Headache in children: overview and treatment approaches …

Nina F. Schor MD PhD

Headache & Pain

Updated 12.02.2023
Released 03.15.2010
Expires For CME 12.02.2026

Headache in children: overview and treatment approaches

Author: Nina F. Schor MD PhD

See Contributor Disclosures

Editor: Stephen D Silberstein MD

Headache in children: overview and treatment approaches

In This Article

Quick Link

Introduction

Overview

Primary headaches, particularly those that are recurrent or chronic, in childhood are increasingly being recognized as a significant neurologic health problem. The high incidence and prevalence of headaches in the pediatric population has a significant impact on children and their families. Migraine remains under-recognized, under-diagnosed, and ultimately under- or inappropriately treated in this population; this has potential long-term consequences with regards to disease progression. The author has addressed the key issues of: (1) using practical diagnostic criteria for clinical practice, (2) which acute medication should be chosen, (3) when to use preventive therapy in childhood, and (4) which preventive therapies have the best therapeutic index. This article serves as a quick reference for the diagnosis and management of primary headache disorders in children and adolescents. Effective intervention may prevent progression and lifelong consequences, including the development of comorbidities. Early diagnosis and an integrative treatment approach are essential to minimize the impact on a child's quality of life.

Key points

	• According to the American Migraine Prevalence and Prevention study (AMPP), the migraine prevalence in adolescents is 14%.
	• The first triptan to receive United States Food and Drug Administration approval for the acute treatment of adolescent migraine pain was almotriptan (12.5 mg tablet).
	• Amitriptyline (1 mg per kilogram of body weight per day), topiramate (2 mg per kilogram per day), and placebo had equivalent (50% to 60%) efficacy in reduction of headache frequency by 50% in children and adolescents 8 to 17 years of age with migraine.

Epidemiology and classification

In a metaanalysis of 64 cross-sectional studies on headaches in children and adolescents performed over a 25-year period with an aggregate population of 227,249 children from 32 different countries, the estimated mean prevalence of headache was 54.4%, and the estimated mean prevalence of migraine was 9.1% (92). In a study performed on 7643 school children in Austria, 44.3% of whom filled out the study questionnaires, prevalence and attributable burden of all headache, undifferentiated headache, migraine, tension-type headache and headache on greater than or equal to 15 days per month (chronic headache) were assessed using the Headache-Attributed Restriction, Disability, Social Handicap and Impaired Participation questionnaire for children and adolescents and the KIDSCREEN questionnaire for health-related quality of life (55). The 1-year prevalence of headache was 75.7%, increasing with age and higher in girls (82.1%) than in boys (67.7%; p < 0.001). Undifferentiated headache, migraine, tension-type headache, and chronic headache were reported by 26.1%, 24.2%, 21.6%, and 3.0% of participants, respectively. Attributable burden was high, with 42% of those with headache experiencing restrictions in daily activities. Medication use (50% overall) was highest in chronic headache (67%) and still considerable in undifferentiated headache (29%). Health-related quality of life was reduced for all headache types except undifferentiated headache. Participants in single parent or blended families had a higher probability of migraine (respectively, OR 1.5, p < 0.001; OR 1.5, p < 0.01).

Using the Pediatric Migraine Disability Assessment (PedMIDAS) questionnaire, an analogous school-based study performed in Norway on 493 adolescents (12 to 18 years of age) revealed the 1-year prevalence of any headache, migraine, probably migraine, and tension-type headache was 88%, 23%, 15%, and 58%, respectively (33). Interestingly, 9% of participants had more than one type of headache, and the duration, rather than the frequency, of individual headaches correlated best with the magnitude of the burden perceived by the participants. Participants with headaches lost up to nine days of activity each year due to their headaches. A study of 7361 children (age 7 to 18 years) in Hungary revealed the 1-year prevalence of migraine to be 12.5%, but requiring a headache duration of four hours in 15- to 18-year-olds, and 1 hour below 15 years of age lowered the 1-year prevalence to 9.1% (30). Another study of 2466 children (ages 3 to 18) presenting to a single hospital in South Korea demonstrated an apparent 3-fold increase in the number of children presenting to the hospital with headache between 2005 and 2016 (27). However, over that period, classification criteria transitioned from International Classification of Headache Disorders-2 (ICHD-) to ICHD-3, and it is not clear what role this transition, differential patient and family reporting bias, and/or changes in hospital utilization and outpatient census may have played in this increase. Interestingly, all of the increase was accounted for by changes in frequency of nonmigraine, nontension-type headaches.

The American Migraine Prevalence and Prevention study (AMPP) used a validated headache questionnaire that was mailed to 120,000 households representative of the United States population. The headache questionnaire was developed to investigate the epidemiology of migraine and the medical treatments utilized (87; 09; 71). This study included 162,576 participants with a migraine prevalence of 5.6% in males and 17.1% in females. Of the 18,968 individuals that met the ICHD-2 criteria for migraine, 823 were between the ages of 12 and 17 years. A subanalysis of AMPP restricted to adolescents found a 1-year ICHD-2 migraine prevalence of 6.3% to 5% in boys and 7.7% in girls (87; 04). For acute treatment, they found that 49.0% used over-the-counter remedies, 20.1% used prescription remedies, and 28.8% used both. The adolescents were more likely to use over-the-counter remedies (59.3%) compared to prescription medications (16.5%) or a combination (22.1%) (87; 04). The majority of adolescents (63.7%) never used preventative medication for migraine, with just 10.6% reporting current use. One of the many observations in this study was the effect of the socioeconomic status and the familial pattern of migraine. If there was a family history of migraine, there was no effect on the prevalence due to the socioeconomic status. However, when there was not a family history, the odds ratio of having migraine increased with a lower socioeconomic status. Further analysis is needed to explain the balance between the genetic and environmental components of migraine.

The relationship of female gender, particularly after puberty, to increased incidence of migraine is long-established. The associated symptom profile also differs significantly between female and male adolescents with migraine, with adolescent girls having non-headache migraine-associated symptoms of all kinds more frequently than adolescent boys (06). Studies also suggest an association between obesity and migraine and provide less robust evidence for an association between obesity and tension-type headache (51).

International Classification of Headache Disorders (ICHD-1) criteria were initially developed to advance the clinical and scientific study of headache but were criticized for a lack of sensitivity and specificity in diagnosing pediatric headaches, especially migraine. Some of the suggested modifications were adopted in the footnotes to the criteria for migraine in the second edition of the International Classification of Headache Disorders (ICHD-2) (19). This improved the sensitivity from the ICHD-1, yet it remained incomplete (24).

A subsequent iteration of this classification system, ICHD-3, is currently in use, and Table 1 presents its diagnostic criteria for migraine without aura (1.1) and migraine with aura (1.2). Note that, in section 1.1, footnote 3 and the comments that follow it, ICHD-3 has addressed the concerns raised with regard to the short duration, the higher likelihood of a bilateral location, and the difficulty in describing the headache features and associated symptoms seen in pediatric migraines (84).

In a study evaluating the sensitivity of ICHD-2 criteria for pediatric migraine, headache characteristics in 260 patients aged 18 years and younger diagnosed with migraine were summarized from standard intake questionnaires, and physician-assigned clinical diagnoses were used as the gold standard for assessing the validity of ICHD-2 criteria (24; 03). Among the 260 patients clinically diagnosed with migraine, 70.4% met ICHD-1 criteria, and 61.9% met ICHD-2 criteria, including the 4- to 72-hour headache duration. When a 1- to 72-hour duration specified in the ICHD-3 footnote is used, 71.9% met the criteria. The most common reasons that patients’ headaches did not meet the standard criteria were the requirements for unilateral location, headache duration, and number of associated symptoms. When the ICHD-2 criteria were modified to the criteria now found in ICHD-3 (Table 1), including bilateral headache, headache duration of 1 to 72 hours, and nausea and/or vomiting plus two of five other associated symptoms (photophobia, phonophobia, difficulty thinking, lightheadedness, or fatigue), the sensitivity for diagnosing migraine improved to 84.4% (24; 70; 03). The suggestion has been made that childhood syndromes associated with a family history of migraine, like neck-tongue syndrome, be brought to the attention of the neurology community (01).

New tools and biomarkers need to be developed and integrated into the diagnostic process. Researchers have begun to examine additional tools for children to augment these criteria and include the use of drawings for the pediatric population (75; 74; 34; 09). Advanced imaging techniques can distinguish migraine from tension headache in children in the mechanistic research setting. For example, children with either tension-type or migraine headache demonstrate increased ADC signal in the hippocampus and brainstem on diffusion-weighted MRI scans relative to age-matched controls, whereas only children with migraine demonstrate increased ADC signal in the thalamus (65). However, imaging is not recommended for children with uncomplicated, primary headache. Symptoms and/or signs indicative of secondary headache (eg, papilledema, headache with cough or Valsalva, nocturnal or early morning headache) should trigger performance of imaging studies (07).

Tension-type headaches are generally considered mild, recurrent headaches, and many features of tension-type headaches are the opposite of migraine. Epidemiology studies have varied on the prevalence of these headaches in children due to the present criteria. One study in which 466 of 4812 children and adolescents in Shanghai, China had experienced at least one headache in the three months preceding the study indicated that 29.1% of the participants with headache had tension-type headache (28).

Cluster headaches can begin at any age, but the mean age of onset is approximately the late twenties. Childhood and adolescent onset of cluster headaches has been reported, but these early-onset cases appear to be rare. Only 18% of patients had their onset of cluster headaches prior to 18 years of age, and 2% began before 10 years of age (49). In the study in China reported by Jin and colleagues, only 6.2% of the 466 children with recent headache met ICHD-2 criteria for cluster headache (28).

With the first occurrence of headache in a child, differential diagnosis includes secondary (ie, symptomatic) headaches for which making the diagnosis depends critically on a high index of suspicion and discovery and treatment of the underlying primary cause (Table 2).

Table 1. Migraine Without and With Aura (ICHD-3 – 1.1, 1.2)

1.1 Migraine without aura
A. At least five attacks fulfilling criteria B through D B. Headache attacks lasting 4 to 72 hours (untreated or unsuccessfully treated)
		- Sleep is also considered part of the headache duration. (Footnote 2) - In children, 1 to 72 hours is allowed. If between 1 and 2 hours daily, corroboration is required. (Footnote 3)
C. Headache has at least two of the following characteristics:
	1. Unilateral location
		- Bilateral headache is most common in children. Most common in frontal area. (Footnote 5,6) - Exclusive occipital location is worrisome based on meta-analysis. (Footnote 6)
	2. Pulsating quality 3. Moderate or severe pain intensity 4. Aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
D. During headache at least one of the following occurs:
	1. Nausea and/or vomiting 2. Photophobia and phonophobia
E. Not accounted for by another ICD-3 diagnosis
Notes:
1. One or a few migraine attacks may be difficult to distinguish from symptomatic migraine-like attacks. Furthermore, the nature of a single or a few attacks may be difficult to understand. Therefore, at least five attacks are required. Individuals who otherwise meet criteria for 1.1 Migraine without aura but have had fewer than five attacks should be coded 1.5.1 Probable migraine without aura.
2. When the patient falls asleep during migraine and wakes up without it, duration of the attack is reckoned until the time of awakening.
3. In children and adolescents (aged under 18 years), attacks may last 2-72 hours (the evidence for untreated durations of less than two hours in children has not been substantiated).

Comments

Migraine headache in children and adolescents (aged under 18 years) is more often bilateral than is the case in adults; unilateral pain usually emerges in late adolescence or early adult life. Migraine headache is usually frontotemporal. Occipital headache in children is rare and calls for diagnostic caution. A subset of otherwise typical patients have facial location of pain, which is called “facial migraine” in the literature; there is no evidence that these patients form a separate subgroup of migraine patients. In young children, photophobia and phonophobia may be inferred from their behavior. Migraine attacks can be associated with cranial autonomic symptoms and symptoms of cutaneous allodynia.

Migraine without aura often has a menstrual relationship. ICHD-3 (beta) offers criteria for A1.1.1 Pure menstrual migraine and A1.1.2 Menstrually-related migraine, but in the Appendix because of uncertainty over whether they should be regarded as separate entities.

Very frequent migraine attacks are now distinguished as 1.3 Chronic migraine. When there is associated medication overuse, both diagnoses, 1.3 Chronic migraine and 8.2 Medication-overuse headache, should be applied. 1.1 Migraine without aura is the disease most prone to accelerate with frequent use of symptomatic medication.

Regional cerebral blood flow imaging shows no changes suggestive of cortical spreading depression (CSD) during attacks of migraine without aura, although blood flow changes in the brainstem may occur, as may cortical changes secondary to pain activation. This contrasts with the pathognomonic spreading oligemia of migraine with aura. Although the bulk of the literature suggests that CSD does not occur in migraine without aura, some recent studies disagree. Furthermore, it has been suggested that glial waves or other cortical phenomena may be involved in migraine without aura. The messenger molecules nitric oxide (NO), 5-hydroxytryptamine (5-HT) and calcitonin gene-related peptide (CGRP) are involved. Although the disease was previously regarded as primarily vascular, the importance of sensitization of pain pathways, and the possibility that attacks may originate in the central nervous system, have gained increasing attention over the last decades. At the same time, the circuitry of migraine pain, the trigeminovascular system, and several aspects of its neurotransmission peripherally and in the trigeminal nucleus caudalis, the central mesencephalic grey and the thalamus, have been recognized. New highly receptor-specific acute medications such as the triptans, which are 5HT1B/D receptor agonists, 5-HT1F receptor agonists and CGRP receptor antagonists have demonstrated efficacy in the acute treatment of attacks. Because of their high receptor-specificity, their mechanism of action provides new insight into migraine mechanisms. It is now clear that migraine without aura is a neurobiological disorder; clinical as well as basic neuroscience has advanced our knowledge of migraine mechanisms, and continues to do so.

1.2 Migraine with aura
	1.2.1 Migraine with typical aura
		1.2.1.1 Typical aura with headache 1.2.1.2 Typical aura without headache
	1.2.2 Migraine with brainstem aura 1.2.3 Hemiplegic migraine
		1.2.3.1 Familial hemiplegic migraine (FHM)
			1.2.3.1.1 Familial hemiplegic migraine type 1 (FHM1) 1.2.3.1.2 Familial hemiplegic migraine type 2 (FHM2) 1.2.3.1.3 Familial hemiplegic migraine type 3 (FHM3) 1.2.3.1.4 Familial hemiplegic migraine, other loci
		1.2.3.2 Sporadic hemiplegic migraine (SHM)
	1.2.4 Retinal migraine
From: (International Headache Society Classification ICHD-3)

Table 2. Differentiating Characteristics of Common Primary and Secondary Headache Syndromes

	Migraine	Tension-type headache	Increased intracranial pressure with or without mass lesion	Subarachnoid hemorrhage	Sinusitis	Infectious meningitis
WHO	Peaks in adolescence and in paramenopausal women; M = F, prepubertal; F > M, postpubertal; family history positive	M = F; school age, adolescence, adult; uncommonly associated bony cervical abnormalities	Any age; those predisposed to pseudotumor, tumor, intraparenchymal intracranial bleeding	Any age	Ethmoid and maxillary sinusitis – can be any age, but usually school age through adulthood; frontal sinusitis – after 7 years of age; sphenoid sinusitis – in late adolescence or adulthood	Any age
WHAT	Sleep- or food-deprivation; stress; hormonal changes; accompanied by nausea, vomiting, photo-/phonophobia; osmophobia; sometimes preceded by aura; sometimes aura alone (without headache); childhood migraine equivalents often without headache; often made better by sleep	Stress; sustained neck and upper back posture; bruxism	Often not particularly severe; dull, achy character; worse with supine position; better when upright; often accompanied by early morning vomiting	Severe; intense; underlying predisposition to hemorrhage (eg, aneurysms, trauma, hypertension, coagulation, and platelet disorders)	Achy, pressure; made worse by side-to-side forceful head movement; made worse with forceful sniffing; accompanied by nasal congestion and discharge, especially if purulent; may be associated with fever; percussion over sinuses elicits tenderness	Wide range of severity depending on infectious agent; associated with fever, meningismus, photophobia without phonophobia or osmophobia
WHERE	More often bilateral in children than adults; often unilateral by late adolescence	Band-like around head; at occipitonuchal junction	Diffuse, whole head; sometimes nuchal component	Pain may start focal; becomes diffuse; if patient upright, can track down neck and back	Over relevant sinuses	Diffuse over head; neck pain prominent
WHEN	Escalating intensity over minutes; parabolic time course of intensity; rarely awakens child from sleep; if present first thing on awakening in morning, gets worse once child is up and about	Escalating over hours; worse later in the day; sustained intensity sometimes for days	Insidious onset; awakens child from sleep; worse on first awakening than on proceeding through day	Instantaneously at its worst; may get better over seconds to minutes – particularly if patient is upright	Insidious onset; can worsen over days	Varies in time course depending on infectious agent
WHY	Genetics; hormonal; deviation from routine; stress	Stress; muscle tension from sustained posture	Abnormal CSF dynamics; mass lesion	Underlying reason or source for bleeding	Infection; anatomic and/or immunologic predisposition	Infection
HOW	Roles for chemokines, cation channels, neuro- and vasoreactivity	Muscle contraction	Impingement or stretch on meninges, ependyma, or vessel walls	Impingement or stretch on meninges, ependyma, or vessel walls; chemical inflammation of meninges and ependyma	Stretch on lining of sinuses; inflammation from infection	Inflammation of meninges

Impact

Pediatric migraines can have a significant impact in the lives of children and their parents. The impact of a migraine can be measured by both the disability to participate desired in activities and the effect on the individual’s quality of life. Several tools have been developed to evaluate the disability of migraine. In adults, this can be addressed by using the MIDAS (Migraine Disability Assessment) tool (78; 77; 76; 43). The MIDAS was not adequate for pediatrics due to the differences in lifestyles of children; subsequently, the PedMIDAS was developed (21). The scoring system was centered on patient-based disability and has a higher scoring range than the MIDAS because children are likely to miss out on school, home, and social activities more frequently than adults (23). PedMIDAS can be used clinically to identify the impact of migraine in the individual pediatric patient as well as their response to treatment. For example, a study from Izmir, Turkey used the PedMIDAS effectively to evaluate and compare prophylactic treatment of migraine in children with topiramate, propranolol, and flunarizine (81).

The impact of headache can also be assessed by measuring an individual’s quality of life. The Short Form-20 has been used for assessing quality of life in adults (53). In pediatric headache patients, a useful tool is the PedsQL 4.0 (83). PedsQL is a 23-question tool with separate, developmentally appropriate versions for age with opportunity for parent and child response. PedsQL is able to identify a significant impact of the quality of life for pediatric headache patients aged 5 to 17 years (60). When the PedsQL was used to compare rheumatologic diseases, oncologic diseases, cardiac diseases, and migraine, it demonstrated an impact on quality of life similar in all disease states as related to emotional and school development. Some studies have raised the question of whether recurrent migraines have negative effects on specific aspects of cognition and metacognition or the ability to monitor and control one’s own cognitive processes (13; 45; 79).

One study utilized the Strengths and Difficulties Questionnaire to discern and compare emotional and behavioral comorbidities in children with migraine or tension headache (68). Children with migraine had higher levels of emotional difficulties than strengths and higher emotional difficulties scores than children with tension headache. Scores for behavioral difficulties were not significantly different between children with migraine and children with tension headache. In children with migraine, the magnitude of the emotional difficulties score correlated with the duration of treatment (whether pharmacological or non-pharmacological) required to achieve 50% reduction in headache frequency.

Treatment

A comprehensive integrative treatment plan for pediatric headaches includes acute, preventative, and bio-behavioral therapy. A practice parameter reviewed the available evidence for both acute and preventative therapies in detail as related to the pediatric population (36; 26). Advances in this area have included acute treatments with several triptans, preventative treatment with topiramate (88) and levetiracetam (26), and the use of supplements including CoQ10 (22) and butterbur root extract (52).

Ginkgolide B and a mixture of feverfew, magnesium, and an extract of the plant Andrographis paniculata have been purported to have preventive value in childhood headache (11; 47).

Acute treatment. An effective acute treatment plan should end the episodic headache and return the child to normal functioning in 1 to 2 hours. The ultimate goal of this treatment should be a quick response with return to normal activity and without relapse. In the pediatric population, the nonspecific medications including NSAIDs (ibuprofen, naproxen sodium) and general pain relievers (acetaminophen) are frequently used. Two studies have evaluated the efficacy of ibuprofen in children. Hämäläinen reported a comparative, double-blinded, placebo-controlled, crossover study of placebo versus ibuprofen versus acetaminophen (18); the study indicated that ibuprofen was superior to both placebo and acetaminophen at both the 1- and 2-hour time point. Lewis performed a similar study on a group of children using a dose of ibuprofen at 7.5 mg/kg versus placebo; again, ibuprofen was more beneficial (40). The proper use of ibuprofen and other NSIADs includes: (1) early treatment, (2) effective doses (7.5 to 10.0 mg/kg), and (3) avoidance of overuse (limited to one to two headaches treated per week).

If this initial strategy of using over-the-counter medications is ineffective or not completely effective, migraine-specific therapy is often required. Children often report that the NSAIDs will work for the majority of their headaches, but they occasionally will have a moderate to severe migraine during which the response is incomplete or the treatment completely ineffective. When needed, triptans (migraine-specific medications) may be added to the treatment plan. Seven triptans are currently approved for adult migraine in the United States. Almotriptan (12.5 mg tablet) has been approved for the treatment of migraine pain in the adolescent population aged 12 to 17 years (42); it has been demonstrated to be statistically beneficial over placebo in adolescents. In Europe, several triptans, including nasal sumatriptan, have been approved for the use of adolescent migraine. Double-blinded, placebo-controlled studies have been performed in adolescents using almotriptan, eletriptan, rizatriptan, sumatriptan, and zolmitriptan. In six crossover and 11 parallel group trials, significant efficacy in children and adolescents was found for sumatriptan (10 to 20 mg nasal spray), zolmitriptan (2.5 to 5 mg tablet), rizatriptan (5 to 10 mg tablet), and almotriptan (12.5 to 25 mg tablet). Although the trials were heterogenous with respect to the triptans and the dosage, the pooled responder rate of triptans for two hours pain-free was 36.0% in crossover trials and 32.5% in parallel group trials, both significantly better than placebo in each case. Triptans also showed a significantly higher pain reduction rate at two hours than placebo both in crossover and parallel group trials. The rate of adverse events was significantly higher after triptans than after placebo. However, triptans were well tolerated in all trials (37; 12). Efficacy in children and adolescents in several placebo-controlled trials has also been noted for intranasal sumatriptan (16).

In an early intervention, open-labeled study with sumatriptan RT 100 mg tablet formulation in 35 adolescent migraine patients, 32 reported control of at least one migraine attack, and 23 reported control of four migraine attacks over a 6-month period. The adolescents were instructed to administer sumatriptan RT 100 mg tablet within 30 minutes of attack onset while pain was still mild. Pain-free response two hours postdose (primary endpoint) was reported in 71% of the 112 attacks treated. Migraine-free response (ie, no pain, nausea, vomiting, photophobia, or phonophobia and no use of rescue medication) two hours postdose was reported in 69% of attacks. Response rates were consistent from attack to attack. Rescue medication was used in 19% of migraine attacks. In 112 attacks, a total of 25 adverse events (none serious) were reported in nine patients. The most common adverse events were worsening of symptoms (n=5), neck pain (n=4), and chest tightening (n=4). Early intervention with sumatriptan RT 100 mg tablets constitutes a promising approach to treating migraine in adolescents and warrants further assessment in controlled clinical trials (91). One study has been conducted to examine efficacy and safety of the combination drug sumatriptan RT 85 mg and naproxen sodium 500 mg in adolescents. In this study, 94 subjects treated 347 attacks in total, treating 277 with sumatriptan/naproxen sodium and 70 with placebo. Compared with placebo, sumatriptan/naproxen sodium produced significantly higher 2-hour pain-free rates (sumatriptan/naproxen sodium 37%, placebo 18%; P < .004). Compared with placebo, 24 hour pain-free rates were higher with sumatriptan/naproxen sodium than placebo, but this difference was not statistically significant (89), perhaps reflecting the shorter timeframe without treatment of pediatric migraine relative to its adult counterpart.

A few placebo-controlled clinical trials for acute treatment, or for that matter preventative treatment, agents among adolescents have consistently shown statistically significant superiority. This is often explained by the high placebo response rates in adolescent migraineurs. Many other factors may play a contributory role: the choice of efficacy endpoints, timing of assessments, and time to treatment initiation. In order to fully determine the clinical benefit of migraine-specific therapies in the setting of adolescent migraine, innovative study designs are needed. A study design built around an initial placebo challenge before patients are randomized to active therapy with an acute treatment agent may be one approach by which this could be achieved. Although these studies are being designed and preformed, we presently must use the results of the available studies (despite their limitations) to determine how to manage childhood headache in routine practice (88).

One new therapy for acute migraine in adults is a specific antagonist at the 5HT(1F) receptor. This specificity of ditans make them nonvasoactive and safer than triptans for those with cardiovascular disease. An open-label, phase I study in children indicates that ditans are safe in children; a placebo-controlled efficacy study is underway (82).

Patients and their parents should be advised to avoid the overuse of acute medications. Medication overuse or analgesic rebound headaches can frequently lead to an increase in headache frequency and require cessation of acute therapy for recovery. Any patient having at least one headache per week should be considered a candidate for preventative medication with a “rescue” option for breakthrough headaches.

Treatment aimed at reduction in headache frequency. Strategies for reduction in headache frequency and resultant disability include lifestyle changes (eg, institution of more regular eating and sleeping habits, reduction in modifiable social and environmental exposures), preventative medication, and bio-behavioral treatment (58) have demonstrated that amitriptyline (1 mg per kilogram of body weight per day), topiramate (2 mg per kilogram per day), and placebo had equivalent (50% to 60%) efficacy in reduction of headache frequency by 50% in children and adolescents 8 to 17 years of age with migraine. Adverse effects were more frequent with amitriptyline or topiramate than with placebo. For children with chronic migraine (15 more headache days per month), addition of cognitive behavioral therapy to amitriptyline was more effective in reduction of headache frequency than addition of headache education to amitriptyline (31). Compliance was equivalent in the two alternative regimens (32). Injection of lidocaine and methylprednisolone into the greater occipital nerve appears to be both safe and effective in children with primary headache that is chronic and refractory to other therapies (62). At the present time, antibodies against calcitonin gene‐related peptide or its receptor are not recommended for use in children, as neither their efficacy nor their safety have been demonstrated (73). However, preliminary results of ongoing randomized, controlled trials in children and adolescents are promising (26; 54). Choice of treatment modality for a given child involves multifactorial consideration, discussion with the child and family, and flexibility as the disorder and circumstances evolve over time.

OnabotulinumtoxinA has been used in adults for frequent and chronic migraine. Although there are no definitive studies in children and adolescents, what studies exist have been promising, with statistically significant reduction in frequency and severity of headaches over that seen with placebo (82).

When the frequency increases to three to four migraines per month, with increased disability, a preventative therapy plan should be developed in the adolescent patient. Two to three migraines per month should be considered the threshold for considering preventative treatment in young children. Implementation of this approach often falls to the neurologist, as in a study of 106 consecutive patients seen in a headache clinic, although 62% met published criteria (39) for needing prophylaxis, prophylaxis was initiated by the referring physician in only 30% of the patients (67).

A comprehensive integrative approach may need to include, at least temporarily, preventative medication as well as incorporation of bio-behavioral management. The impact of migraine on the pediatric patient should be routinely measured by increased use of assessment tools such as PedMIDAS and the PedsQL (21; 23; 60).

The goal of preventative treatment is to reduce headache frequency and decrease headache disability. Ultimately, the goal is to maintain this reduction at an acceptable level for a long enough period of time so the preventative medication can be discontinued and the bio-behavioral therapy alone can sustain this response. Again, there are no absolutes as to what this frequency must be nor for how long, but in general most patients can be successfully weaned off of their preventative medication once they are at one to two headaches per month for 3 to 6 months. This time period may be altered based on the school year. Children typically experience decreases in headache frequency over the summer when they are out of school. Early summer provides an opportunity to reduce medication. Headaches often worsen in the fall with the start of the school year as well as in late spring. Thus, these are less desirable times to discontinue preventative medication.

Presently, in the United States only topiramate is FDA-approved as a preventative medication for the treatment of migraine in children age 12 and over (29). As in adults, preventative medications are grouped into: antiseizure medications, antidepressant medications (especially the tricyclic antidepressants), anti-serotonergic medications, and antihypertensive medications, including both beta-blockers and calcium channel blockers (36). The antiseizure medications currently being used include divalproate sodium and topiramate (both approved by the FDA for the prevention of migraine in adults) (46; 69) as well as gabapentin, levetiracetam, and zonisamide. Although a Cochrane review concluded that there was no evidence for efficacy of pregabalin or gabapentin in adults with migraine (41), a randomized comparative effectiveness study of propranolol and pregabalin for prophylaxis of childhood migraine suggested that pregabalin is superior to propranolol in this regard (02).

For children, the effective doses for most preventative anti-seizure medications have not been established, but in general the doses should be slowly increased, typically increasing the dose as tolerated over 6 to 8 weeks to the lower dosages used for epilepsy (90).

Lewis and colleagues completed a randomized, double-blind, placebo-controlled, multicenter, 16-week study evaluated the efficacy and safety of topiramate for the prevention of pediatric migraine (38). The primary efficacy measure was the percent reduction in the monthly migraine attack rate compared with baseline. The percent reductions in the monthly rates of migraine days, headache days, migraine attacks, migraine days with rescue medication, and the 50% responder rate were also evaluated. A total of 106 pediatric subjects with migraine with a mean (±SD) age of 14.2 (±1.6) years were randomized to topiramate 50 mg/day, topiramate 100 mg/day, or placebo. Topiramate 100 mg/day, but not 50 mg/day, resulted in a statistically significant reduction from baseline compared with placebo in the monthly migraine attack rate (72.2% vs. 44.4%) during the last 12 weeks of double-blind treatment. In addition, topiramate 100 mg/day, but not 50 mg/day, resulted in statistically significant percent reductions from baseline compared with placebo in the monthly rates of migraine days, headache days, and migraine attacks (24-hour rule; 48-hour rule). The 50% responder rate was statistically significantly higher for the topiramate 100 mg/day treatment group compared with placebo. Topiramate 100 mg/day for preventive treatment of migraine was both effective and well tolerated in pediatric migraine subjects.

For antidepressant medications, amitriptyline is the most widely used tricyclic antidepressant for headache prevention. In the pediatric population, the efficacy data are limited by open-labeled or small sample studies (35; 20). Other antidepressants have been used to a lesser degree with mixed results.

Antihypertensive agents have also been used for headache prevention and include beta-blockers (44; 93) and calcium channel blockers with flunarizine, available in Europe for migraine prevention (17; 72) with grade I evidence of its effectiveness (36).

New approaches to frequent and chronic migraine in adults include anti-CGRP monoclonal antibodies and small molecule CGRP receptor antagonists (termed “gepants”), for both of which there are ongoing pediatric trials (82).

Additional prevention agents may include some nonpharmaceutical treatments and supplements including: riboflavin (66; 05), coenzyme Q10 (63; 64), butterbur extract (57), melatonin (14), feverfew with Andrographis paniculata, and magnesium (47). Their effectiveness and usefulness in children has yet to be rigorously demonstrated.

When pharmacologic treatment is chosen to reduce headache frequency, the key to successful use of preventative medications is to slowly titrate the dose to an effective level. This requires an understanding by the patient and parent that it may take several weeks to months before an effective level and, thus, an effective response, is achieved. The most effective levels have yet to be established in children although adult guidelines may be useful for adolescents. Nearly one third of adolescent migraineurs met criteria for preventative therapy whereas only 19% have received it. Prospective studies are needed to fully evaluate the efficacy of preventative management in this population and to establish whether early intervention might slow this disease progression (87).

Several different devices that modulate the activity of the brain, spinal cord, or peripheral nerves, called neuromodulatory devices, have been approved in the U.S. and Europe for use in adults with acute or chronic migraine and have been proposed for prevention of episodic primary headache in children and adolescents. Towards the standardization of and the application of rigorous methods to the clinical evaluation of these devices, the International Headache Society has published guidelines for these clinical trials in adults and children with migraine (80). The challenge is that most of these have not been adequately tested in children, although there are some data suggestive of both efficacy and safety in adolescents. At present, most insurance companies will not pay for these devices for use in children and adolescents and their long-term cost can be prohibitive for many families (82).

Bio-behavioral treatment. The third component of a comprehensive integrative treatment plan is bio-behavioral therapy. This incorporates normalizing a pediatric patient’s lifestyle as well as establishing long-term healthy goals. In addition, attention to the contribution of adverse psychosocial circumstances and events to the origin of childhood headache is critical to treating underlying precipitants (54; 56; 94). Bio-behavioral therapy can roughly be divided into treatment adherence, lifestyle management, and psychological intervention including biofeedback-assisted relaxation training and cognitive behavioral therapy. Treatment adherence involves educating the patient and parent about the importance of compliance with their treatment plan and identifying obstacles that may limit the effectiveness of the plan. Adjustment of lifestyle habits includes identification of triggers for pediatric headaches, such as inadequate nutrition, skipping meals, and altered sleep patterns. This discussion includes the importance of adequate fluid hydration with limited use of caffeine, regular exercise, and adequate nutrition (25; 10). Additional psychological intervention can include biofeedback-assisted relaxation therapy, which has been shown to be effective in the pediatric population (08; 86; 61; 59), and cognitive behavioral therapy, which demonstrated sustained effectiveness for at least three months after initiation (50; 15).

References

01: Allen NM, Dafsari HS, Wraige E, Jungbluth H. Neck-tongue syndrome: an underrecognized childhood onset cephalalgia. J Child Neurol 2018;33(5);347-50. PMID 29451061
02: Bakhshandeh Bali M, Rahbarimanesh AA, Sadeghi M, Sedighi M, Karimzadeh P, Ghofrani M. Comparison of propranolol and pregabalin for prophylaxis of childhood migraine: a randomised controlled trial. Acta Med Iran 2015;53(5):276-80. PMID 26024701
03: Bigal ME, Lipton RB, Winner P. Epidemiology and classifiction of headache. In: Winner P, Lewis DW, Rothner AD, editors. Headache in Children and Adolescents. 2nd Ed. Hamilton,ON: BC Decker, 2008:1-18.
04: Bigal ME, Lipton RB, Winner P, Reed ML, Diamond S, Stewart WF. Migraine in adolescents: association with socioeconomic status and family history. Adolescent analysis of AMPP study. Neurology 2007;69(1):16-25. PMID 17606878
05: Boehnke C, Reuter U, Flach U, Schuh-Hofer S, Einhaupl KM, Arnold G. High-dose riboflavin treatment is efficacious in migraine prophylaxis: an open study in a tertiary care centre. Eur J Neurol 2004;11(7):475-7. PMID 15257686
06: Buse DC, Loder EW, Gorman JA, et al. Sex differences in the prevalence, symptoms, and associated features of migraine, probable migraine and other severe headache: results of the American Migraine Prevalence and Prevention (AMPP) study. Headache 2013;53(8):1278-99. PMID 23808666
07: Camargo A, Kanekar S. Neuroimaging in pediatric headache. Neurol Clin 2022;40(3):679-98. PMID 35871791
08: Daly E, Donn P, Galliher M, Zimmerman J. Biofeedback applications to migraine and tension headaches: a double-blinded outcome study. Biofeedback Self Regul 1983;8(1):135-52. PMID 6882811
09: Diamond S, Bigal ME, Silberstein S, Loder E, Reed M, Lipton RB. Patterns of diagnosis and acute and preventive treatment for migraine in the United States: results from the American Migraine Prevalence and Prevention study. Headache 2007;47(3):355-63. PMID 17371352
10: Ernst MM, Powers SW. Nonpharmacologic treatment of headache: hidden opportunities. In: Winner P, Lewis DW, Rothner AD, editors. Headache in Children and Adolescents. 2nd Ed. Hamilton,ON: BC Decker, 2008:255-81.
11: Esposito M, Ruberto M, Pascotto A, Carotenuto M. Nutraceutical preparations in childhood migraine prophylaxis: effects on headache outcomes including disability and behaviour. Neurol Sci 2012;33(6):1365-8. PMID 22437495
12: Evers S. The efficacy of triptans in childhood and adolescence migraine. Curr Pain Headache Rep 2013;17(7):342. PMID 23709234
13: Faedda N, Natalucci G, Calderoni D, Cerutti R, Verdecchia P, Guidetti V. Metacognition and headache: which is the role in childhood and adolescence? Front Neurol 2017;8:650. PMID 29312108
14: Fallah R, Shoroki FF, Ferdosian F. Safety and efficacy of melatonin in pediatric migraine prophylaxis. Curr Drug Saf 2015;10(2):132-5. PMID 24909684
15: Fisher E, Law E, Dudeney J, Palermo TM, Stewart G, Eccleston C. Psychological therapies for the management of chronic and recurrent pain in children and adolescents. Cochrane Database Syst Rev 2018;9(9):CD003968. PMID 30270423
16: Goldman RD, Meckler GD. Intranasal sumatriptan for migraine in children. Can Fam Physician 2015;61(5):435-7. PMID 25971759
17: Guidetti V, Moscato D, Ottaviano S, Fiorentino D, Fornara R. Flunarizine and migraine in childhood: an evaluation of endocrine function. Cephalalgia 1987;7(4):263-6. PMID 3427627
18: Hamalainen ML, Hoppu K, Valkeila E, Santavuori P. Ibuprofen or acetaminophen for the acute treatment of migraine in children. Neurology 1997;48:103-7. PMID 9008503
19: Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders. Cephalagia 2004;24(Supplement 1):1-160. PMID 14979299
20: Hershey AD, Powers SW, Bentti AL, Degrauw TJ. Effectiveness of amitriptyline in the prophylactic management of childhood headaches. Headache 2000;40(7):539-49. PMID 10940092
21: 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
22: Hershey AD, Powers SW, Vockell AL, et al. Coenzyme Q10 deficiency and response to supplementation in pediatric and adolescent migraine. Headache 2007a;47(1):73-80. PMID 17355497
23: Hershey AD, Powers SW, Vockell AL, LeCates SL, Segers A, Kabbouche MA. Development of a patient-based grading scale for PedMIDAS. Cephalalgia 2004;24(10):844-9. PMID 15377315
24: Hershey AD, Winner P, Kabbouche MA, et al. Use of the ICHD-II criteria in the diagnosis of pediatric migraine. Headache 2005;45(10):1288-97. PMID 16324160
25: Hershey AD, Winner P, Kabbouche MA, Powers SW. Headaches. Curr Opin Pediatr 2007b:1-7. PMID 18025933
26: Iannone LF, De Cesaris F, Geppetti P. Emerging pharmacological treatments for migraine in the pediatric population. Life 2022;12:536. PMID 35455026
27: Jeong YJ, Lee YT, Lee IG, Han JY. Primary headaches in children and adolescents – experiences at a single headache center in Korea. BMC Neurol 2018;18(1):70. PMID 29783930
28: Jin Z, Shi L, Wang YJ, et al. Prevalence of headache among children and adolescents in Shanghai, China. J Clin Neurosci 2013;20(1):117-21. PMID 23098390
29: Kacperski J. Prophylaxis of migraine in children and adolescents. Paediatr Drugs 2015;17(3):217-26. PMID 25792525
30: Kobor J, Nyári T, Benedek G, Túri S. Age-related prevalence and features of migraine headache in Hungarian schoolchildren and adolescents. Eur J Paediatr Neurol 2013;17(6):600-7. PMID 23746927
31: Kroner JW, Peugh J, Kashikar-Zuck SM, et al. Trajectory of improvement in children and adolescents with chronic migraine: results from the Cognitive-Behavioral Therapy and Amitriptyline Trial. J Pain 2017;18(6):637-44. PMID 28108386
32: Kroon Van Diest AM, Ramsey R, Kashikar-Zuck S, et al. Treatment adherence in child and adolescent chronic migraine patients: results from the Cognitive Behavioral Therapy and Amitriptyline Trial. Clin J Pain 2017;33(10):892-8. PMID 28118256
33: Krogh AB, Larsson B, Linde M. Prevalence and disability of headache among Norwegian adolescents: a cross-sectional school-based study. Cephalalgia 2015;35(13):1181-91. PMID 25720767
34: Larsson B, Sund AM. One-year incidence, course, and outcome predictors of frequent headaches among early adolescents. Headache 2005;45(6):684-91. PMID 15953301
35: Levinstein B. A comparative study of cyproheptadine, amitriptyline, and propranolol in the treatment of adolescent migraine. Cephalagia 1991;11:122-3.
36: Lewis D, Ashwal S, Hershey A, Hirtz D, Yonker M, Silberstein S. Practice parameter: pharmacological treatment of migraine headache in children and adolescents: report of the American Academy of Neurology Quality Standards Subcommittee and the Practice Committee of the Child Neurology Society. Neurology 2004;63(12):2215-24. PMID 15623677
37: Lewis D, Winner P, Hershey A, Wasiewski S. Efficacy of zolmitriptan nasal spray in adolescent migraine. Pediatrics 2007;120:390-6. PMID 17671066
38: Lewis D, Winner P, Saper J, et al. A 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
39: 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 2002a;59(4):490-8. PMID 12196640
40: Lewis DW, Kellstein D, Dahl G, et al. Children's ibuprofen suspension for the acute treatment of pediatric migraine. Headache 2002b;42(8):780-6. PMID 12390641
41: Linde M, Mulleners WM, Chronicle EP, McCrory DC. Gabapentin or pregabalin for the prophylaxis of episodic migraine in adults. Cochrane Database Syst Rev 2013;6:CD010609. PMID 23797675
42: Linder SL, Mathew NT, Cady RK, et al. A randomized, double-blind, placebo-controlled study of oral almotriptan 6.25 mg, 12.5 mg, and 25 mg in the acute treatment of migraine in adolescents. Headache 2006;46:834.
43: Lipton RB, Stewart WF, Sawyer J, Edmeads JG. Clinical utility of an instrument assessing migraine disability: the Migraine Disability Assessment (MIDAS) questionnaire. Headache 2001;41(9):854-61. PMID 11703471
44: Ludvigsson J. Propranolol used in prophylaxis of migraine in children. Acta Neurol Scand 1974;50:109-15. PMID 4839065
45: Margari L, Palumbi R, Lecce PA, et al. Non-verbal cognitive activities in children and adolescents affected by migraine and tension-type headache: an observational study using the Leiter-3. Front Neurol 2018;9:78. PMID 29556207
46: Mathew NT, Saper JR, Silberstein SD, et al. Migraine prophylaxis with divalproex. Arch Neurol 1995;52:281-6. PMID 7872882
47: Moscano F, Guiducci M, Maltoni L, et al. An observational study of fixed-dose Tanacetum parthenium nutraceutical preparation for prophylaxis of pediatric headache. Ital J Pediatr 2019;45(1):36. PMID 30871574
48: Munakata J, Harard E, Serrano D, et al. Economic burden of transformed migraine: results from the American Migraine Prevalence and Prevention (AMPP) Study. Headache 2009:(49)4:498-508. PMID 19245386
49: Newman LC, Maytal J. Cluster and the trigeminal autonomic cephalalgias. In: Winner P, Lewis DW, Rothner AD, editors. Headache in Children and Adolescents. 2nd Ed. Hamilton,ON: BC Decker, 2008:147-61.
50: Ng QX, Venkatanarayanan N, Kumar L. A systematic review and meta-analysis of the efficacy of cognitive behavioral therapy for the management of pediatric migraine. Headache 2017;57(3):349-62. PMID 28028812
51: Oakley CB, Scher AI, Recober A, Peterlin BL. Headache and obesity in the pediatric population. Curr Pain Headache Rep 2014;18(5):416. PMID 24695998
52: Oelkers-Ax R, Leins A, Parzer P, et al. Butterbur root extract and music therapy in the prevention of childhood migraine: An explorative study. Eur J Pain 2008;12(3):301-13. PMID 17659990
53: Osterhaus JT, Townsend RJ, Gandek B, Ware JE Jr. Measuring the functional status and well-being of patients with migraine headache. Headache 1994;34:337-43. PMID 7928312
54: Papetti L, Sforza G, Frattale I, et al. The enigma of new daily persistent headache: what solutions for pediatric age? Curr Pain Headache Rep 2022;26(2):165-72. PMID 35064916
55: Philipp J, Zeiler M, Wöber C, et al. Prevalence and burden of headache in children and adolescents in Austria - A nationwide study in a representative sample of pupils aged 10-18 years. J Headache Pain 2019;20(1):101. PMID 31694547
56: Polese D, Belli A, Esposito D, et al. Psychological disorders, adverse childhood experiences and parental psychiatric disorders in children affected by headache: A systematic review. Neurosci Biobehav Rev 2022;140:104798. PMID 35907492
57: Pothmann R, Danesch U. Migraine prevention in children and adolescents: results of an open study with a special butterbur root extract. Headache 2005;45(3):196-203. PMID 15836592
58: 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
59: Powers SW, Hershey AD. Biofeedback for childhood migraine. In: Maria BL, editor. Current Management in Child Neurology. 2nd ed. Hamilton, Ontario: BC Decker, 2002:83-5.
60: Powers SW, Patton SR, Hommel KA, Hershey AD. Quality of life in paediatric migraine: characterization of age-related effects using PedsQL 4.0. Cephalalgia 2004;24(2):120-7. PMID 14728707
61: Powers SW, Spirito A. Biofeedback. New York: Wiley 1998.
62: Puledda F, Goadsby PJ, Prabhakar P. 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
63: Rozen TD, Oshinsky ML, Gebeline CA, et al. Open label trial of coenzyme Q10 as a migraine preventive. Cephalalgia 2002;22(2):137-41. PMID 11972582
64: Sandor PS, Di Clemente L, Coppola G, et al. Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. Neurology 2005;64(4):713-5. PMID 15728298
65: Santoro JD, Fokert ND, Yang QZ, et al. Brain diffusion abnormalities in children with tension-type and migraine-type headaches. AJNR Am J Neuroradiol 2018;39(5):935-41. PMID 29545251
66: Schoenen J, Jacquy J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine prophylaxis: a randomized controlled trial. Neurology 1998;50:466-70. PMID 9484373
67: Schor NF. Brain imaging and prophylactic therapy in children with migraine: recommendations versus reality. J Pediatr 2003;143(6):776-9. PMID 14657827
68: Shimomura H, Tokunaga S, Taniguchi N, et al. Emotional and behavioral problems in children with migraine and tension-type headache. Brain Dev 2021;43(8):826-32. PMID 33985794
69: Silberstein SD. Divalproex sodium in headache: literature review and clinical guidelines. Headache 1996;36(9):547-55. PMID 8916563
70: Silberstein S, Loder E, Diamond S, Reed ML, Bigal ME, Lipton RB. Probable migraine in the United States: results of the American Migraine Prevalence and Prevention (AMPP) study. Cephalalgia 2007b;27(3):220-34. PMID 17263769
71: Silberstein SD, Lipton RB, Winner P, et.al. Examining the case definition for migraine: potential areas for modification of ICHD-II criteria. Headache 2007a.
72: Sorge F, De Simone R, Marano E, Nolano M, Orefice G, Carrieri P. Flunarizine in prophylaxis of childhood migraine: a double-blind, placebo-controlled, crossover study. Cephalalgia 1988;8(1):1-6. PMID 3282670
73: Szperka CL, VanderPluym J, Orr SL, et al. Recommendations on the use of anti-CGRP monoclonal antibodies in children and adolescents. Headache 2018;58(10):1658-69. PMID 30324723
74: Stafstrom CE, Goldenholz SR, Dulli DA. Serial headache drawings by children with migraine: correlation with clinical headache status. J Child Neurol 2005;20(10):809-13. PMID 16417875
75: Stafstrom CE, Rostasy K, Minster A. The usefulness of children's drawings in the diagnosis of headache. Pediatrics 2002;109(3):460-72. PMID 11875142
76: Stewart WF, Lipton RB, Dowson AJ, Sawyer J. Development and testing of the migraine disability assessment (MIDAS) questionnaire to assess headache-related disability. Neurology 2001;56(6 Suppl 1):S20-8. PMID 11294956
77: Stewart WF, Lipton RB, Kolodner KB, Sawyer J, Lee C, Liberman JN. Validity of the migraine disability assessment (MIDAS) score in comparison to a diary-based measure in a population sample of migraine sufferers. Pain 2000;88:41-52. PMID 11098098
78: Stewart WF, Lipton RB, Whyte J, et al. An international study to assess reliability of the migraine disability assessment (MIDAS) score. Neurology 1999;53:988-94. PMID 10496257
79: Tarantino S, Checchi MP, Papetti L, et al. Interictal cognitive performance in children and adolescents with primary headache: A narrative review. Front Neurol 2022;13:898626. PMID 35911918
80: Tassorelli C, Diener HC, Silberstein SD, et al. Guidelines of the International Headache Society for clinical trials with neuromodulation devices for the treatment of migraine. Cephalalgia 2021;41(11-12):1135-51. PMID 33990161
81: Topcu Y, Hiz Kurul S, Bayram E, Sozmen K, Yis U. The Paediatric migraine disability assessment score is a useful tool for evaluating prophylactic migraine treatment. Acta Paediatr 2014;103(11):e484-9. PMID 25048365
82: VanderPluym JH, Victorio MCC, Oakley CB, Rastogi RG, Orr SL. Beyond the guidelines: A narrative review of treatments on the horizon for migraine in children and adolescents. Neurology 2023;101(18):788-97. PMID 37604658
83: Varni JW, Seid M, Kurtin PS. PedsQL 4.0: reliability and validity of the Pediatric Quality of Life Inventory version 4.0 generic core scales in healthy and patient populations. Med Care 2001;39(8):800-12. PMID 11468499
84: Virtanen R, Aromaa M, Rautava P, et al. Changing headache from preschool age to puberty: a controlled study. Cephalalgia 2007;27(4):294-303. PMID 17376106
85: Waldie KE, Thompson JM, Mia Y, Murphy R, Wall C, Mitchell EA. Risk factors for migraine and tension-type headache in 11 year old children. J Headache Pain 2014;15:60. PMID 25205384
86: Werder D, Sargent J. A study of childhood headache using biofeedback as a treatment alternative. Headache 1984;24:122-6. PMID 6376425
87: Winner P, Diamond S, Reed ML, Bigal M, Lipton R. Migraine prevalence, disability and prevention need in a community sample of adolescents: results from the American Migraine Prevalence and Prevention (AMPP) study. Presented at the 48th Annual Scientific Meeting of the American Headache Society. Los Angeles, CA. June 22-25, 2006a.
88: Winner P, Hershey AD, Wasiewski W, et al. On behalf of the Adolescent Migraine Steering Committee. Issues in the design of adolescent migraine studies with triptan agents. Headache 2007.
89: Winner P, Linder S, Hershey AD. Consistency of response to sumatriptan/naproxen sodium in a randomized placebo-controlled, cross-over study for the acute treatment of migraine in adolescence. Headache 2015;55(4):519-28. PMID 25881677
90: Winner P, Linder SL, Yonker ME. Pharmacologic treatment of headache. In: Winner P, Lewis DW, Rothner AD, editors. Headache in Children and Adolescents. 2nd Ed. Hamilton, ON: BC Decker, 2008:229-53.
91: Winner P, Nelsen A. Early intervention in adolescent migraineurs: efficacy and tolerability of 100 mg sumatriptan. Presented at the 49th Annual Scientific Meeting of the American Headache Society, Chicago, IL. June 7-11, 2007.
92: Wober-Bingol C. Epidemiology of migraine and headache in children and adolescents. Curr Pain Headache Rep 2013;17(6):341. PMID 23700075
93: Ziegler DK, Hurwitz A. Propranolol and amitriptyline in prophylaxis of migraine. Arch Neurol 1993;50:825-30. PMID 8352668
94: Ziplow J. The psychiatric comorbidities of migraine in children and adolescents. Curr Pain Headache Rep 2022;25(11):69. PMID 34766216

Contributors

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

Author

Nina F. Schor MD PhD

Dr. Schor of the National Institutes of Health has no relevant financial relationships to disclose.
See Profile

Editor

Stephen D Silberstein MD

Dr. Silberstein, Director of the Jefferson Headache Center at Thomas Jefferson University has no relevant financial relationships to disclose.
See Profile

Former Authors

Paul Winner DO

Patient Profile

Age range of presentation: 0 month to 18 years
Sex preponderance: male=female
Heredity: heredity may be a factor

ICD & OMIM codes

ICD-9: Migraine with aura (classical migraine): 346.00

Migraine without aura (common migraine): 346.10
ICD-10: Migraine with aura [classical migraine]: G43.1

Migraine without aura [common migraine]: G43.0

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Headache in children: overview and treatment approaches

Also Relevant

Activity-related headache
Childhood migraine
Cluster headache
Headache guidelines
Tension-type headache

Headache in children: overview and treatment approaches …

Headache in children: overview and treatment approaches

Introduction

Overview

Key points

Childhood primary headaches as a neurologic health problem

Epidemiology and classification

Table 1. Migraine Without and With Aura (ICHD-3 – 1.1, 1.2)

Comments

Table 2. Differentiating Characteristics of Common Primary and Secondary Headache Syndromes

Impact

Treatment

Conclusion

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Acute cerebellar ataxia in children

Zika virus: neurologic complications

Headache associated with intracranial neoplasms

Cerebral edema in childhood

CNS germinoma

Vein of Galen malformations

Patent foramen ovale

Acupuncture

Headache in children: overview and treatment approaches

Introduction

Overview

Key points

Childhood primary headaches as a neurologic health problem

Epidemiology and classification

Table 1. Migraine Without and With Aura (ICHD-3 – 1.1, 1.2)

Comments

Table 2. Differentiating Characteristics of Common Primary and Secondary Headache Syndromes

Impact

Treatment

Conclusion

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Acute cerebellar ataxia in children

Zika virus: neurologic complications

Headache associated with intracranial neoplasms

Cerebral edema in childhood

CNS germinoma

Vein of Galen malformations

Patent foramen ovale

Acupuncture

This is an article preview.
Start a Free Account
to access the full version.