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Recognizing and Diagnosing
Abdominal Migraines
Debbie M. Popovich, MSN, CPNP, Denise M. Schentrup, DNP, ARNP-BC,
& Allison L. McAlhany, MSN, CPNP
ABSTRACT
Abdominal migraine affects 1% to 4% of children and is a
variant of migraine headaches. Onset is seen most often
between the ages of 7 to 12 years, with girls affected more
often than boys. Presenting symptoms include acute incapacitating non-colicky periumbilical abdominal pain that lasts
for 1 or more hours. Pallor, anorexia, nausea, vomiting,
photophobia, or headache may be associated with the episodes, and a family history of migraine headaches often is
noted. The diagnostic process begins with a thorough history and physical examination and often follows a series
of exclusions or elimination of other organic causes. Limited
research exists regarding treatment options, but they may
include pharmacologic intervention and prevention
based on lifestyle modifications. J Pediatr Health Care.
(2010) 24, 372-377.
KEY WORDS
Abdominal migraine, migraine, abdominal pain, headache,
periumbilical pain, cyclic vomiting syndrome
Abdominal migraine (AM) affects as many as 1% to
4% of all children in the United States (Collins &
Debbie M. Popovich, Assistant Professor, University of Florida
College of Nursing, Gainesville, FL.
Denise M. Schentrup, Clinical Assistant Professor, University of
Florida College of Nursing, Gainesville, FL.
Allison L. McAlhany, Clinical Assistant Professor, University of
Florida College of Nursing, Gainesville, FL.
Conflicts of interest: None to report.
Correspondence: Debbie M. Popovich, MSN, CPNP, University of
Florida College of Nursing, PO Box 100197, Gainesville, FL 32610;
e-mail: [email protected].
0891-5245/$36.00
Copyright Q 2010 by the National Association of Pediatric
Nurse Practitioners. Published by Elsevier Inc. All rights
reserved.
doi:10.1016/j.pedhc.2009.11.003
372
Volume 24 Number 6
Thomas, 2007; Rasquin et al., 2006). However, it often
is overlooked as children are tested by any number of
specialists for a multitude of organic conditions before
the correct diagnosis is made. To some extent, the inability of many children to adequately describe their
pain experience may hinder efforts at diagnosis, and
migraine experts, usually neurologists, do not often
see children presenting with AMs (Russell, Abu-Arafeh,
& Symon, 2002). Nurse practitioners and pediatricians
are more familiar with this syndrome but may lack
knowledge about recently published criteria to aid in
diagnosing it.
Diagnostic criteria for AM was added to the International Headache Society’s International Classification
of Headache Disorders-II (ICHD-II) as recently as 2004
(Box 1) and to the Rome III Pediatric Criteria for
Functional Gastrointestinal Disorders (FGIDs) in 2006
(Box 2) (Rasquin et al., 2006). The two criteria differ in
the number of episodes required for diAM is characterized
agnosis. The Rome III
by acute,
criteria suggest the diparoxysmal
agnosis after two
episodes, whereas the
episodes of
ICHD-II requires five
abdominal pain
episodes for a diagnofollowed by intense
sis of AM. Fortunately,
use of either of these
periumbilical pain.
criteria to aid in diagnosis may considerably shorten what has been a typically
protracted evaluation process.
In simplest terms, AM is characterized by acute, paroxysmal episodes of abdominal pain followed by
intense periumbilical pain. Typically there is no accompanying headache with the abdominal symptoms. The
condition is more prevalent in girls than in boys (3:2).
The mean age of onset is 7 years, with a peak at 10 to
12 years of age for both sexes (Rasquin et al., 2006). Occasionally, it may persist into adulthood, although this
is quite uncommon. Dignan and colleagues (2001)
Journal of Pediatric Health Care
BOX 1. Diagnostic criteria for abdominal
migraine as established by the International
Headache Society and reported by the
International Classification of Headache
Disorders II, 2004
Definition
An idiopathic recurrent disorder occurring primarily in
children and characterized by episodic midline abdominal
pain manifesting in attacks normality between episode
intensity and associated with vasomotor symptoms,
nausea, and vomiting.
Criteria
A. At least five attacks fulfilling criteria B-D
B. Attacks of abdominal pain lasting 1 to 72 hours
C. Abdominal pain has all the following characteristics:
1. Midline location, periumbilical or poorly localized
2. Dull or ‘‘just sore’’ quality
3. Moderate to severe intensity
D. During abdominal pain, at least 2 of the following:
1. Anorexia
2. Nausea
3. Vomiting
4. Pallor
E. Not attributed to another disorder; history and physical
examination findings do not suggest gastrointestinal or
renal disease, or such disease has been ruled out by
appropriate investigations
found that AM did persist into the late teens in 38% of
their 54 cases.
SYMPTOMATOLOGY
AM symptoms are characterized by acute episodic, midline periumbilical abdominal pain that is dull in nature,
lasting for several hours to days, and associated with
flushing, pallor, anorexia, nausea, vomiting, and photophobia (Lewis, 2009). Symptoms recur at least twice
a year, and the child is typically pain free in between
episodes. A family history of migraine headaches is
common. In a prospective study, researchers reviewed
150 case histories of AM over a 10-year period. A family
history of cephalic migraines in first-degree relatives
was identified in 90% of cases (Bentley, Kehely, AlBayaty, & Michie, 1995). A clinical retrospective survey
of 5848 pediatric ambulatory patients revealed that 65%
of cases with AM/cyclical vomiting had a family history
of migraine (Al-Twaijri & Shevell, 2002). In a 2005 study,
Stickler (2005) also reported that mothers and grandmothers of patients with AM were twice as likely to
experience migraines when compared with a control
group with no migraine history.
Brams introduced the term abdominal migraine
nearly a century ago, in 1922. He believed the condition
was under-diagnosed by gastroenterologists and neurologists. The onset of abdominal pain was described
www.jpedhc.org
BOX 2. Rome III diagnostic criteria* for
abdominal migraine
For a diagnosis of abdominal migraine, all of the following
must apply:
1. Paroxysmal episodes of intense, acute periumbilical
pain that lasts for 1 hour or more
2. Intervening periods of usual health lasting weeks to
months
3. Pain interferes with normal activities
4. Pain is associated with two or more 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
patient’s symptoms
*Criteria fulfilled two or more times in the preceding 12
months.
as abrupt, recurrent, and persistent for 3 to 4 days and
ending just as abruptly. The interval between attacks
of pain was symptom free (Brams, 1922). Dignan et al.
(2001) thought it was common for pediatric abdominal
pain to give way to migraine headaches. They tracked
54 children with AM into young adulthood and found
that 70% were present or past sufferers of migraine
headaches, compared with only 20% of matched control
subjects. Other researchers suggest that AM, cyclic vomiting syndrome, and migraine headache comprise a continuum of a single disorder and that affected individuals
often progress from one clinical symptom to another
(Abu-Arafeh & Russell, 2002). Cyclic vomiting syndrome
and AM have been used interchangeably, but there are
significant differences to support their separation,
mainly the presence or absence of migraine headache
(Catto-Smith & Ranuh, 2003).
The principle textbook on migraines, The Headaches,
second edition (2000), devoted a chapter on migrainerelated syndromes in children, including AM. Because
of widespread acceptance by health care providers of
AM as a unique diagnostic entity, the Headache Classification Subcommittee of the International Headache Society (2004) included AM in the second edition of their
classification within the group ‘‘Childhood periodic
syndrome precursor of migraine’’ and coded it as 1.3.2.
PATHOPHYSIOLOGY
Several hypotheses have been investigated to determine the pathogenesis and pathophysiology of abdominal migraine pain. Factors include IgE-mediated
diet-induced allergy, gut mucosal immune responses,
phenol sulfotransferase enzyme M and P catabolism
November/December 2010
373
of catecholamines and monoamines, and the permeability of the gut mucosal surface (Bentley et al.,
1995). Weydert, Ball, and Davis (2003) discussed the relationship between the gut and the central nervous system (CNS). Derived from the same embryologic tissues,
the enteric nervous system and CNS have direct effects
on each other. These investigators proposed that stress
increases CNS arousal, during which neuropeptides
and neurotransmitters are released. This situation, in
turn, leads to dysregulation of the gastrointestinal system. While the consistent symptom is episodic abdominal pain with clear-cut symptom-free intervals, the
pathophysiology of pain is beyond the scope of this
discussion.
CASE STUDY
A 15-year-old girl presented as a new patient with intermittent episodes of abdominal pain and vomiting since
infancy, occurring up to four times per month. Symptoms included non-radiating abdominal pain and vomiting. Pain was not relieved with bowel movements or
position change and continued for 24 hours. There
were no identified triggers, and headache was denied.
No other associated symptoms were reported. Previous
evaluations included a complete blood cell count with
differential, a complete metabolic panel , erythrocyte
sedimentation rate, urinalysis, urine culture, serum human chorionic gonadotropin, thyroid studies, serum
amino and urine organic acids, lipase, amylase, toxicology, and hemoglobin electrophoresis; all results were
normal. Findings of an abdominal x-ray, abdominal/renal ultrasound, and upper gastrointestinal study with
small bowel follow-through also were normal. Past
medications included Zofran (ondansetron) and Phenergan (promethazine) without improvement. Fioricet,
prescribed for the mother’s migraine headaches, was
marginally effective. Nonpharmacologic treatment failures included dietary restrictions and stress reduction
strategies. There is a reported history of migraine headache in the patient’s mother. Her examination was
within normal limits in all systems. The child’s history
and symptoms met ICHD-II criteria for AM. Successful
treatment included administration of prophylactic tricyclic antidepressants. Follow-up evaluation revealed
a marked reduction in episodes of abdominal pain.
other causes of intermittent severe abdominal pain
should be considered and systematically excluded. In
contrast to acute and chronic abdominal pain, an
explanation for recurrent abdominal pain is seldom
found (Russell et al.,
2002). It is estimated that
Ultimately,
only 5% to 10% of children
diagnosis is
with recurrent abdominal
based on the
pain have an underlying
organic process that conmedical history,
tributes to their pain (Weyabsence of
dert et al., 2003).
abnormality, and
The health care provider
must conduct a thorough
fulfillment of
physical examination and
recognized
obtain the health history
criteria.
of the child and his or her
family.
Collins
and
Thomas (2007) identified ‘‘red flag’’ signs and symptoms
suggestive of organic diseases (Box 3), which suggest
a higher likelihood of pathology requiring subspecialty
referral and possible endoscopy. Catto-Smith and Ranuh
(2003) recommended initial diagnostic studies (Box 4),
and Diamond (2002) advocated for the consistent inclusion of appendicitis, volvulus, bowel malrotation, and
posterior fossa tumors as part of the AM differential diagnosis. Ultimately, diagnosis is based on the medical history, absence of abnormality, and fulfillment of
recognized criteria.
MANAGEMENT
Treatment and management of AM in children should be
kept simple and are determined by the severity, frequency, and impact on the daily life of the child and
BOX 3. Red flags suggesting further workup
needed
Unexplained subjective and objective findings including:
d
d
d
d
d
DIAGNOSIS
When accompanied by a history of migraine headaches,
the diagnosis of AM is straightforward (Collins &
Thomas, 2007). AM is excluded, however, if any of the
following are present: mild symptoms not interfering
with daily activities; burning pain; non-midline abdominal pain; symptoms consistent with food allergy or
other gastrointestinal disease; attacks lasting less than
1 hour; or persistence of symptoms between attacks
(Lewis, Yonker, Winner, & Sowell, 2005). In all other
cases, the diagnosis should remain presumptive, and
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Volume 24 Number 6
d
d
d
d
d
d
d
d
d
d
Change in growth patterns includes height and weight
Recurrent unexplained fevers
Pain radiating to the back
Bilious emesis
Visible or occult blood in stool
Chronic diarrhea (lasting >2 weeks and >20 mL/kg per
day)
Mouth ulcers
Dysphagia
Rashes with no identifiable cause
Nighttime symptoms
Arthritis
Anemia
Pale mucus membranes
Delayed puberty
Family history of inflammatory bowel disease
Journal of Pediatric Health Care
BOX 4. Initial diagnostic studies for
consideration in children presenting with
possible cyclic vomiting syndrome or
abdominal migraine
Blood studies
d Hemoglobin, white count and differential
d C-reactive protein
d Electrolytes, creatinine and glucose
d Liver function tests
d Pancreatic enzymes
d Pregnancy test
Urine and stool studies
d Urinalysis with microscopy and culture
d Stool occult blood and microscopy
Radiologic studies
d Ultrasound of liver, gall bladder, biliary tract, pancreas,
adrenal glands, and kidneys
d Upper GI series
d Magnetic resonance imaging or CT of brain
Endoscopy
d Esophagogastroduodenoscopy
d Colonoscopy
with ileoscopy (to exclude Crohn’s
disease)
Data from Pareek, Fleisher, & Abell, 2007.
his or her family. According to recently published
findings, the Franklin (1952) approach remains the
cornerstone for management of AM: explanation, reassurance, search for possible triggers, and behavioral
approaches (Russell, Symon, & Abu-Arafeh, 2007).
Severe and protracted episodes of emesis, however,
may warrant hospitalization and require intravenous
fluids to counteract dehydration.
NONPHARMACOLOGIC THERAPY
Because minimal data are available regarding AM
treatment, Lewis et al. (2005), Russell et al. (2002), and
Diamond (2002) offered experiential and anecdotal
rather than evidence-based nonpharmacologic recommendations, beginning with family education and avoidance of triggers. Suggested strategies for identified
triggers include the following:
d
d
d
d
d
d
Effective coping strategies to prevent and relieve stress
Bedtime fiber snack to prolong the glycemic effect
and avoid hypoglycemia and related acute morning
attacks
Frequent travel stops to prevent motion sickness
Routine bedtime to prevent altered sleep patterns
Use of a hat or sunglasses to eliminate glare and
diminish bright lights
Use of a diet low in amines, which includes many
food that begin with the letter ‘‘C’’—that is, chocolate,
cocoa, citrus, caffeine (cola, coffee, tea), cheese, and
www.jpedhc.org
d
colorings (in sweets and chewing gum); additives
such as monosodium glutamate (MSG); currants, raisins, and black grapes; and flavorings such as those
in snacks like potato chips
Identifying specific foods by restricting the diet and
gradually re-introducing foods over a 2-week period
PHARMACOLOGIC THERAPY
Abnormal concentrations of vasoactive amines, such as
noradrenaline and serotonin, typically are found in
adults who have migraine headaches. Anti-migraine
drugs are intended to prevent the painful events by interfering with the biochemical pathways. There are no
studies evaluating similar biochemical imbalances in
children with AM; however, pharmacologic management in the treatment of migraine headaches has
proved to be effective in treatment of AM (Tan, Sahami,
Peebles, & Shaw, 2006). Lewis et al. (2005) also
suggested that treatment guidelines for migraine headaches may prove to be efficacious for the management
of AM. In the practice guidelines published in 2004,
Lewis et al. summarized data from numerous studies
that focused on abortive treatment, specifically nasal
sumatriptan, as well as preventive treatment of
migraines in children, noting that similar treatment
has been proven effective in persons with AM.
Catto-Smith and Ranuh (2003) found tricyclic antidepressants to be effective prophylactic agents, and Lewis,
Winner, Hershey, and Wasiewski (2007) also found
propranolol (2 to 4 mg/kg/day) and cyproheptadine
(0.25 to 1.5 mg/kg) to be effective. Lewis (2009) also
noted that cyproheptadine at a starting dose of 2 to
4 mg at bedtime is a simple, effective, and safe strategy
for children younger than 10 years who are not overweight. Lewis (2007) incorporates the work of a number
of other researchers (Ahonen, Hamalainen, Rantala, &
Hoppu, 2004; Major, Grubisa, & Thie, 2003; Uberall,
2001; Winner et al., 2000) when he states the following:
The agents studied most rigorously for the acute
treatment of migraine [headache] are ibuprofen
(10 mg/kg/dose), acetaminophen (10-15 mg/kg/
dose) for children under 12 years of age, and sumatriptan nasal spray, all of which have shown
safety and efficacy in controlled trials (2007,
p. 50).
Although none of the selective serotonin receptor
agonists or triptans have been approved by the Food
and Drug Administration for use with children and adolescents, multiple studies have demonstrated their
safety for children’s use (Major et al., 2003). Thus far,
only sumatriptan in the nasal spray form, 5 and
20 mg, has demonstrated efficacy in adolescents (Ahonen et al., 2004; Lewis et al., 2004; Uberall, 2001; Winner
et al., 2000).
In their review of the literature for pediatric migraines, Shah and Kalra (2009) observed that oral
November/December 2010
375
formulations of selective serotonin receptor agonists
were not beneficial in children. Zolmitriptan nasal spray
(2.5 to 5 mg), demonstrated efficacy when evaluated in
12-to 17-year-old children (Lewis et al., 2007). Lewis and
colleagues’ practice parameters (2004) addressed the
limitations of pharmacologic agents, reporting inconclusive data regarding preventive treatment of migraine
headaches. They concluded that further research is warranted before specific pharmacologic agents can be
suggested. (An up-to-date reference list for AM is available online at the Web site for the Cyclic Vomiting
Syndrome Association: www.cvsaonline.org).
NURSING PRACTICE IMPLICATIONS
Initial consideration of the diagnosis of AM is
warranted if a child presents with intermittent severe
abdominal pain without an identifiable cause. Symptom-free periods between episodes are essential to
the diagnosis. A thorough history and physical examination is essential to rule out any physical causes of
pain. The diagnosis should be made after other organic causes are ruled out. Initial episodes may mimic
appendicitis or obstruction, and often an ab.use of the
dominal scan is needed
Rome III and
to rule out acute proICHD-II criteria to
cesses. The provider
should encourage the
aid in diagnosis
caregiver to document
may
the frequency of epiconsiderably
sodes, precipitating factors,
and
treatment
shorten what has
interventions. A symptom
been a typically
diary can identify triggers
protracted
and effective treatment
strategies. Pharmacologic
evaluation
and non-pharmacologic
process.
measures
should
be
attempted, and caregivers
should be educated about the potential adverse effects of pharmacologic treatment. The goal of therapy
is to abort episodes quickly to prevent interference
with daily activities. Referrals to neurology and psychology specialists may be necessary for alternative
treatments such as biofeedback if interventions are
not successful.
CONCLUSION
AM, along with organic causes, must be considered in
any child presenting with severe episodic abdominal
pain, with or without headache. A thorough history
and physical is essential for making the diagnosis, and
use of the Rome III and ICHD-II criteria to aid in diagnosis may considerably shorten what has been a typically
protracted evaluation process. Caregiver education
about management of symptoms is also essential, and
treatment should be individualized, because patient
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Volume 24 Number 6
responses to treatment will vary. Pharmacologic
treatment is currently limited but has been implemented in children who do not respond to nonpharmacologic therapy and whose symptoms have
a negative impact on daily activities. The overall
goal of treatment is to limit occurrence of episodes
and thus improve quality of life for children and adolescents who have this disorder.
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CONTACT INFORMATION:
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