abdominal migraine was first used by William A. Brams, MD in 1922 to describe functional epigastralgia that occurs in patients at periodic intervals. He also noted that there was a strong association of the condition with migraine. Most patients had migraine themselves or had a family history of migraine. Abdominal migraine (AM) is one of the most common causes of functional abdominal pain in children and is currently recognized as a type of pediatric migraine variant. Despite the presence of well-defined diagnostic criteria, AM is still a lesser known entity and is underdiagnosed by both general pediatricians and pediatric gastroenterologists.1-4 Since most of the literature pertaining to AM comes from Europe and UK, this inadequate awareness about AM among clinicians in USA may lead to underdiagnosis of the condition4-15.

A Chronic and recurrent abdominal pain is a very distressing symptom that causes significant morbidity in affected children impairing their school performance and overall quality of life5-6.  Chronic abdominal pain in childhood accounts for 2% to 4% of office visits to primary care clinicians and about half of  the referrals to pediatric gastroenterologists.2 It also utilizes a lot of health resources with frequent emergency room visits, hospitalizations, and expensive laboratory and imaging services.  More awareness about the essential clinical characteristics of the disease would improve diagnostic accuracy and optimal utilization of health resources and also improve long-term outcomes in affected children.

Chronic abdominal pain occurs in 11% to15% of children and adolescents6-16 The overall prevalence of AM is around 1% to 9%.  And is most commonly seen in children aged 4 to 15 years of age. With an average age of diagnosis of 3 to 10 year. The peak incidence is at 7 years. Most of the studies have shown a higher prevalence in girls than in boys, similar to other functional gastrointestinal diseases (FGIDs) and cephalic migraine.

The pathophysiology of this functional disorder has not yet been fully described. Several hypotheses have been postulated to explain it, but none have been definitely confirmed.  1- The hypothesis of visceral hyperalgesia is actually the most accepted of all for all functional gastro-intestinal disorders (FGID’s). This theory is based on the strong association between the enteric nervous system and central nervous system (CNS) and their common embryonic origin. Patients with FGIDs have a low threshold for nociceptive stimuli. A variety of ill-defined factors including genetic, environmental and psychosocial (early stressors in life) predispose an individual to visceral hyperalgesia. Postulated mechanisms for visceral hyperalgesia include sensitization of primary sensory neurons and central spinal neurons, altered descending inhibitory control, and impaired stress response. This in turn causes alteration of bowel–gut axis and causes abnormal secretion of excitatory neurotransmitters such as serotonin. Serotonin plays a key role in the regulation of gastrointestinal (GI) motility, secretion, and sensation. The bidirectional communication between the brain–gut neurons through various neural and hormonal circuits may lead to changes in the CNS and cause other associated symptoms such as headache. Stimulation of the autonomic nervous system and sympathetic hyperactivity may account for symptoms such as pallor. Novel imaging techniques such as functional magnetic resonance imaging have shown defective visceral pain processing pathways in patients with FGID. Although, the theory of visceral hyperalgesia has not been specifically proven in patients with AM, it holds the most evidence-based explanation for all FGIDs. 2- Hypothesis: “Altered gut motility”: Patients with AM may have abnormal gut motility. It is postulated that functional abdominal pain results from distension of the GI tract and abnormal contractions which cause hyperalgesia. A study conducted in Sri Lanka from 2007 to 2012 looked at gastric motility parameters in 17 children aged 4–12 years with AM compared to healthy controls, found that gastric emptying rate and antral motility parameters were significantly lower in children with AM. Gastric emptying rate had a significant negative correlation with the average duration of pain episodes. The amplitude of antral contractions negatively correlated with scores obtained for severity of symptoms. These findings suggest a possible role of abnormal gastric motility in the pathogenesis of AM. 3- “Altered gut permeability” (leaked Gut) hypothesis: Gut permeability may be altered in patients with AM. Mucosal permeability is an indirect function of gut health. Bentley et al in 1995 compared the gut mucosal permeability children with diagnosis of AM and healthy controls. They found that gut mucosal permeability was significantly increased in patients with AM when compared to healthy controls.  4- “Diet-induced allergy and altered mucosal immunity hypothesis”: Dietary factors may also contribute to the symptoms of AM. The role of diet in patients with cephalic migraine has been extensively studied. The incidence of cephalic migraine is significantly higher in patients with atopy and other allergic disorders.  In vitro studies have shown that enterocytes can express  Major histocompatibility complex (MHC) class II antigen and secrete specific chemokines to stimulate epithelial lymphocytes and activate immune response under the influence of dietary antigens; more recently, there has been evidence showing that the mucosal immune system is the master regulator of the gut–brain axis.35 The adaptive immune system (T-cells in particular) and the innate immune system (mucosal lymphoid cells, mast cells, and mononuclear phagocytic cells) play a key role in maintaining gut–brain homeostasis and are disrupted in patients with FGIDs. A disrupted immune system is involved in the pathogenesis of cephalic migraine as well. Further research specifically focused on altered immune responses in patients with AM would help in identifying new treatment strategies. 5- “Abnormal neuroregulation hypothesis”: Abnormalities in the metabolism of neurotramitters causing an imbalance between excitatory amino acids and inhibitory amino acids have been well studied in cephalic migraine. A similar mechanism might be involved in the pathogenesis of AM. In the CNS, glutamic acid and aspartic acid are the main excitatory neurotransmitters, whereas gamma aminobutyric acid (GABA) is the inhibitory neurotransmitter. The balance between these two systems regulates the function of other circuits of the brain involving dopamine, serotonin, and norepinephrine. CNS hyper excitability plays a central role in the pathogenesis of cephalic migraine.

Other factors may also play a roll, like: genetic, environmental, dietary, psychosocial stressors; by activating the trigeminal-vascular system and cause the release of inflammatory neuropeptides and neurotransmitters including catecholamine gene-related peptide, substance-P, serotonin, adenosine diphosphate, platelet activating factor, nitric oxide resulting in migraine headache. A similar mechanism involving increased activity of excitatory amino acids might play a role in the pathogenesis of AM. This can explain the possible efficacy of certain medications that increase GABA (valproate) in patients with AM.

Clinical diagnostic: AM is a well-recognized entity with specific diagnostic criteria. Is characterized by paroxysmal episodes of intense periumbilical, midline, or diffuse abdominal pain lasting ≥1 hour3-5-12. Abdominal pain is the most severe and distressing symptom and is incapacitating and interferes with normal activities. After appropriate evaluation, symptoms cannot be fully explained by another medical condition. The pain may be associated with at least two of the following features: anorexia, nausea, vomiting, headache, photophobia, or pallor. Stereotypical pattern and symptoms are seen in the individual patient. At least two episodes in a 6-month period are needed to confirm the diagnosis.

Differential Diagnosis: The paroxysmal nature of the illness, the presence of possible triggers that may include: Exposure to  bright or flickering light, alterations of sleep patterns, Exercise, travel, prolonged fasting, school or family stressors and dietary triggers (Citrus food, Caffeine, Cheese, Carbonated drinks, Coloring and Flavorings) helps in stablishing the diagnostic; but others G.Is. and functional entities should be ruled out, including, but not limited to: Gastrointestinal disorders: Acid peptic disease (esophagitis, gastritis, peptic ulcer disease), Eosinophilic diseases (esophagitis, gastritis, enteropathy), Celiac Disease, Gallbladder disease (choledochal Cyst, chlolithiasis, cholesystitis), Gastroesophageal reflex, Small bowel disorders. Other functional abdominal pain disorders: (functional dyspepsia, irritable bowel syndrome, cyclic vomiting syndrome, other functional abdominal pain, not otherwise specified). Chronic hepatitis, lactose intolerance, surgical causes like hernias, appendicitis and intussusception. Central nervous system disorders, posterior fossa disorders, epilepsy among others.

Management: There is no consensus over if the abdominal migraine should or should not be treated, as children feels well between episodes10-14. The severity, frequency, and morbidity associated with episodes of abdominal migraine must be taken into account. This impose the need for a careful analysis of the potential benefits of different treatment options against the risk of unpleasant side effects and possible harm.  Given the episodic nature of this GI disorder, the likely psychosocial factors involved and the lack of knowledge regarding its pathophysiology, treatment options are divided in Nonpharmacological and Pharmacological alternatives.

Nonpharmacological therapy: Is frequently the first-line of treatment of abdominal migraine. Often a detailed explanation of the disease and its prognosis is all that is required in cases of mild abdominal migraine. In particular, families should be reassured that serious abdominal pathology is absent and that symptoms will likely subside with advancing age. Once children have been reassured and the migrainous nature of the pain has been explained, some may be able to recall triggers for the pain. There is a minimal evidence base for this, but from their experience, Russell et al suggested that triggers may include stress, travel, prolonged fasting, exposure to flickering lights, exercise, and alterations of sleep patterns. Avoidance of known or suspected triggers may improve the frequency or severity of attacks, although there is no enough evidence to support this theory.  Dietary modifications include:  increased fiber, reduced lactose, and a “few foods” diet, each with a paucity of evidence to support them. Feldman et al studied the effect of increasing fiber in the diet of children who had abdominal migraine. They reported a significant benefit of increased fiber in their study of 52 children. The authors concluded that 50% of children in the fiber group had a 50% reduction in the number of episodes of abdominal pain, compared with only 27% in the control group. Historically, a reduced lactose diet has been advocated for the treatment of abdominal migraine. Barr and Liebman, demonstrated that a significant proportion of children with recurrent abdominal migraine had an abnormal lactose tolerance test and showed complete resolution of symptoms with a lactose-free diet. However, these children would not meet the definition criteria for abdominal migraine which excludes organic disease. Russell et al described the “few foods or “oligo-antigenic” diet as a dietary modification the authors applied within their own practice for children with abdominal migraine. The authors listed a number of foods, including chocolate, citrus fruits, caffeine, cheese, and colorings that may trigger abdominal migraine and should thus be avoided. The “few foods” diet treatment requires careful supervision by a dietician and is reserved for those children who have frequent attacks (>2 per week). The child is commenced on a diet consisting of a very small number of foods that do not usually evoke symptoms. The number of foods the child can eat is then increased by one food per week. In an audit of their results for this mode of treatment, the authors reported a successful outcome in 17 of 22 patients with abdominal migraine, although further study is needed.

Of the nonpharmacological treatment options available, psychotherapy, in particular cognitive behavior therapy (CBT) appears to have the most promising outcome. Meta-analysis of well-designed studies has shown psychotherapy to be effective in both children and adults with chronic functional abdominal pain.  In order to carry out psychotherapy effectively, psychoeducation must first be addressed. This includes an introduction to the concept of pain, epidemiology, and natural history of the disease process and coping strategies including stress reduction. Cognitive behavior therapy can then be used with the idea that pain may not be purely caused by nociception but may also be caused by possible secondary gain, including parental attention and time away from school.

Cognitive behavioral therapy versus standard pediatric care was assessed by Sanders et al.  Forty-four children aged 7–14 years who had recurrent abdominal pain were observed. They were randomly assigned to either the cognitive behavior therapy group or the standard pediatric care group. At 6 months, the cognitive behavior therapy group were pain-free in 55.6% and 70% of cases based on diary and parental assessment, respectively. These figures were 58.8% and 82.4% at 12 months. The results in this group were significantly better than in the standard pediatric care group, which showed percentages of children pain-free at 12 months of 36.8% and 42.1% by diary and parental assessment, respectively.

The pharmacological therapy: Drug therapy has often been reserved for patients displaying severe, frequent symptoms or those refractory to nonpharmacological therapy. The criteria for selecting children is poorly defined and may be based more on the viewpoint of the families involved than on any objective measure of severity. The agents available are primarily used due to their proven or presumed activity in migraine headache and for that reason much of the research has been based on serotonin antagonists, beta blockers, or calcium channel inhibitors. The conclusion stated that, in the majority of patients with abdominal migraine, prophylaxis with propranolol is effective. It is believed that this effect is a direct result of its beta blocking action, but the exact mechanism in unknown. Serotonin antagonists such as cyproheptadine and pizotifen have also been studied in the treatment of abdominal migraine. The authors concluded that most patients benefit from prophylactic treatment and that cyproheptadine probably works via its anti-serotonin action. In addition to the beta-blockers and serotonin antagonists discussed above, the calcium channel antagonist, flunarizine, has also been used successfully in the treatment of childhood and adult migraine. Kothare performed a retrospective analysis of all patients seen in a neurology clinic in Bombay, India, the authors concluded that flunarizine is a safe, once-daily option for abdominal migraine prophylaxis. However, they conceded that although its efficacy in this study matches its efficacy in migraine demonstrated in large open US trial, larger studies would need to be conducted to confirm this observation. Other available treatments are valproic acid and sumatriptan which are two of the latest agents studied in relation to abdominal migraine with successful results according to the authors; however, this evidence is limited to small case series containing only two patients each. It is thought that these medications may work due to similarities in the underlying pathophysiology of migraine and abdominal migraine, although firm evidence for the etiology of abdominal migraine is lacking. As with all the above mentioned pharmacological therapies, larger and more robust studies are required before a consensus of opinion can be reached.

The take away of this article is that AM is a functional abdominal pain disorder (FAPD) characterized by paroxysmal episodes of periumbilical pain and other vasomotor or GI symptoms severe enough to interfere with daily activities. It is considered as a precursor of migraine headaches and shares a similar pathophysiology and treatment responses. A comprehensive history, physical examination, appropriate diagnostic tests (only if needed), and use of well-defined guidelines will aid in the timely diagnosis of AM and optimize treatment outcomes. Although precise diagnostic criteria are present, it continues to be an underdiagnosed entity. Increasing awareness among the scientific community combined with more research studies focusing on epidemiology, pathophysiology, effective treatment options, and long-term prognosis would help improve the quality of life of affected children and limit health care utilization.

*Douglas Mendez, MD, MSc.                                                                                                                                                                                  Staff Associate Officer of Research                                                                                                                                                                                                   GH Sergievsky Center & Taub Institute                                                                                                                                                                         Columbia University Irving Medical Center


1 -. Di Lorenzo C, Colletti RB, Lehmann HP, et al. Chronic abdominal pain in children: a technical report of the American Academy of Pediatrics         and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition: AAP Subcommittee and NASPGHAN Committee on Chronic Abdominal Pain. J Pediatr Gastroenterol Nutr. 2005;40(3):249–261. [PubMed] [Google Scholar]

2- Abu-Arafeh I, Russell G. Prevalence and clinical features of abdominal migraine compared with those of migraine headache. Arch Dis Child. 1995;72:413–417.

3-  McFerron BA, Waseem S. Chronic recurrent abdominal pain. Pediatr Rev. 2012;33(11):509–517.[PubMed] [Google Scholar]

4-   Carson L, Lewis D, Tsou M, et al. Abdominal migraine: an under-diagnosed cause of recurrent abdominal pain in children. Headache. 2011;51:707–712.

5-  Feldman W, Rosser W, McGrath P. Recurrent abdominal pain in children. Can Fam Physician. 1988;34:629–630. [PMC free article] [PubMed] [Google Scholar]

6-  Mortimer MJ, Kay J, Jaron A. Clinical epidemiology of childhood abdominal migraine in an urban general practice. Dev Med Child Neurol. 1993;35:243–248.

7-  Drossman DA, Hasler WL. Rome IV – functional GI disorders: disorders of gut-brain interaction. Gastroenterology. 2016;150(6):1257–1261. [PubMed] [Google Scholar]

8-  Cuvellier JC, Lepine A. Childhood periodic syndromes. Pediatr Neurol. 2010;42:1–11.

9-  Napthali K, Koloski N, Talley NJ. Abdominal migraine. Cephalalgia. 2016;36(10):980–986. [PubMed] [Google Scholar]

10- Cullen KJ, MacDonald WB. The periodic syndrome: its nature and prevalence. Med J Aust. 1963;ii:167–173.

11-  Winner P. Abdominal migraine. Semin Pediatr Neuro. 2016;23(1):111–113. [Google Scholar]

12-  Farquhar HG. Abdominal migraine in children. Br Med J. 1956;1: 1082–1085.

13-  Wang SJ. Abdominal migraine. In: Greenamyre JT, editor. MedLink Neurology. San Diego, CA: MedLink Corp; 2013. Online October 8, 2016. [Google Scholar]

14- Olesen J. The International Classification of Headache Disorders, Second Edition. Cephalalgia. 2004;24 Suppl 1:9–160.

15- Carson L, Lewis D, Tsou M, et al. Abdominal migraine: an underdiagnosed cause of recurrent abdominal pain in children. Headache. 2011;51(5):707–712. [PubMed] [Google Scholar]

16- Bufler P, Gross M, Uhlig HH. Recurrent abdominal pain in childhood. Deutsches Arzteblatt International. 2011;108:295–30


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