Migraine in childhood …

Yasmine Elhefnawy MD FAAP

Headache & Pain

Updated 12.22.2025
Released 07.11.1994
Expires For CME 12.22.2028

Migraine in childhood

Author: Yasmine Elhefnawy MD FAAP

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Editor: Alcy R Torres MD FAAP

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Migraine in childhood

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Introduction

Overview

Childhood migraine is common, affecting 9% to 10% of children. Migraine in children commonly causes bilateral or midfrontal headaches. The peak incidence of migraine in males of all ages is 10 to 14 years, and for females, it is 20 to 24 years. Parents’ biggest concerns regarding the etiology of childhood headaches are brain tumors or vascular problems, particularly aneurysms. However, these concerns are usually unwarranted when the examination is normal, and the headaches are episodic. The CHAMP trial has led some clinicians to question the utility of pharmacological treatment for migraine. However, many pharmacological approaches are still warranted. Newer targeted medications include antagonists to calcitonin-gene-related peptides, which are gaining interest in the pediatric population. The benefits of a healthy lifestyle and nonpharmacologic treatments to prevent acute migraine and to forestall chronic migraine remain the mainstay of management. Some neuromodulation devices are approved in children and adolescents with migraines, but potential barriers to access include high cost and lack of insurance coverage. The author reviews the clinical manifestations and discusses treatment strategies.

Key points

	• Migraines are one of the most disabling conditions globally, and they often start during childhood and adolescence.
	• Headache duration may be as short as 30 minutes, especially in children younger than 7 years of age with migraines (76).
	• Many children and teenagers have migraine headaches. However, the lack of normality between attacks should raise concern about the accuracy of the diagnosis.
	• Neuroimaging is usually not necessary.
	• No migraine aura lasts more than 60 minutes.
	• Medications are helpful, particularly acutely, but lifestyle changes and nonpharmacologic methods are important treatment modalities.

Historical note and terminology

The first reliable description of migraine was probably given by Aretaios of Kappadokia in the first century A.D., when he described “heterocrania.” In the second century A.D., Galen used the word “hemicrania,” from which the word “migraine” derives, as a synonym for “heterocrania.” In Medieval Europe, Hildegard von Bingen suggested that migraine was often unilateral because the pain was so severe that it could not be tolerated if it were on both sides of the head. During the Renaissance, explanations for unilaterality included the separation by the falx cerebri. During this time, it was also postulated that migraine was caused by yellow bile and, furthermore, that the vapors proposed by the Galenic theorists could ascend (as from the stomach to the brain). In this theory, anatomic connections were not necessary (42). The first unmistakable descriptions of migraine with aura were from the 17th century and included the observations of Charles Le Pois, who described premonitory symptoms of his own migraine. Since then, many other investigators have described their own auras. In the 19th century, Liveing and Gowers contributed to the knowledge of the relationship between migraine and epilepsy. In the early 20th century, Moebius coined the term “status migrainosus,” which was similar to the term for the prolonged epileptic state (42).

Even though Tissot, Calmeil, and Liveing mentioned patients whose migraine started during childhood (13), the onset of migraine in early childhood (between the ages of 1 and 4 years) was not well described until the early 20th century (91). Edward Flatau's book, La Migraine, published in 1912, was the most comprehensive review to that time. Among the therapies he reviewed, ergotamine is the primary medication still used. In 1926, Maier reported a successful clinical trial of ergotamine in migraine. The work of H G Wolff, Headache and Other Head Pain, published in 1948, is considered a classic and was a forerunner to much of the successful migraine research of the 20th century. Traditionally, many doubted that migraine was much of a problem in childhood, but the important epidemiological studies of Bille established the high prevalence of childhood migraine (13).

Clinical manifestations

Presentation and course

The most notable symptom of childhood migraine is headache, which is accompanied by aura in about one third of patients. A key clinical feature, however, is normality between attacks. Although a unilateral, throbbing headache is typical with adult migraine, it is more common for children to complain of bilateral or midfrontal headaches. Even though the headache is often bilateral, its onset may be unilateral. If usual questioning does not disclose the location and quality of the headache, the child can be asked to point to the location of onset, and the examiner can supply several adjectives to determine the quality of the pain (eg, pounding, pressing, and burning); however, as with all leading questions, the examiner must be wary that the child might just pick an answer whether true or not. Clues to a diagnosis of migraine in young children are often obtained from the parents describing the physical appearance and the behavior of their child. One measure of morbidity is how much school is missed due to migraine attacks. In a survey, 10% of children with migraine missed 1 day of school over a 2-week period, and nearly 1% missed 4 days (82). A Brazilian study found that children with migraines had significantly poorer school performance than children not suffering migraines (11). This may be related to the disability posed by the migraine or potentially a learning disability that triggers migraine chronicity. The use of a migraine disability assessment tool may help specify associated disabilities and is useful for comparison at follow-up (36). A headache diary kept by a parent or child is also useful at follow-up (69). A visual aura of scintillating scotomata or flashing lights or, less commonly, a sensory or motor disturbance may precede the headache by 20 to 60 minutes in a third of migrainous children (63), but the pathognomonic fortification spectrum with its gradually expanding “C” shape with a scintillating border is rarely reported.

Migraine aura in childhood (patient depiction)

This picture was drawn by an 8-year-old boy who experienced a visual aura of silver spots lasting 2 or more minutes before the onset of midfrontal pounding headaches. His mother had the same aura, but it lasted 15 to 20 minutes. (...

Visual symptoms are usually homonymous, and motor or sensory symptoms are usually unilateral. In children, gastrointestinal symptoms are especially prominent, but the headaches, sometimes lasting less than an hour or so, are usually of shorter duration than those of adults. Facial pallor commonly occurs before or with the headache, and photophobia and phonophobia may also occur. Although most children with migraine do not experience syncope, migraine is second only to vasovagal syncope as a cause of syncope in children (61), and many children report a lightheaded dizziness with the headaches. Cutaneous allodynia occurs in some children with migraine, sometimes expressed as their hair hurting, such as when combing hair, touching their head, or wearing a hat (54). Nonheadache symptoms often precede the headache and include irritability, malaise, and hyperactivity. Factors often mentioned as precipitating or exacerbating the headache include stress, light, irregular schedule (eg, meals, sleep times), menses, minor head trauma, heavy exercise, environmental heat, and weather. Medications that may increase the likelihood of headaches include adrenergic agonists (eg, for asthma or ADHD), oral contraceptives, and others. Unfavorable lifestyles (including obesity, low physical activity, and cigarette smoking) are associated with an increased prevalence of headaches. Among 112 adolescents with migraine who underwent a weight-loss program, the 40 who became migraine-free lost more weight than the 72 who continued to experience migraine (93). Dietary substances are generally less important as triggering factors (eg, chocolate, cheese, caffeine, alcohol, nitrites [“hot dog headache”], and monosodium glutamate) (43).

The criteria for different headache types in the International Classification of Headache Disorders (ICHD-3) (35) may be used for children. However, if a child has not yet had five attacks or if the headaches last less than 1 hour or so, the IHS criteria may be too restrictive (89). As of 2016, the full headache classification can be accessed digitally: https://www.ichd-3.org.

Diagnostic criteria. Migraine has three basic types: (1) migraine without aura, (2) migraine with aura, and (3) chronic migraine (35). For all types, a criterion is that the headache is not better accounted for by an alternative diagnosis (eg, infection, mass lesion, or others).

Migraine without aura.

• Five headache attacks lasting for 2 to 72 hours (the minimum is 4 hours for adults). If a child falls asleep during the headache, the time asleep is part of the headache duration (69).

• At least two of the following headache characteristics: (1) unilateral pain, (2) pulsatility, (3) moderate or severe pain intensity, and (4) aggravation by or causing avoidance of routine physical activity. For children and adolescents, bilateral headaches are more likely. Unilateral headaches often start to occur in late adolescence. In addition, during the headache, the individual must have at least one of the following: (1) nausea or vomiting or (2) photophobia and phonophobia.

Migraine with aura. This diagnosis requires one or more fully reversible aura symptoms to indicate focal cerebral cortical or brainstem dysfunction. No migraine aura lasts more than 60 minutes. A typical aura may include visual, sensory, or speech symptoms and is usually followed by a typical migraine headache. Aura without headache is exceedingly rare in children and should raise suspicion for a structural lesion (eg, occipital arteriovenous malformation). ICHD-3 provides diagnostic criteria for aura as shown below.

C. At least three of the following six characteristics:
	1. At least one aura symptom spreads gradually over 5 or more minutes.
	2. Two or more aura symptoms occur in succession
	3. Each individual aura symptom lasts 5 to 60 minutes ¹
	4. At least on aura symptome is unilateral ²
	5. At least one aura symptom is positive ³
	6. The aura is accompanied, or followed within 60 minutes, by headache
(35) ¹ When, for example, three symptoms occur during an aura, the acceptable maximal duration is 3×60 minutes. Motor symptoms may last up to 72 hours. ² Aphasia is always regarded as a unilateral symptom; dysarthria may or may not be. ³ Scintillations and pins and needles are positive symptoms of aura.

Chronic migraine. Chronic migraine is diagnosed when headaches occur for 15 days or more per month for at least 3 months, and migraine headache (with or without aura) occurs on at least 8 of those days. Tension-type headaches usually occur on the remaining headache days. The most common cause for chronic migraine is medication overuse, though there are some controversies. If medication overuse is present, diagnoses of both chronic migraine and medication-overuse headaches are appropriate. The demarcation is arbitrary between chronic migraine (15 headache days or more per month for 3 or more months) and episodic migraine (fewer than 15 days per month), and there is no biological difference between the two types (01). During some months (eg, school holidays and summer vacation), a child with chronic migraine can have fewer than 15 headache days per month, and during those months, the child would carry a diagnosis of episodic migraine (96).

Subforms of migraine with aura. Please note that many of the headache types commonly referred to as “complicated migraine” are classified as subtypes of migraine with aura.

	• Migraine with typical aura (visual, sensory, or speech/language)
	• Migraine with brainstem aura (previously termed basilar-type migraine)
	• Hemiplegic migraine (sporadic or familial)
	• Retinal migraine. This subform is characterized by a monocular aura based on changes in retinal vessels and is not due to vascular changes in the visual cortex. Because a subjective impression of a monocular change might be incorrect, the monocularity must be confirmed by testing vision using at least a cover/uncover test. In children, retinal migraine is almost never diagnosed. In the rare reports of occurrence in children, there is typically reliance on the child’s subjective impression rather than testing of vision (62). As yet, details are lacking to confirm that this subform occurs in children. Even in adults, retinal migraine is extremely rare.

Migraine with brainstem aura (basilar-type migraine) has aura symptoms referable to brainstem dysfunction (vertigo, tinnitus, impaired hearing, ataxia, dysarthria, nystagmus, diplopia, or impaired consciousness or somnolence) and usually has typical aura symptoms as well (visual, sensory, or speech/language). Headache usually occurs within 60 minutes of the auras. There is no motor weakness, which is the key clinical feature differentiating it from hemiplegic migraine.

Hemiplegic migraine occurs both sporadically and as an inherited autosomal dominant trait. It is a migraine with aura that includes motor weakness. Fully reversible motor weakness occurs as an aura and is accompanied by reversible auras of sensory, visual, or speech/language dysfunction, with headache often occurring during or within 60 minutes of an aura. The motor weakness can last up to 72 hours (and rarely weeks), but the nonmotor auras last 5 to 60 minutes. At least one aura is typically unilateral. Symptoms of brainstem dysfunction often occur. Rarely, during an attack of hemiplegic migraine, there can be altered consciousness, confusion, fever, and CSF pleocytosis mimicking meningoencephalitis. Some of the familial patients have cerebellar signs and may have serious complications, including coma from mild head injury (22). In the familial type of hemiplegic migraine, genetic etiologies have been determined for three subtypes, with each having a mutation in a different gene: CACNA1A (calcium channel), ATP1A2 (K/Na-ATPase), and SCN1A (sodium channel).

Childhood episodic syndromes that may be associated with migraine (03). As mentioned above, the evaluation must determine that an alternative disorder does not account for the symptoms.

	• Recurrent gastrointestinal disturbance includes two entities: cyclical vomiting syndrome, which commonly presents between 4 and 18 years of age, and abdominal migraine, which often presents from 5 to 10 years of age.
	• Benign paroxysmal vertigo of childhood, which often presents from 2 to 5 years of age.
	• Benign paroxysmal torticollis, which often presents in the first 1 to 2 years of life.

The subgroup of episodic syndromes associated with migraine are either precursors to migraine or are considered migraine equivalents. However, a clear link with migraine remains questionable. The most common of these is recurrent gastrointestinal disturbance, which comprises two disorders: abdominal migraine, with its recurrent abdominal pain, and cyclical vomiting. Other possible migraine equivalents include benign paroxysmal vertigo and benign paroxysmal torticollis. Some consider acute confusional migraine as part of this group. These episodic syndromes are more likely to be accepted as migraine equivalents if the child also has typical episodes of migraine headache that include similar symptoms. For example, coexisting migraine headaches are most typical with abdominal migraine and cyclical vomiting and occur in 70% of the patients, whereas they are least frequent with benign paroxysmal vertigo (10%) (06). Although some children with these syndromes later develop migraine, others do not. No diagnostic marker for migraine can verify a relationship between migraine and episodic syndromes, and the existence of these disorders as forms of migraine remains uncertain.

Episodic entities of less certain status. These three entities are included in the appendix of the headache classification, indicating their uncertain status as childhood episodic syndromes that may be associated with migraine (35).

	• Infantile colic. Episodes of excessive crying occur from birth to 4 months of age in otherwise healthy children. These children are more likely to develop future migraines and have a family history of migraine.
	• Alternating hemiplegia of childhood. With onset before 18 months of age, this disorder is often associated with a mutation of the ATP1A3 gene.
	• Vestibular migraine. This is rare in childhood, but some children with benign paroxysmal vertigo evolve to vestibular migraine.

Migraine variants. (47)

	• Acute confusional migraine
	• Alice in Wonderland syndrome. Perceptual distortions of body image, visual size, or time (associated with headache).
	• Ophthalmoplegic migraine. This is no longer accepted as a form of migraine. The accepted term is “recurrent painful ophthalmoplegic neuropathy.”

Prognosis and complications

In Bille's large study, 35% to 50% of the children with migraine became asymptomatic after 4 to 6 years of observation (13). When Bille re-evaluated his cohort near the age of 50 years, more than half of the subgroup who had “pronounced” migraine at about 6 years still had migraine at the age of 50. However, one fourth of the subgroup stopped having migraine by the age of 25 years (14). A more recent study re-evaluated headache prognosis in patients 25 years after they were initially observed in a headache clinic as children between 2 and 15 years of age (58). Sixty-six percent reported ongoing migraines though with significant improvement, and 33% had experienced remission(boys tended to remit more than girls). A larger study at Cincinnati Children's Hospital showed similar rates with improvement in 56% of cases (67). The odds of worsening were significantly higher with increasing age, female sex, chronic migraine, status migrainosus, depressive symptoms, higher PedMIDAS scores, and use of nutraceuticals, whereas the odds of worsening were lower for summer visits, caffeine drinkers, higher headache frequencies, and use of pharmaceuticals.

Migraine is a disabling disease and represents an ongoing global public health concern. Migraine ranks second among all human diseases in terms of years lived with disability (YLWD), according to the 2019 Global Burden of Disease study, and is the most disabling neurologic disease in children and adolescents. Incidence, prevalence, and disability-adjusted life years (DALYs) in both adult and pediatric populations increased further over the years, according to the 2021 Global Burden of Disease study. Prevalence of migraine and DALYs were found to be the highest in adolescents 15 to 19 years of age.

Migraine, especially migraine with aura, is considered an independent vascular risk factor for cerebrovascular and cardiovascular events. This is hypothesized to be related to underlying endothelial dysfunction in individuals with migraines. Using estrogen-containing hormonal contraceptive pills further increases those risks, a fact that started a controversy in the field. A large study examined the use of modern combined hormonal contraceptives in females 18 to 45 years of age who were diagnosed with migraine with aura (41). Results showed that exposure to modern combined hormonal contraceptives was not associated with a significant increase in vascular risk in women with migraine with and without aura who have no prior cardiovascular events. However, in those who never received combined hormonal contraceptives, migraine with aura was associated with higher vascular risks compared to migraine without aura. Many adolescents need combined hormonal contraceptives for management of various conditions like dysmenorrhea, menorrhagia, and endometriosis. Although there are no dedicated studies in the pediatric population looking at vascular risk factors while using combined hormonal contraceptives, the data from the adult population suggest the safety of low estrogen-containing options.

Clinical vignette

I evaluated this boy at 12 years of age. He had headaches from the age of 7 to 8 years old, which later began worsening. The severe headaches lasted for several hours and required him to lie down and sleep twice per month. He missed 4 days of school because of headaches. His mother could tell when a headache was coming because there was a different look in his eyes. She thought the whites of his eyes became darker, and his eyes appeared sunken. He seemed confused and dazed with the headache. The headaches were exacerbated by activity, heat, and loud noises. Sleep provided relief. The headaches were associated with abdominal pain and anorexia. There was no photophobia, nausea, vomiting, or aura. He had no history of seizures, head trauma, or loss of consciousness. Family history was positive for severe headaches in his father when he was about the same age. Physical and neurologic examinations were normal, with blood pressure 110/60 and pulse 90. He was treated with propranolol long-acting 60 mg daily. His mother telephoned a few weeks later. She was worried because she said his blood pressure and pulse were low and reported blood pressure 100/41 and pulse 52. She stopped propranolol for several days, and he had a severe headache. I reassured her that these changes in pulse and blood pressure in a child/teenager with a healthy heart were of no concern. Propranolol was restarted. When he returned 4 weeks after the initial visit, he was free of headaches and asymptomatic, with a pulse of 58. He submitted an illustration of his headaches.

Childhood migraine (patient depiction)

This picture was drawn by 12-year-old boy. When narrating the picture, the boy explained that the man in the foreground holding his forehead and looking ill is himself as an adult; his soccer game has been interrupted by a headach...

Biological basis

	• Migraine tends to run in families.
	• Onset is influenced by environmental, psychosocial, and pain-processing factors among others.
	• Definite genetic causes are known for familial hemiplegic migraine.
	• Activation of the trigiminovascular system is the basis of migraine pathogenesis.

Etiology and pathogenesis

A large proportion of children with migraine have a family history of migraine. Furthermore, children with headaches associated with acute illnesses are more likely to have a family history of migraine (48). However, even though 72% to 89% of migrainous children have a positive family history, the relative contributions of genetics or other factors generally remain unclear. One estimate suggests 52% heritability (102). But for specific types of migraine, the role of genetics is more certain. In the familial type of hemiplegic migraine, genetic etiologies have been determined for three subtypes, with each having a mutation in a different gene: CACNA1A (calcium channel), ATP1A2 (Na/K-ATPase), and SCN1A (sodium channel). For the autosomal dominantly inherited familial hemiplegic migraine 1, there is a mutation in a calcium-channel gene in up to 75% of cases. Surprisingly, familial hemiplegic migraine is one of three allelic disorders (ie, different alleles of the same gene) due to defects in calcium channel alpha 1A subunit gene (CACNA1A) on chromosome 19p13, the others being episodic ataxia type 2 and chronic spinocerebellar ataxia type 6. In other families with familial hemiplegic migraine 2, the chromosome 1q23 gene for sodium-potassium ATPase pump is associated with familial hemiplegic migraine, benign familial infantile convulsions, permanent mental retardation, and a family history of confusional migraine (92). A third subform of familial hemiplegic migraine is due to mutations of the sodium-channel gene SCN1A.

The exact pathogenesis of childhood migraine is unknown but is felt to represent the interaction of several factors: genetic predisposition, environmental predisposition (eg, hormonal and psychosocial influences), physiological and biochemical abnormalities, precipitating factors, and processing of pain impulses. Regarding genetic predisposition, a genome-wide study has implicated primary involvement of genes related to vascular control (32).

The trigeminovascular system, referring to the trigeminal innervation of the cranial vessels, has been linked to the pathophysiology of migraine. Activation of trigeminal nerve terminals by various triggers provokes several events, which include (1) the release into the cranial circulation of neuropeptides, including calcitonin gene-related peptide (CGRP, a vasodilator peptide), (2) vessel leakage, and (3) mast-cell degranulation. Neuropeptides are thought to play a role in several aspects of migraine, including migraine pain, lowering of the pain-response threshold, and allodynia, sensitivity to stimuli that are usually not considered uncomfortable (eg, discomfort when combing hair). Sumatriptan normalizes elevated levels of CGRP and relieves the headache. Moreover, treatment with an antagonist of CGRP relieves migraine (21). Abnormalities of ion channels leading to neuronal hyperexcitability have been confirmed in familial hemiplegic migraine (92; 23).

Epidemiology

	• The onset of adult migraine is often during pediatric years.
	• Prevalence of migraine in children and adolescents is rising globally, mainly among adolescents and male populations.
	• Migraine is associated with multiple comorbidities including mental health disorders, which are on their own considered global public health problem.

Migraine is common during childhood. The global average prevalence of pediatric migraine is 11% and increases with age. The burden of migraine in children and adolescents has trended upward over the years, more significantly among adolescents aged 15 to 19 years and among males. Lower socioeconomic status is associated with an increased prevalence of migraine (87).

Migraine affects 9.1% of children (98), as contrasted with 6% of men and 18% of women (23). Generally, boys and girls are affected equally before puberty, but girls are affected roughly three times more than boys after puberty (90). Fluctuations in estrogen levels during adolescence may trigger migraine by affecting hypothalamic function and neuronal excitability, whereas testosterone may confer a protective effect in males (17).

As a chronic problem, childhood headaches (migraine and other types) are more prevalent than asthma, with headaches occurring in 60% and asthma in 13% (66). Adolescents with migraine, however, have several comorbidities, including asthma, seasonal allergies, epilepsy, persistent nightmares, and motion sickness (53). Wagner and colleagues found that depression occurs at all ages, more commonly in children with either migraine or epilepsy as compared to controls with lower-leg fractures (95). However, when comparing migrainous adolescents with migrainous preadolescents, depression is more than twice as common in adolescents (95). Migraine age-of-onset influences familial clustering of migraine. If a patient has onset of migraine headaches before 16 years of age, it is more likely that other family members will have migraine (85). As mass shootings of children have become more common, morbidities in survivors are being recognized, among them a greater risk for headaches. Following a mass shooting at a camp for adolescents in the Utoya islet in Norway in 2011 that killed 69 and severely wounded 33 people, all 358 adolescent survivors participated in the study and had an increased odds ratio for both migraine (odds ratio 4.27) and tension-type headaches (odds ratio 3.39) (84).

The two basic types of migraine occur in children. According to a meta-analysis by Onofri and colleagues in 2023, the prevalence of migraine without aura is 8%, and prevalence of migraine with aura 3% (66). The prevalence of both migraine without aura and migraine with aura increases with increasing age (63). Thus, incidence rates for migraine in children were estimated as 9 per 100,000 person-years in 0- to 4-year-olds and 151 per 100,000 in 15- to 19-year-olds (83). Note that the age of peak incidence of migraine varies by sex; for males of all ages (including adults), the peak incidence is 246 per 100,000 person-years for 10 to 14-year-olds, whereas the peak for females is 689 per 100,000 for 20- to 24-year-olds (83). Adult migraine often starts in childhood. When adults with migraine are questioned regarding onset, half report onset before 20 years of age, whereas one fourth report onset before the age of 10 years (78). The prevalence of abdominal migraine, for which diagnostic criteria and a verifiable relationship with migraine remain controversial, peaks at the ages of 5 to 9 years (64).

Differential diagnosis

In the presence of the following features, the diagnosis of migraine is fairly secure: (1) a positive family history of similar illness; (2) a typical history of migraine; (3) a normal examination; (4) normal health between attacks. At different times, a child can have either type of migraine, ie, migraine without aura and migraine with aura. Other combinations may suggest alternative diagnoses. For example, a structural brain lesion may be responsible if a neurologic aura lasts longer than 60 minutes or if headaches typically awaken a child from sleep. In the emergency department, about 10% of headaches in children are thought to be primary headaches, mostly migraine, and most of the remainder are due to concurrent illness or minor head trauma (45). In general, most of the headaches in children and adolescents are primary headache, including migraine and tension headaches, and a minority are posttraumatic or due to medication overuse (03). Less common are those due to brain tumors and vascular lesions.

Confusing conditions

Disorders that may have migraine-like headaches include the following:

Chronic daily headaches. These children typically have one of three entities: chronic migraine, chronic tension-type headaches, or new daily persistent headaches. Chronic migraine and chronic tension-type headaches, which often overlap in the same child, evolve from episodic headaches to extremely frequent or even continuous daily headaches (or at least 15 or more headache days per month). New persistent daily headaches begin without a prior history of headaches. Daily or chronic headaches are sometimes associated with an infection or physical stress and uncommonly related to idiopathic intracranial hypertension without papilledema (12). The evolution to daily headaches is often related to medication overuse or to concurrent psychological problems. In adults, cutaneous allodynia can be a risk factor for chronic migraine, but allodynia is not associated with chronic migraine in children (54). Over time, the frequency of chronic migraine headaches might improve to that of episodic migraine headaches. The improvement might take years, and some patients shift over the years between episodic migraine and chronic migraine (96).

Brain tumors. Other tumor manifestations usually develop within 4 months of headache onset (38).

Vascular malformations. Headaches are always on one side, and sometimes a cranial bruit is heard.

Hydrocephalus. Check the head circumference for macrocephaly.

Idiopathic intracranial hypertension (pseudotumor cerebri). Other clinical features may include positional headaches, pulsatile tinnitus, and episodes of transient visual obscuration. Papilledema and sixth nerve palsy may be present on examination; less commonly, there is no papilledema (12).

Posterior reversible encephalopathy syndrome. Headaches have been associated with white matter lesions and related to various disorders, including hypertension, renal disease, chemotherapeutic agents, and malignancies. More commonly in children, renal disease, extreme hypertension, and papilledema are combined with occipital edema (46).

Head trauma. In the case of post-concussion, there are no tests or measures other than self-report to confirm that headache or other complaints are due to persisting postconcussive symptoms (101). Standardized symptom rating scales may be useful.

Various inflammatory disorders.

Mitochondriopathies. Including mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS).

Seizures. Epilepsy is the favored diagnosis when the aura is especially brief, consciousness is altered, and there is focal epileptiform discharges on electroencephalogram. A therapeutic trial with antimigrainous or antiepileptic drugs is rarely helpful in the differential diagnosis because many of these drugs can be used for either migraine or epilepsy (eg, topiramate and valproate).

Cluster headaches or chronic paroxysmal hemicrania. These headache types are rare in children. The hallmark of diagnosis is unilateral headache associated with autonomic symptoms like conjunctival injection, eyelid puffiness, drooping, tearing, nasal congestion, ear fullness, hemifacial flushing, and anhydrosis.

Abdominal disorders. Primary abdominal disorders may cause recurrent episodes of prominent vomiting and abdominal pain, whereas metabolic disorders (eg, heterozygous ornithine transcarbamylase deficiency) may add severe headaches to the abdominal symptoms.

Associated or underlying disorders

Obesity. Obesity is associated with increased risk and greater severity of migraine in children and adolescents. A meta-analysis conducted by Quispe-Vicuna and colleagues in 2023 showed that excess weight and obesity increased the odds of migraine based on eight studies (75).

Attention deficit hyperactivity disorder. Patients with ADHD have twice the risk of developing migraine compared to controls. The association is strongest among children younger than 12 years, followed by adolescents aged 12 to 17 years. The risk is not significant in young adults, underscoring the importance of acknowledging this association when addressing pediatric migraines (39). Stimulants used to treat ADHD can cause side effects of headaches, which can present as migraine in genetically predisposed patients.

Other psychiatric conditions. Anxiety, panic disorders, eating disorders, depression, and posttraumatic stress disorders are often reported in association with migraine (60). Internalizing disorders in children with migraine had 4.69-fold higher odds of experiencing mixed anxiety or depressive disorders (27).

Sleep disorders. Sleep disorders are highly prevalent in pediatric migraine and are frequently associated with a higher headache severity and lower response to acute therapy (94). In a study that included 185 children with migraine referred to sleep clinics, snoring was reported in 66% of patients, and 40% were diagnosed with obstructive sleep apnea. Obstructive sleep apnea, insomnia, and periodic limb movement disorders are often associated with migraines (09).

Atopic conditions. A meta-analysis including 10 studies found that allergic diseases overall confer a 1.52-fold increased risk of migraine, with specific odds ratios of 1.49 for asthma, 2.16 for allergic rhinitis, and 1.27 for atopic dermatitis (40).

Hypertension. A large cross-sectional study of over 2 million adolescents found that 0.7% of those with migraine had hypertension compared to 0.2% of nonmigraineurs (05). This may be related to a shared underlying mechanism of endothelial dysfunction.

Epilepsy. There is a bidirectional relationship between epilepsy and migraine. Meta-analyses demonstrate an approximately 80% bidirectional increase in prevalence between the two conditions (100). Specific epilepsy syndromes like self-limited epilepsy with centro-temporal spikes and juvenile myoclonic epilepsy demonstrated significantly higher migraine prevalence.The association is more prevalent in children 10 years or older, and migraine onset typically occurs after epilepsy diagnosis (50). In children, migraine with aura confers an eight-fold increased risk for developing subsequent epilepsy (OR 8.1, 95% CI 2.7-24.3), whereas migraine without aura does not increase epilepsy risk (77). Both epilepsy and migraine share pathophysiology, including cortical hyperexcitability, impaired ion homeostasis, and dysfunctional neurotransmission. Shared genetic mutations, particularly in genes encoding ion channel subunits such as CACNA1A, SCN1A, and ATP1A2, support a common channelopathy model (33; 71).

Diagnostic workup

	• Except for some cases of hemiplegic migraine with a CSF pleocytosis, standard laboratory tests on blood, CSF, and urine are normal.
	• No laboratory test is diagnostic for migraine.
	• Unless there is a specific indication, tests are unnecessary.
	• Neuroimaging and various conditions that represent indications for testing are discussed below.

Indications for laboratory testing. In children with sickle cell disease, low hemoglobin is associated with headaches. However, even children with sickle cell disease and at higher risk for silent cerebral infarction do not require neuroimaging for recurrent headaches if they are neurologically normal (25). Standard CSF analysis is usually normal, even with hemiplegic migraine. However, the syndrome HaNDL might mimic hemiplegic migraine. HaNDL rarely occurs in children and can be excluded if CSF is normal (31). In general, if lumbar puncture demonstrates abnormalities, then a process other than migraine should be considered (eg, inflammatory disease, mitochondriopathy, hemorrhage). EEG is not recommended for routine evaluation of migraine (56) but may be performed if there is a clinical suspicion for seizures, realizing that abnormalities occur frequently in children with migraine and, in most cases, do not clearly define an epileptic disorder. Migraine-associated EEG abnormalities are relatively common: 10% to 75% in total (paroxysmal in 20% to 30%). For example, midtemporal or central spikes have been reported in 9% of children with migraine who did not have seizures (51). With occipital epilepsy, but not with migraine, spikes occur when the eyes are closed (fixation off phenomenon). In children with typical migraine (ie, migraine with or without aura) and who have normal physical and neurologic examinations, brain MRI is normal or has findings that do not require surgical treatment (56). Subsequent studies support this conclusion. Thus, brain MRIs were performed in 375 of 926 pediatric patients with migraine. Among them, 24 (6%) had nonprogressive, predominantly frontal T2/FLAIR white-matter hyperintensities, and none had stroke. Other MRI abnormalities were not clearly related to the migraine headaches (Chiari malformations, arachnoid cysts, pineal or other cysts, etc.) (59). It has been shown that T2/FLAIR white-matter hyperintensities are no more common in children with migraine than those without migraine (04). A head CT scan, eg, in the emergency department, is not helpful unless the child has acute abnormalities other than headache.

Lewis and colleagues created a practice parameter for children aged 3 to 18 years that recommends consideration of neuroimaging in children with an abnormal neurologic examination or for children with other physical findings that suggest disease of the central nervous system (56). I often perform neuroimaging in the following situations:

	• Any neurologic abnormality (including seizures, reduced visual acuity, alteration of consciousness, elevation of intracranial pressure, or deterioration in cognition, motor skills, personality or behavior).
	• Evidence of a systemic disorder, which might affect the brain, including a drop-off in growth rate or diabetes insipidus.
	• Infant or toddler (especially with enlarging head).
	• Neurologic involvement during the attack, other than a typical visual aura.
	• Headaches that always occur on one side (fixed laterality or side-locked headache).
	• Headaches that last several days or attacks that are not responding to treatment.
	• Headaches characterized by nocturnal awakening from sleep or associated with coughing, straining, or changing position.

Management

	• For some children, analgesics and rest may be the only treatments necessary.
	• If migraine headaches prevent a child from playing or going to school, preventative treatment is often indicated.
	• Routine treatments for migraine include the following five methods that are described more fully below:
		(1) intermittent headache medications, including analgesics, triptans or a combination of both;
		(2) antidopaminergic antinausea agents: promethazine 12.5 to 25 mg (oral, rectal, or topical gel), and oral metoclopramide 5 to 10 mg;
		(3) prophylaxis with a daily preventive medication, such as propranolol or nadolol, amitriptyline, antiepileptic agents (eg, topiramate, valproic acid, levetiracetam) or a CGRP antagonist.
		(4) injectable CGRP monoclonal antibodies and onabotulinumtoxinA injections are options for refractory cases.
		(5) counseling and avoidance of triggering factors;
		(6) alternative methods, such as neuromodulation, relaxation training, biofeedback, or acupuncture. However, some alternative methods require further research to confirm efficacy (86; 34).

Drug treatment

(72; 69; 70)

Acute headaches. With regard to medication management, at full dose per weight, ibuprofen, naproxen, or acetaminophen are efficacious when given rapidly, ie, during a migraine aura or as soon after headache onset as possible. However, if the individual typically has severe headaches inadequately responsive to analgesics, add a triptan to the analgesic. For analgesics, the following are suggested: acetaminophen with a dosage of 15 mg/kg every 4 to 6 hours; ibuprofen 10 mg/kg every 6 to 8 hours; naproxen or aspirin 15 mg/kg every 4 to 6 hours. Do not use aspirin for pre-teenagers or those at risk for Reye syndrome. Caution should be taken not to combine NSAIDs.

The CDC does not recommend using NSAIDs or acetaminophen before vaccines, and the COVID-19 vaccine is no exception. However, these agents are indicated for postvaccination symptoms, including headache (28). The four triptans approved for pediatric use, sumatriptan plus naproxen (12 years and older), rizatriptan (6 years or older), almotriptan (12 years and older), and zolmatriptan (12 years and older), are used for severe headaches or migraine with aura. Rapid treatment with a nasal or oral triptan plus ibuprofen or naproxen is helpful for about 70% to 80% of headache episodes. Preceding the dose of a nasal triptan with a hard candy can ameliorate the side effect of bad taste. Based on the study of Linder and colleagues, the FDA in June 2009 approved oral almotriptan malate as the first triptan approved for use in adolescents aged 12 to 17 years old. The 25 mg dose showed a statistically significant decrease in headache at the 2-hour time point (57). In March 2012, rizatriptan was FDA-approved for treating headaches in children ages 6 to 17 years (5 mg once for those less than 40 kg and 10 mg once for those more than 40 kg weight). In May 2015, Treximet (sumatriptan/naproxen) was approved by the FDA for adolescents 12 years and older at a new dosage-strength recommendation of 10 mg sumatriptan and 60 mg naproxen given once per 24 hours with a maximum dose of 85 mg sumatriptan and 500 mg naproxen per 24 hours. In addition, reports have confirmed the safe use of nasal triptans, acetaminophen, and ibuprofen for children as young as 4 years of age, and oral and subcutaneous triptans are often used for children as young as 6 years of age. Experience in children is limited for intravenous dihydroergotamine, but it seems to have the same safety profile as in adults. Triptans and dihydroergotamine should not be used for hemiplegic migraine, migraines with brainstem aura, or for children who have cardiac disease or hypertension. Opioids and barbiturate-combination medications are usually avoided in outpatient treatment of pediatric headaches. In pediatric emergency departments from 2009 to 2019, opioid treatment for migraine decreased, particularly in hospitals with clinical guidelines for treating childhood migraines (29).

Chronic migraine. Chronic migraine occurs relatively infrequently in children. According to ICHD3, the definition of chronic migraine is having headaches on 15 or more days per month for a duration of 3 months. At least eight of the 15 headaches should fulfill the criteria of migraine. Preventative treatment should be considered for both episodic migraine (fewer than 15 headache days per month) and, most importantly, chronic migraine.

Preventive treatment. The first step in prevention should include journaling headaches and identifying triggers that need to be avoided or mitigated. Lifestyle modifications are necessary and are often effective without the need for pharmacological management, especially regular meal schedules, adequate sleep, and limited screen exposure (65). Initiation of pharmacological preventive treatment is indicated if the above measures are ineffective or if the headaches are severe or especially frequent (more than two to three per month). It can be difficult for the clinician to determine whether preventive treatment is effective due to the prominent placebo effect in childhood migraine, ie, a placebo response rate close to 60% (73; 01). Other than limited evidence supporting the preventive use of topiramate and trazodone, pediatric migraine studies have not found effective preventive treatments, but this should not be interpreted as meaning there are no effective treatments (10). However, exciting developments are on the horizon with regard to the clinical use of CGRP antagonists. In August 2025, fremanezumab was the first CGRP monoclonal antibody to be approved by the US FDA for children 6 years or older (if weight is at least 45 kg). Compared to placebo, fremanezumab showed a statistically significant reduction of migraine days in patients 6 to 17 years of age.

More caution is now exercised regarding potential adverse effects of medications in view of studies showing that active medications are often no more useful than placebo (10). For instance, in the Childhood and Adolescent Migraine Prevention (CHAMP) trial, children were treated for 24 weeks. Surprisingly, topiramate or amitriptyline was no more effective than a placebo for preventing migraine headaches (73). If preventive medications are chosen, propranolol or nadolol (beta-blockers) can be given daily. For those weighing less than 30 kg, the dosage is 1 mg/kg per dose given three times daily. For those weighing more than 30 kg, nadolol is started at 40 or 80 mg as a single daily dose and increased every 2 weeks as limited by side effects such as fatigue, depression, or sleep disturbances. Special caution is necessary for those for whom beta-blockade could cause problems, eg, asthmatics (beta-blockers may worsen bronchospasm), allergic individuals receiving desensitization shots, children taking insulin (beta-blockers can mask symptoms of anaphylaxis or hypoglycemia), or children with congestive heart failure, orthostatic hypotension, or renal insufficiency. Other oral medications might be useful when administered daily: amitriptyline or nortriptyline starting at 10 mg, verapamil, cyproheptadine (4 mg tab) starting at one-half tab once or twice daily, particularly for children, who have vestibular migraine (02), antiepileptic agents (topiramate, divalproex, topiramate, levetiracetam, and as used more in the past, phenobarbital and phenytoin), trazodone, and naproxen sodium. Amitriptyline combined with cognitive behavioral therapy was more effective than amitriptyline alone. However, there is a Food and Drug Administration warning about suicidal thoughts and behavior for children treated with amitriptyline. In a study using divalproex sodium ER, 500 mg/day for 15 days and then 1000 mg/day, the median rate of headaches decreased by 75% when comparing the first month of therapy to the fourth month. However, the decrease in the mean rate was less than 50%. Adverse effects were like those in adults (08). In a study of topiramate in adolescents, the 100 mg dose was superior to the 50 mg dose. Topiramate not only decreased headaches but also decreased absenteeism (55). Oral chlorpromazine has not been studied for migraine in children but may be used intermittently at doses of 2.5 to 5 mg every hour for four to five doses until sleep or headache relief occurs.

Treatment with CGRP antagonists. In adults, preventive treatment using CGRP antagonists includes injectable anti-CGRP monoclonal antibodies and oral small-molecule CGRP antagonists (gepants). Fremanezumab, which is the only FDA-approved CGRP monoclonal antibody medicine in the pediatric population, is injected subcutaneously at a dose of 225 mg monthly (15). At this time, it is only indicated for episodic migraines; studies are still underway for chronic migraines. Post-pubertal children who have failed other treatments can be considered for treatment with a CGRP antagonist at the lowest available dose. For example, rimegepant is an orally available CGRP antagonist dosed at 75 mg orally daily that was shown to be effective in an adult trial using 75 mg every other day (21). Relative contraindications to either small-molecule CGRP antagonists or anti-CGRP monoclonal antibodies include impairment of the blood-brain barrier, severe cardiovascular conditions, stroke or risk factors for stroke, and pregnancy, including planned pregnancy or breastfeeding (88). Trials of rimegepant treatment for migraine in children aged 6 to 17 years are ongoing and have completion dates estimated for 2026, 2027, and 2031. More information can be accessed at the following site:clinicaltrials.gov. In adults, CGRP-targeting therapies are now first-line therapy for prevention of migraine (19).

Injections. An effective treatment modality is injecting the greater occipital nerve with a combination of lidocaine and methylprednisolone acetate (74). OnabotulinumtoxinA (BOTOX®) injections, according to the PREEMPT (2010) protocol and based on adult data, have been a safe option for pediatric patients; however, they require at least 31 injections in the face, head, neck, and shoulders, which may not be acceptable to pediatric patients. There are multiple retrospective studies supporting the efficacy and safety of BOTOX® in the prevention of migraine in the pediatric population (49). However, the only randomized controlled trial did not meet the efficacy endpoints, again due to improvement of the placebo arm, a result similar to the CHAMP study that was previously mentioned (97).

Nutraceuticals. One should remain cautious with the use of alternative pharmacologic treatments that might have adverse side effects, particularly nutraceuticals, many of which have not been adequately studied. Nutraceuticals are often considered by parents or physicians because of purported safety or as a “natural” remedy but are not proven effective for the preventive or immediate treatment of pediatric migraine. Furthermore, these substances are not regulated by the FDA for purity, safety, or efficacy. Nutraceuticals include butterbur, riboflavin, ginkgolide B, magnesium, coenzyme Q10, polyunsaturated fatty acids, and oral melatonin (07; 18; 81; 68).

Prolonged migraine. Especially severe and prolonged migraine attacks can be treated with oral prednisone (initially 2 mg/kg per day up to 60 mg per day) for a tapering 6- to 14-day course when other agents are unsuccessful or before instituting systemic therapy. A short course of olanzapine has been used for refractory migraines, but caution should be taken with concurrent use of an antidopaminergic antiemetic to avoid extrapyramidal complications (44).

Hospital treatment. For emergency department treatment, dopamine antagonists are often used and might include prochlorperazine, metoclopramide, or promethazine. Prochlorperazine was the most effective and promethazine the least (80). A dopamine antagonist is usually combined with intravenous hydration, intravenous ketorolac, and diphenhydramine. For status migrainosus, consider intravenous or intramuscular administration of a drug like valproate sodium (10 to 15 mg/kg), magnesium sulfate (1 to 2 grams), metoclopramide (5 to 10 mg) or prochlorperazine (2.5 to 5 mg) (72; 80). Dexamethasone has shown benefit in reducing rates of rebound migraines following discharge from the emergency department; however, a similar effect was not reported in the pediatric population (20). Metoclopramide or prochlorperazine can be followed 20 minutes later by intravenous dihydroergotamine with an initial dose of 0.5 to 1 mg. In general, dihydroergotamine should not be used within 24 hours of a triptan. Status migrainosus, frequently associated with prolonged vomiting, may require hospitalization employing intravenous rehydration and treatment with metoclopramide and dihydroergotamine as above, and then dihydroergotamine every 8 hours for several days. A proportion of children whose status migrainosis has been refractory to the above treatments respond favorably to peripheral nerve blocks (30). Locations for superficial nerve blocks can include the tissue near the greater occipital nerve, lesser occipital nerve, supraorbital nerve, and auriculotemporal nerve. Morphine or intravenous chlorpromazine is sometimes added.

Nonpharmacologic treatments

Counseling. Additional aspects of counseling include the following: (1) reassurance that there is not a brain tumor or disease; (2) avoidance of triggering factors (especially stress, irregular or inadequate sleep, and irregular meal schedules); (3) the benign nature of migraine with regard to health; (4) the importance of using analgesics early in the headache; and (5) counseling about the risk of medication overuse headache.

Lifestyle adjustments. Advice regarding the benefits of adequate rest and relaxation can provide long-lasting benefits (24). Although stress is often an unavoidable part of life, sometimes stress can be reduced, eg, the child can more completely prepare for an upcoming examination, parents and children can be counseled regarding conflict resolution, and bullies can be avoided. The headache may be exacerbated by stress related to emotional or cognitive problems resulting from or causing school failure or child abuse. Addressing these problems may reduce the frequency of these headaches. Inadequate sleep might be due to obstructive sleep apnea, among other possibilities. Factors associated with recurrent headaches in adolescents include lack of physical activity, being overweight, use of alcohol and caffeine, exposure to tobacco, and poor sleep habits (70).

Relaxation, biofeedback, and psychological treatments. Cognitive-behavioral therapy, relaxation, meditation, and hypnosis have all been used with varying degrees of success. Although it is still not certain which children will benefit most from these therapies, a study that used network meta-analysis confirmed that these categories of nonpharmacologic therapies (lumped) were effective for pediatric migraine, but when categories of treatment were separated into components (split), the treatment effect was no longer statistically significant (52).

Neuromodulation. Neuromodulation devices are gaining interest in children with growing evidence. Three devices are FDA-approved for the pediatric population (remote electrical neuromodulation, single-pulse transcranial magnetic stimulation, and noninvasive vagus nerve stimulation). Based on the relatively good efficacy and the low rate of side effects in adults, repetitive neuromuscular magnetic stimulation for migraine prevention and remote electrical neuromodulation for acute migraine might be effective and acceptable in children (16). A 2023 study of remote electrical neuromodulation that used the Nerivio® device recruited 1,629 adolescents (average age 15.9 years, 80.6% female). For the measures 2 hours following Nerivio treatment in groups that used only the remote electrical neuromodulation without rescue medication, consistent pain relief occurred in 60.3% of 262, consistent pain freedom in 26.3% of 289, and consistent relief of functional disability in 41.2% of 255 users. Consistency was defined as the response occurring in at least 50% of treatments (26). It should be noted that this study included no control groups or sham treatments (26). The Nerivio® device is a nonpharmacologic abortive and preventative migraine treatment that requires a prescription. It is a battery-operated device controlled by a smartphone app. Nerivio was initially FDA-approved for patients 12 years and older. In November 2024, the FDA approval was extended down to age 8 years. A study by Hershey and colleagues in 2024 documented the potential for the remote electrical neuromodulation device to increase compliance with treating migraines in the school setting, as it is a self-led treatment (37).

A single-pulse Transcranial Magnetic Stimulation (sTMS) device or SAVI Dual is FDA-approved as a preventative and abortive treatment for migraine in patients 12 years and older. Side effects include mild discomfort. Disadvantages also include being a large and bulky device that may be less portable than other devices.

Non-invasive vagus nerve stimulation or GammaCore™ is also FDA-approved for patients 12 years and older for both prevention and acute migraine treatment. Both SAVI and GammaCore are FDA-approved based on safety reports and adult data. There are no dedicated pediatric studies to investigate efficacy. Cost and lack of insurance coverage are barriers to neuromodulation devices’ access. Nerivio® is showing some progress with some private insurance companies to expand coverage and improve access.

References

01: Abu-Arafeh I, Hershey AD, Diener HC, Tassorelli C. Guidelines update: Guidelines of the International Headache Society for controlled trials of preventive treatment of migraine in children and adolescents, 1st edition - an experience-based update. Cephalalgia 2023;43(5):3331024231178239. PMID 37226450
02: Abu-Arafeh I, Howells R. Management of migraine in children and adolescents. In: Swanson JW, Matharu M, editors. Handbook of Clinical Neurology. Vol 199 (3rd series), 1st edition. Cambridge: Elsevier, 2024:487-502.**
03: Abu-Arafeh I, Morozova M. Migraine in children and adolescents: Assessment and diagnosis. In: Swanson JW, Matharu M, editors. Handbook of Clinical Neurology. Vol 199 (3rd series), 1st edition. Cambridge: Elsevier, 2024:475-85.**
04: Ackley E, Asamoah P, Mirsky D, et al. Dots and spots: a retrospective review of T2-hyperintense white matter lesions in pediatric patients with and without headache. Headache 2023;63(5):611-20. PMID 37114889
05: Akavian I, Nitzan I, Twig G, et al. Association between migraine and hypertension in 2 million adolescents. Hypertension 2025;82(11):e337-45. PMID 40904275
06: Al Twaijri WA, Shevell MI. Pediatric migraine equivalents: occurrence and clinical features in practice. Pediatr Neurol 2002;26(5):365-8. PMID 12057796
07: Alstadhaug KB, Odeh F, Salvesen R, et al. Prophylaxis of migraine with melatonin: a randomized trial. Neurology 2010;75(17):1527-32. PMID 20975054
08: Apostol G, Lewis DW, Laforet GA, et al. Divalproex sodium extended-release for the prophylaxis of migraine headache in adolescents: results of a stand-alone, long-term open-label safety study. Headache 2009;49(1):45-53. PMID 19040679
09: Armoni Domany K, Nahman-Averbuch H, King CD, et al. Clinical presentation, diagnosis and polysomnographic findings in children with migraine referred to sleep clinics. Sleep Med 2019;63:57-63. PMID 31606650
10: Arruda MA. No evidence of efficacy or evidence of no efficacy. JAMA Pediatr 2013;167(3):300-2.** PMID 23358915
11: Arruda MA, Bigal ME. Migraine and migraine subtypes in preadolescent children: association with school performance. Neurology 2012;79(18):1881-8. PMID 23109652
12: Beri S, Gosalakkal JA, Hussain N, Balky AP, Parepalli S. Idiopathic intracranial hypertension without papilledema. Pediatr Neurol 2010;42(1):56-8. PMID 20004864
13: Bille B. Migraine and school children. Acta Paediatr Scand 1962;51(Suppl 136):1-151.
14: Bille B. A 40-year follow-up of school children with migraine. Cephalalgia 1997;17(4):488-91; discussion 487. PMID 9209767
15: Blair HA. Fremanezumab: pediatric first approval. Paediatr Drugs 2025;27(6):771-5. PMID 41021201
16: Borner C, Urban G, Beaulieu LD, et al. The bottom-up approach: non-invasive peripheral neurostimulation methods to treat migraine: A scoping review from the child neurologist's perspective. Eur J Paediatr Neurol 2021;32:16-28. PMID 33743386
17: Borsook D, Erpelding N, Lebel A, et al. Sex and the migraine brain. Neurobiol Dis 2014;68:200-14. PMID 24662368
18: Bruijn J, Duivenvoorden H, Passchier J, et al. Medium-dose riboflavin as a prophylactic agent in children with migraine: a preliminary placebo-controlled, randomised, double-blind, cross-over trial. Cephalalgia 2010;30(12):1426-34. PMID 20974610
19: Charles AC, Digre KB, Goadsby PJ, Robbins MS, Hershey A, American Headache Society. Calcitonin gene-related peptide-targeting therapies are a first-line option for the prevention of migraine: An American Headache Society position statement update. Headache 2024;64(4):333-41. PMID 38466028
20: Cobb-Pitstick KM, Hershey AD, O'Brien HL, et al. Factors influencing migraine recurrence after infusion and inpatient migraine treatment in children and adolescents. Headache 2015;55(10):1397-403. PMID 26345726
21: Croop R, Lipton RB, Kudrow D, et al. Oral rimegepant for preventive treatment of migraine: a phase 2/3, randomised, double-blind, placebo-controlled trial. Lancet 2021;397(10268):51-60. PMID 33338437
22: Curtain RP, Smith RL, Ovcaric M, et al. Minor head trauma-induced sporadic hemiplegic migraine coma. Pediatric Neurology 2006;34:329-32. PMID 16638514
23: Dodick DW. Migraine. Lancet 2018;391(10127):1315-30. PMID 29523342
24: Dooley J, Bagnell A. The prognosis and treatment of headaches in children--a ten year follow-up. Can J Neurol Sci 1995;22:47-9. PMID 7750073
25: Dowling MM, Noetzel MJ, Rodeghier MJ, et al. Headache and migraine in children with sickle cell disease are associated with lower hemoglobin and higher pain event rates but not silent cerebral infarction. J Pediatr 2014;164(5):1175-80.e1. PMID 24529619
26: Esparham A, Stark-Inbar A, Jekel L, et al. Acute treatment of migraine in adolescents: real-world analysis of remote electrical neuromodulation (REN). Pediatr Neurol 2023;142:51-5. PMID 36931109
27: Falla K, Kuziek J, Mahnaz SR, Noel M, Ronksley PE, Orr SL. Anxiety and depressive symptoms and disorders in children and adolescents with migraine: a systematic review and meta-analysis. JAMA Pediatr 2022;176(12):1176-87. PMID 36315158
28: Gelfand AA, Poland G. Migraine treatment and COVID-19 vaccines: no cause for concern. Headache 2021;61(3):409-11. PMID 33543775
29: Genadry KC, Monuteaux MC, Neuman MI, Lowe DA, Lee LK. Disparities and trends in migraine management in pediatric emergency departments, 2009-19. Acad Pediatr 2023;23(1):76-84. PMID 35609775
30: Goenka A, Chikkannaiah M, Fonseca LD, Kumar G. Peripheral nerve blocks: a tool for inpatient pediatric status migrainosus. Pediatr Neurol 2023;138:81-6. PMID 36423569
31: Goncalves D, Meireles J, Rocha R, Sampaio M, Leão M. Syndrome of transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL): a pediatric case report. J Child Neurol 2013;28:1661-3. PMID 23076427
32: Gormley P, Anttila V, Winsvold BS, et al. Meta-analysis of 375,000 individuals identifies 38 susceptibility loci for migraine. Nat Genet 2016;48(8):856-66. PMID 27322543
33: Gotra P, Bhardwaj N, Ludhiadch A, Singh G, Munshi A. Epilepsy and migraine shared genetic and molecular mechanisms: focus on therapeutic strategies. Mol Neurobiol 2021;58(8):3874-83. PMID 33856647
34: Graff DM, McDonald MJ. Auricular acupuncture for the treatment of pediatric migraines in the emergency department. Pediatr Emerg Care 2018;34(4):258-62. PMID 27139637
35: Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. As of 2016, the full headache classification can be accessed digitally: https://www.ichd-3.org. Cephalalgia 2018;38(1):1-211. PMID 29368949
36: Hershey AD, Powers SW, Vockell AL, LeCates S, Kabbouche MA, Maynard MK. PedMIDAS: development of a questionnaire to assess disability of migraines in children. Neurology 2001;57(11):2034-9. PMID 11739822
37: Hershey AD, Shmuely S, Stark-Inbar A, et al. Patterns, barriers, and preferences of treating migraine within the school setting: a survey study of students. Children (Basel) 2024;11(11):1286. PMID 39594861
38: Honig PJ, Charney EB. Children with brain tumor headaches. Distinguishing features. Am J Dis Child 1982;136:121-4. PMID 7064925
39: Hsu JW, Chen LC, Huang KL, et al. The influence of sex on major psychiatric comorbidities and parental psychiatric disorders in 22,698 children and adolescents with ICD-9-CM-based autism spectrum disorder. Eur Arch Psychiatry Clin Neurosci 2024;274(1):19-25. PMID 36459229
40: Huang X, Jiang Y, Huang X, et al. The association between allergic diseases and migraine: a systematic review and meta-analysis. Int Arch Allergy Immunol 2025;186(12):1166-75. PMID 40188820
41: Ihara K, Pike CW, Hui G, et al. Estrogen exposure from modern contraceptives and vascular risk in women with migraine: A nationwide electronic medical record database study. Cephalalgia 2025;45(12):3331024251404924. PMID 41406065
42: Isler H. Historical background. In: Olesen J, Tfelt-Hansen P, Welch KM, editors. The headaches. New York: Raven Press Ltd, 1993:1-8.
43: Jansen SC, van Dusseldorp M, Bottema KC, Dubois AE. Intolerance to dietary biogenic amines: a review. Ann Allergy Asthma Immunol 2003;91:233-40. PMID 14533654
44: Jimenez XF, Sundararajan T, Covington EC. A systematic review of atypical antipsychotics in chronic pain management: olanzapine demonstrates potential in central sensitization, fibromyalgia, and headache/migraine. Clin J Pain 2018;34(6):585-91. PMID 29077621
45: Kan L, Nagelberg J, Maytal J. Headaches in a pediatric emergency department: etiology, imaging, and treatment. Headache 2000;40:25-9. PMID 10759899
46: Kandt RS, Caoili AQ, Lorentz WB, Elster AD. Hypertensive encephalopathy in children: neuroimaging and treatment. J Child Neurol 1995;10:236-9. PMID 7642896
47: Kandt RS, Goldstein GW. Steroid-responsive ophthalmoplegia in a child: diagnostic considerations. Arch Neurol 1985;42:589-91. PMID 4004604
48: Kandt RS, Levine RM. Headache and acute illness in children. J Child Neurol 1987;2:22-7. PMID 3624825
49: Karian V, Morton H, Schefter ZJ, et al. OnabotulinumtoxinA for pediatric migraine. Pain Manag Nurs 2023;24(6):610-16. PMID 37183070
50: Kelley SA, Hartman AL, Kossoff EH. Comorbidity of migraine in children presenting with epilepsy to a tertiary care center. Neurology 2012;79(5):468-73. PMID 22744668
51: Kinast M, Leuders H, Rothner AD, Erenberg G. Benign focal epileptiform discharges and childhood migraine. Neurology 1982;32:1309-11. PMID 6813763
52: Koechlin H, Kossowsky J, Lam TL, et al. Nonpharmacological interventions for pediatric migraine: a network meta-analysis. Pediatrics 2021;147(4):e20194107. PMID 33688031
53: Lateef TM, Cui L, Nelson KB, Nelson KB, Nakamura EF, Merikangas KR. Physical comorbidity of migraine and other headaches in US adolescents. J Pediatr 2012;161(2):308-13. PMID 22381023
54: Levinsky Y, Zeharia A, Eidlitz-Markus T. Cephalic cutaneous allodynia in children and adolescents with migraine of short duration: a retrospective cohort study. Cephalalgia 2019;39(1):61-7. PMID 29732930
55: Lewis D, Winner P, Saper J, et al. Randomized, double-blind, placebo-controlled study to evaluate the efficacy and safety of topiramate for migraine prevention in pediatric subjects 12 to 17 years of age. Pediatrics 2009;123(3):924-34. PMID 19255022
56: Lewis DW, Ashwal S, Dahl G, et al. Practice parameter: evaluation of children and adolescents with recurrent headaches: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology 2002;59(4):490-8. PMID 12196640
57: Linder SL, Mathew NT, Cady RK, Finlayson G, Ishkanian G, Lewis DW. Efficacy and tolerability of almotriptan in adolescents: a randomized, double-blind, placebo-controlled trial. Headache 2008;48(9):1326-36. PMID 18484981
58: Lopes CF, Dos Santos TP, Martins IP. Prognosis of headache in children: a 25-year follow-up. Childs Nerv Syst 2022;38(3):619-26. PMID 35059785
59: Mar S, Kelly JE, Isbell S. Aung WY, Lenox J, Prensky A. Prevalence of white matter lesions and stroke in children with migraine. Neurology 2013;81:1387-91. PMID 24042095
60: McGinley JS, Savord A, Buse DC, Wirth RJ, Lipton RB. Longitudinal assessment of comorbidities and co-occurring conditions in adolescents with migraine: a secondary analysis of the National Longitudinal Study of Adolescent to Adult Health (Add Health). Headache 2023;63(2):243-54. PMID 36794298
61: McHarg ML, Shinnar S, Rascoff H, Walsh CA. Syncope in childhood. Pediatr Cardiol 1997;18:367-71. PMID 9270107
62: Morishita N, Yamanaka G, Go S, Takeshita M, Tsutsumi N. Pediatric retinal migraine: a case report and literature review. Pediatr Int 2022;64(1):e14922. PMID 34897886
63: Mortimer MJ, Kay J, Jaron A. Epidemiology of headache and childhood migraine in an urban general practice using Ad Hoc, Vahlquist and IHS criteria. Dev Med Child Neurol 1992;34(12):1095-101. PMID 1451940
64: Mortimer MJ, Kay J, Jaron A. Clinical epidemiology of childhood abdominal migraine in an urban general practice. Dev Med Child Neurol 1993;35:243-8. PMID 8462757
65: Nilles C, Williams JV, Patten SB, Pringsheim TM, Orr SL. Lifestyle factors associated with frequent recurrent headaches in children and adolescents: a Canadian population-based study. Neurology 2024;102(6):e209160. PMID 38417103
66: Onofri A, Pensato U, Rosignoli C, et al. Primary headache epidemiology in children and adolescents: a systematic review and meta-analysis. J Headache Pain 2023;24(1):8. PMID 36782182
67: Orr SL, Turner A, Kabbouche MA, et al. Predictors of short-term prognosis while in pediatric headache care: an observational study. Headache 2019;59(4):543-55. PMID 30671933
68: Orr SL, Venkateswaran S. Nutraceuticals in the prophylaxis of pediatric migraine: Evidence-based review and recommendations. Cephalalgia 2014;34(8):568-83. PMID 24443395
69: Oskoui M, Pringsheim T, Billinghurst L, et al. Practice guideline update summary: Pharmacologic treatment for pediatric migraine prevention: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology 2019a;93(11):500-9. PMID 31413170
70: Oskoui M, Pringsheim T, Holler-Managan Y, et al. Practice guideline update summary: Acute treatment of migraine in children and adolescents: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology 2019b;93(11):487-99. PMID 31413171
71: Pascarella A, Marsico O, Abelardo D, et al. Epilepsy and migraine: a diagnostic and therapeutic challenge. Front Pharmacol 2025;16:1649543. PMID 40949139
72: Patterson-Gentile C, Szperka CL. The changing landscape of pediatric migraine therapy: a review. JAMA Neurol 2018;75(7):881-7. PMID 29532087
73: Powers SW, Coffey CS, Chamberlin LA, et al. Trial of amitriptyline, topiramate, and placebo for pediatric migraine. N Engl J Med 2017;376(2):115-24.** PMID 27788026
74: Puledda F, Goadsby PJ, Prabhakar P, et al. Treatment of disabling headache with greater occipital nerve injections in a large population of childhood and adolescent patients: a service evaluation. J Headache Pain 2018;19(1):5. PMID 29340791
75: Quispe-Vicuna C, Soriano-Moreno DR, De-Los-Rios-Pinto A, et al. Association between weight status and migraine in the paediatric population: a systematic review and meta-analysis. Front Neurol 2023;14:1225935. PMID 38033769
76: Raieli V, Pitino R, Giordano G, et al. Migraine in a pediatric population: a clinical study in children younger than 7 years of age. Dev Med Child Neurol 2015;57(6):585-8. PMID 25586426
77: Rajapakse T, Buchhalter J. The borderland of migraine and epilepsy in children. Headache 2016;56(6):1071-80. PMID 27103497
78: Raskin NH, Appenzeller O. Headache. Major Probl Intern Med. Philadelphia: W.B. Saunders, 1980;19:1-244.
79: Russo A, Iannone LF, Orologio I, et al. Safety of onabotulinumtoxin-a for chronic migraine during pregnancy and breastfeeding: a narrative review. Toxins (Basel) 2025;17(4):192. PMID 40278690
80: Sheridan DC, Laurie A, Pacheco S, et al. Relative effectiveness of dopamine antagonists for pediatric migraine in the emergency department. Pediatr Emerg Care 2018;34(3):165-8. PMID 27176905
81: Slater SK, Nelson TD, Kabbouche MA, et al. A randomized, double-blinded, placebo-controlled, crossover, add-on study of CoEnzyme Q10 in the prevention of pediatric and adolescent migraine. Cephalalgia 2011;31(8):897-905. PMID 21586650
82: Stang PE, Osterhaus JT. Impact of migraine in the United States: data from the National Health Interview Survey. Headache 1993;33:29-35. PMID 8436495
83: Stang PE, Yanagihara PA, Swanson JW, et al. Incidence of migraine headache: a population-based study in Olmsted County, Minnesota. Neurology 1992;42:1657-62. PMID 1513451
84: Stensland SO, Zwart JA, Larsen TW, Dyb G. The headache of terror: a matched cohort study of adolescents from the Utøya and the HUNT Study. Neurology 2018;90(2):e111-8. PMID 29237795
85: Stewart WF, Bigal ME, Kolodner K, et al. Familial risk of migraine: variation by proband age at onset and headache severity. Neurology 2006;66:344-8. PMID 16476932
86: Stubberud A, Varkey E, McCrory DC, Pedersen SA, Linde M. Biofeedback as prophylaxis for pediatric migraine: A meta-analysis. Pediatrics 2016;138(2). pii: e20160675. PMID 27462067
87: Sun Q, Xie H, Hao L, et al. Global epidemiology and burden of migraine in children and adolescents from 1990 to 2021: insights from the Global Burden of Disease Study 2021. J Pain Res 2025;18:5265-81. PMID 41084528
88: Szperka CL, VanderPluym J, Orr SL, et al. Recommendations on the use of anti-CGRP monoclonal antibodies in children and adolescents. Headache 2018;58:1501-697. PMID 30324723
89: Torriero R, Capuano A, Mariani R, et al. Diagnosis of primary headache in children younger than 6 years: a clinical challenge. Cephalalgia 2017;37(10):947-54. PMID 27432612
90: Ursitti F, Valeriani M. Migraine in childhood: gender differences. Eur J Paediatr Neurol 2023;42:122-5. PMID 36634526
91: Vahlquist B, Hackzell G. Migraine of early onset. Acta Paediatr 1949;38:622-36.
92: Vanmolkot KR, Stroink H, Koenderink JB, et al. Severe episodic neurological deficits and permanent mental retardation in a child with a novel FHM2 ATP1A2 mutation. Ann Neurol 2006;59:310-4. PMID 16437583
93: Verrotti A, Carotenuto M, Altieri L, et al. Migraine and obesity: metabolic parameters and response to a weight loss programme. Pediatr Obes 2015;10(3):220-5. PMID 24990114
94: Voci A, Bruni O, Ferilli MA, et al. Sleep disorders in pediatric migraine: a questionnaire-based study. J Clin Med 2021;10(16):3575. PMID 34441871
95: Wagner JL, Wilson DA, Smith G, et al. Neurodevelopmental and mental health comorbidities in children and adolescents with epilepsy and migraine: a response to identified research gaps. Dev Med Child Neurol 2015;57(1):45-52. PMID 25088717
96: Wang SJ, Fuh JL, Lu SR. Chronic daily headaches in adolescents: an 8-year follow-up study. Neurology 2009;73(6):416-22. PMID 19605771
97: Winner PK, Kabbouche M, Yonker M, Wangsadipura V, Lum A, Brin MF. A randomized trial to evaluate onabotulinumtoxina for prevention of headaches in adolescents with chronic migraine. Headache 2020 ;60(3):564-75. PMID 32037549
98: Wober-Bingol C. Epidemiology of migraine and headache in children and adolescents. Curr Pain Headache Rep 2013;17(6):341. PMID 23700075
99: Wong HT, Khan R, Buture A, Khalil M, Ahmed F. OnabotulinumtoxinA treatment for chronic migraine in pregnancy: an updated report of real-world headache and pregnancy outcomes over 14 years in Hull. Cephalalgia 2025;45(5):3331024251327387. PMID 40326040
100: Wu X, Zhuang J. Association between migraine and epilepsy: a meta-analysis. Front Neurol 2024;14:1276663. PMID 38249732
101: Yeates KO, Räisänen AM, Premji Z, et al. What tests and measures accurately diagnose persisting post-concussive symptoms in children, adolescents and adults following sport-related concussion? A systematic review. Br J Sports Med 2023;57(12):780-8. PMID 37316186
102: Ziegler DK, Hur YM, Bouchard TJ Jr, Hassanein RS, Barter R. Migraine in twins raised together and apart. Headache 1998;38(6):417-22. PMID 9664744

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Yasmine Elhefnawy MD FAAP

Dr. Elhefnawy of Boston Medical Center has no relevant financial relationships to disclose.
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Editor

Alcy R Torres MD FAAP

Dr. Torres of Boston Medical Center and Boston University Chobanian and Avedisian School of Medicine has no relevant financial relationships to disclose.
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Former Authors

Michael V Johnston MD†
Raymond S Kandt MD
Ann Tilton MD

Patient Profile

Age range of presentation: 1 month to 18 years
Sex preponderance: Prepubertal: no sex preponderance

postpubertal female>male, >3:1
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Migraine with aura [classical migraine]: G43.1

Migraine without aura [common migraine]: G43.0
ICD-11: Migraine without aura: 8A80.0

Migraine with aura: 8A80.1

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Migraine in childhood

Associated Disorders

Acute confusional migraine
Alice in Wonderland syndrome
Migraine with aura
Migraine without aura

Differential Diagnosis

structural brain lesions
concurrent illness
minor head trauma
brain tumor
vascular malformation
- hydrocephalus
- pseudotumor cerebri
- hypertensive encephalopathy
- head trauma with posttraumatic cerebrovascular disease
- head trauma without posttraumatic cerebrovascular disease
- inflammatory disorders
- low-grade viral meningoencephalitis
- connective tissue disease
- mitochondriopathies
- mitochondrial encephalopathy with lactic acidosis and strokelike episodes
- metabolic disorders
- heterozygous ornithine transcarbamylase deficiency
- chronic daily headaches
- medication-overuse headaches
- seizures
- complex partial seizures
- benign occipital epilepsy
- epilepsy
- abdominal disorders

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- Transient global amnesia

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Migraine

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Migraine in childhood

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

Drug treatment

Nonpharmacologic treatments

Special considerations

Pregnancy

Anesthesia

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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