Pediatric Headache 

Updated: Jan 02, 2019
Author: J Ivan Lopez, MD, FAAN, FAHS; Chief Editor: George I Jallo, MD 

Overview

Practice Essentials

Headache is a common reason for pediatric patients to seek medical care. Headaches can result from any of a number of causes, including genetic predisposition, trauma, an intracranial mass, a metabolic or vascular disease, or sinusitis. Recognition that pediatric headaches can result from primary and secondary causes is crucial to their treatment.

Signs and symptoms

In pediatric patients with headache, the history should include the following:

  • Headache onset, duration, and severity

  • Associated symptoms

  • Family history of migraines

  • Medication history

  • Factors that may have precipitated the headache (most often migraine)

Symptoms accompanying migraine headache may vary according to the migraine type present:

  • Migraine with aura: Visual symptoms, sensory symptoms, motor symptoms, speech or language disturbances, and other cognitive effects

  • Complicated migraine: Focal or diffuse neurologic deficits

  • Hemiplegic or hemisensory migraine: Unilateral motor weakness or sensory disturbance that may persist for hours after the headache has subsided

  • Basilar migraine: Vasoconstriction of the basilar and posterior cerebral arteries; diplopia, vertigo, tinnitus, or ataxia

  • Acute confusional states (unusual): Sudden onset of confusion, unresponsiveness, memory disturbances, disorientation, and dysarthria

Distinguishing characteristics of tension headaches include the following:

  • Occurring during times of obvious stress

  • Involving the neck and occiput

  • Continuous pain

  • No nausea, vomiting, or abdominal pain

  • Family history of migraine is less likely

  • In some patients, obvious symptoms of depression; in this subgroup, headaches are relieved when depression is treated

Other types of headache include the following:

  • Cluster headache

  • Sinus headache

  • Head trauma-related headache

  • Intracranial mass-related headache

  • Benign intracranial hypertension

  • Meningeal irritation

  • Medication-overuse headache

Physical examination should include assessment of the following:

  • Vital signs

  • Skin rashes or lesions

  • Signs of neurologic abnormalities

  • Hematomas or other signs of trauma

  • Signs of papilledema or subhyaloid hemorrhage on funduscopy

  • Intracranial hypertension, uncomplicated idiopathic epilepsy, seizures, meningeal irritation

See Clinical Presentation for more detail.

Diagnosis

For migraine or tension headache in pediatric patients, a thorough history and physical examination usually suffice. Laboratory, radiologic, or electroencephalographic (EEG) studies are not useful to confirm the diagnosis of migraine but may help exclude other causes of headache.

For headache associated with head trauma or a significant intracranial hemorrhage, the following laboratory studies may be indicated:

  • Complete blood count

  • Prothrombin time

  • Activated partial thromboplastin time

Lumbar puncture may reveal elevated opening pressure, leukocytosis, elevated protein, and low glucose. It is the most sensitive test in the diagnosis of subarachnoid hemorrhage.

Diagnostic imaging is not routinely indicated unless a structural cause is suspected or, possibly, unless the patient is very young and there is no family history. Modalities include the following:

  • Sinus radiography

  • Computed tomography

  • Magnetic resonance imaging

EEG may be useful to assess the status of an underlying seizure disorder associated with headache or to exclude seizures in children with acute confusional migraines.

See Workup for more detail.

Management

Treatment of pediatric headache is of 3 basic types:

  • Symptomatic

  • Abortive

  • Preventive

Drugs used in symptomatic treatment are chosen according to the following:

  • Headache type and frequency

  • Type of symptoms present

  • Adverse-effect profile

  • Comorbidities present

Nonpharmacologic treatment of migraine and tension-type headaches includes the following:

  • Elimination of identified precipitants

  • Lifestyle changes

  • Stress relief

Abortive therapy for migraine and tension-type headaches may include the following:

  • Triptans (sumatriptan, almotriptan, rizatriptan, and others) (see the image below)

    Trigeminovascular system. The trigeminal nerve fib Trigeminovascular system. The trigeminal nerve fibers around basal cerebral and meningeal vessels are triggered (various stimuli are possible), and a vicious cycle starts in which the nerve terminals release calcitonin gene-related peptide (CGRP), substance P, vasoinhibitory peptide (VIP), and other mediators of local neurogenic inflammation and vasodilatation. The latter further stimulates the nerve endings. On the other end of the nerve, painful messages are transmitted toward central centers, including thalamus and cortex, and the sensation of pain arises. Modern drugs, such as the triptans, act at 3 levels, via 5-HT 1 B and D receptors; they vasoconstrict the vessels, reduce the release of the above-mentioned mediators, and decrease the central transmission of pain impulses.
  • Isometheptene and ergotamines

  • Analgesics

Prophylactic therapy for migraine and tension-type headaches may include the following:

  • Beta-blockers

  • Tricyclic antidepressants (TCAs)

  • Anticonvulsants

  • Calcium channel blockers

Treatment of chronic daily headache (CDH) may include the following:

  • Combination of therapies used for tension and migraine headache

  • Discontinuance of over-the-counter analgesics and all narcotics

  • Tricyclic antidepressants

  • Psychological, behavioral, and relaxation interventions (sometimes with TCAs)

  • Abortive therapy, if the CDH pattern includes well-defined migraine attacks

See Treatment and Medication

Background

Headache is a common reason why pediatric patients seek medical care. Headaches can result from any of a number of causes, such as genetic predisposition, trauma, an intracranial mass, a metabolic or vascular disease, or sinusitis, to name a few. Headaches have a significant impact on the lives of children and adolescents, resulting in school absence, decreased extracurricular activities, and poor academic achievement. (See Etiology and Prognosis.)[1]

Recognition that pediatric headaches can result from primary and secondary causes is crucial to their treatment (see the image below). (See Presentation, Workup, Treatment, and Medication.)

Trigeminovascular system. The trigeminal nerve fib Trigeminovascular system. The trigeminal nerve fibers around basal cerebral and meningeal vessels are triggered (various stimuli are possible), and a vicious cycle starts in which the nerve terminals release calcitonin gene-related peptide (CGRP), substance P, vasoinhibitory peptide (VIP), and other mediators of local neurogenic inflammation and vasodilatation. The latter further stimulates the nerve endings. On the other end of the nerve, painful messages are transmitted toward central centers, including thalamus and cortex, and the sensation of pain arises. Modern drugs, such as the triptans, act at 3 levels, via 5-HT 1 B and D receptors; they vasoconstrict the vessels, reduce the release of the above-mentioned mediators, and decrease the central transmission of pain impulses.

The most common primary headaches in pediatrics are migraine and tension-type headaches, representing the ends of a spectrum of manifestations of similar pain mechanisms. These 2 types of headache can be episodic, or they can exist in a chronic, daily form (present 15 or more days per month for 3 or more months).

Migraine headaches

Migraine headaches account for most primary childhood headaches. More than 90% of patients who present to a neurologist complaining of headache are estimated to have a migraine (Rothrock, personal communication, 2006). Migraine can be divided into 2 groups: migraine with aura, and migraine without aura. (See Presentation.)[2]

Pediatric migraines are often bilateral, and clear localization of the pain can be difficult to obtain from children. Migraines in children are often of shorter duration than they are in adults. Migraine with aura is seen in 14-30% of children with migraine.

Migraine variants are headaches that are accompanied or manifested by transient neurologic symptoms. These symptoms may occur immediately before, during, or after the headache. In some situations, the headache may be mild or nonexistent.

Tension-type headaches

Tension-type headaches are benign. They manifest as a bandlike sensation around the head, and they may be associated with neck and/or shoulder pain. These headaches often become worse as the day progresses and can last for days. They may be associated with stressful events at home or school, and they may be temporarily and relieved by sleep.

International Headache Society classification

The International Headache Society (IHS) has provided diagnostic criteria and a classification scheme for headaches in general.[2, 3, 4, 5, 6, 7] (Pediatric migraine is now distinctly recognized among the primary headache disorders.) Headaches are grouped on the basis of etiology, facilitating proper evaluation and treatment. The 3 main classifications are as follows (see Etiology, Presentation, Workup, and Treatment):

  • Primary headaches - Eg, migraine, tension-type, and cluster

  • Secondary headaches - Eg, related to head/neck trauma, vascular and nonvascular disorders, infection, or psychiatric disorders (except in young children, the frequency of secondary headaches is lower in children than in adults)

  • Cranial neuralgias, central and primary facial pain, and other headaches

Migraine without aura

Migraine without aura is identified by at least 5 attacks fulfilling the following criteria:

  • Duration between 1 and 48 hours

  • At least 2 of the following: (1) unilateral or bilateral, (2) pulsating, (3) moderate to severe in intensity, (4) aggravation by, or causing avoidance of, routine physical activity

  • During the headache, at least 1 of the following must be present: (1) nausea or vomiting, (2) photophobia or phonophobia

In addition, the headache should not be attributed to any other cause.

Migraine with aura

Migraine with aura includes the following types of headache[7] :

  • Typical aura with migraine

  • Typical aura with nonmigraine headache

  • Typical aura without headache

  • Familial hemiplegic migraine (FHM)

  • Sporadic hemiplegic migraine

  • Basilar-type migraine

Typical aura with migraine consists of the presence of the IHS criteria for migraine without aura, along with visual, sensory, or speech symptoms or any combination of the 3. In addition, development is gradual and the aura lasts no more than 60 minutes. Positive and negative features are experienced, and there is complete reversibility of symptoms. (See Presentation.)

Migraine variants

Migraine variants are headaches that are accompanied by or manifested by transient neurologic symptoms. These symptoms may occur immediately before, during, or after the headache. In some situations, the headache may be mild or nonexistent.

Hemiplegic migraine and basilar artery migraine are typical examples of migraine with aura. Hemiplegic migraine, while unusual, is seen more commonly in children than in adults. This type of headache is characterized by abrupt onset of hemiparesis, which usually is followed by a headache. Hemianesthesia may also precede the headache.

Basilar artery migraines are more common in girls. They are characterized by dizziness, weakness, ataxia, and severe occipital headache (with vomiting).

Less common migraine presentations have been described in which head pain is not a prominent feature. The "Alice in Wonderland" syndrome is characterized by distortions of vision, space, and/or time. Patients may note micropsia and/or metamorphopsia, as well as other sensory hallucinations.

Confusional migraine seen in juvenile patients is characterized by impairment of sensorium, agitation, and lethargy; these impairments sometimes progress to stupor. Focal neurologic deficits, such as aphasia, anisocoria, and memory deficits, may also be seen.

Benign paroxysmal torticollis of infancy is characterized by episodes of a head tilt, and benign paroxysmal vertigo of childhood is characterized by recurrent episodes of vertigo and ataxia. The torticollis typically occurs during the first year, whereas the vertigo occurs in young children (usually aged 2-3 years).

Cyclic vomiting and recurrent abdominal pain frequently are considered migraine variants. Before diagnosing either of these entities, primary gastrointestinal (GI) diseases must be excluded.

Classification by temporal pattern

Besides being classified on the basis of associated symptoms, headaches can also be classified by their temporal pattern, as follows:

  • Acute

  • Acute recurrent (episodic)

  • Chronic nonprogressive

  • Chronic progressive

Impact of headache on daily activities and productivity

Headache can lead to psychological impairment and decreased quality of life, especially for persons who experience chronic migraine. Children who suffer from migraine are more impaired than children who do not suffer from headaches or even children who suffer from tension-type headache, in terms of medication use, school nurse visits, and school absences.

Three million bedridden days per month in the US are attributed to headache, and more than 50% of absentees from headache average at least 2 days of absence per month. For almost 1 million children who have migraine, over 150,000 school days are missed.

Etiology

Because the brain is insensate, headache is due to the stimulation of pain-sensitive nerve fibers in large cerebral arteries and veins, the periosteum of the skull, the muscle and skin of the scalp, the sinus mucosa, the temporomandibular joint, the teeth, or the gingiva.

Migraine

Trigeminovascular system activation

Although much remains to be discovered, the pain in migraine attacks is multifactorial. One mechanism suggests activation of the trigeminovascular system. Synaptic boutons of the perivascular branches of the trigeminal nerve at the level of meningeal and basal cerebral vessels release the following proinflammatory mediators when the nerve is stimulated:

  • Substance P

  • Calcitonin gene-related peptide (CGRP)

  • Vasoactive intestinal peptide (VIP)

The initial triggers are still poorly understood. The mediators create neurogenic inflammation, including local rupture of the blood-brain barrier, and trigger vasodilatation, further stimulating the trigeminal nerve terminals. (See the image below.)

Trigeminovascular system. The trigeminal nerve fib Trigeminovascular system. The trigeminal nerve fibers around basal cerebral and meningeal vessels are triggered (various stimuli are possible), and a vicious cycle starts in which the nerve terminals release calcitonin gene-related peptide (CGRP), substance P, vasoinhibitory peptide (VIP), and other mediators of local neurogenic inflammation and vasodilatation. The latter further stimulates the nerve endings. On the other end of the nerve, painful messages are transmitted toward central centers, including thalamus and cortex, and the sensation of pain arises. Modern drugs, such as the triptans, act at 3 levels, via 5-HT 1 B and D receptors; they vasoconstrict the vessels, reduce the release of the above-mentioned mediators, and decrease the central transmission of pain impulses.

On the other end, pain afferent messages are transmitted centrally. Whether this system is abnormal in migraineurs versus healthy people, and whether it is genetically determined, is not known. Evidence exists of cortical hyperexcitability in migraineurs, which may be linked to a defect in the central catecholaminergic systems. Low magnesium levels also may play a role.

White-matter T2 MRI hyperintensities are observed in higher frequency in migraineurs with aura, especially in the posterior circulation territories. The pathophysiologic implication of this remains unclear.

Chronic transformation of migraine is believed to be due to spatial and temporal, central and peripheral sensitization, which correlates clinically with cutaneous allodynia.

Cortical spreading depression

Another mechanism thought to result in migraine headache has its origin in the brain stem. The onset of the aura in migraine headache is thought to be mediated by cortical spreading depression (CSD)—caused by neuronal activation followed by suppression—which spreads over the cortical surface. A simultaneous change occurs in cerebral blood flow, characterized by hyperperfusion, followed by hypoperfusion.

CSD is thought to be caused by either trauma or changes in the local concentrations of hydrogen ions, potassium, and glutamate. CSD activates central nervous system (CNS) nociceptors, possibly through the release of nitric oxide, atrionatriuretic factor, activation of noradrenergic pathways, and/or changes in cerebral blood flow. CSD also causes neurogenic inflammation, which stimulates the release of several different neurotransmitters that lead to cerebral vasodilatation and activation of CNS nociceptors.

Genetic predisposition

Migraine headaches may also have a genetic predisposition; nearly 70% of pediatric patients with migraine have a family history of migraine headache. Some individuals with familial hemiplegic migraine (FHM), a rare migraine subtype, have been found to have several genetic mutations in ion channels responsible for neurotransmitter release within the CNS, which may ultimately affect cortical excitability.[8]

In 1993, a gene mutation was found on chromosome 19, locus p13, in a pedigree experiencing FHM. Later, hemiplegic migraine in other families was mapped to chromosomes 1 and 2. At this time, 3 genes have been discovered, leading to following categories of FHM:

  • FHM I (locus 19, q 13) - Codes for the calcium channel CACNA1A gene

  • FHM II (locus 1, q 21) - Codes for the Na-K ATPase ATP1A2 gene[9]

  • FHM III (locus 2, q 24) - Codes for the sodium channel SCN1A gene[10]

Defects in ion channels resulting in excessive glutamate activity explain the effect of the mutations, which play a role in the aura. Cases of migraine due to a single mutation remain the exception.[11, 12]

Migrainelike headache

It should be clarified that although true migraine is a primary headache disorder, sometimes a migrainelike headache can be secondary to a metabolic or vascular disease. This is the case, for instance, with MELAS (mitochondrial encephalomyopathy, lactic acidosis, stroke), a mitochondrial cytopathy, and with CADASIL (cerebral autosomal dominant angiopathy with subcortical infarcts and leukoencephalopathy), a genetically determined disease of small vessels in the brain. The headache attacks in these disorders are indistinguishable from those of primary, true migraine, but other symptoms and disease features are also present.

Tension-type headache

The causes of tension-type headache are still poorly understood. A combination of muscular factors, abnormal pain-perception mechanisms, and central emotional abnormalities exist, all possibly linked to brain-stem serotonergic interneurons. Furthermore, central and peripheral sensitization is involved. Contrary to common belief, the relevance of muscle contraction itself is marginal, especially in the chronic form.

Posttraumatic headache

Because of their frequency, posttraumatic headaches should be mentioned. The acute phase usually is not a significant concern, because it does not change the initial assessment or management; this headache phase usually is considered nociceptive. Later, however, it can become a chronic, lingering head pain.

This syndrome is variably associated with autonomic symptoms and is often akin to a primary headache syndrome, such as migraine and tension-type headache. It is believed that the trauma has acted as a trigger or exacerbating factor in the genesis of that primary headache. Frequently, psychological disturbances are present and need to be specifically addressed for therapeutic success.

Sinus headache

Often suspected but rarely implied, sinusitis should be excluded as the cause of headache, although acute sinusitis typically presents with systemic and otorhinolaryngologic (ORL) symptoms and signs. Chronic and allergic sinusitis are almost never responsible for headaches.

Benign intracranial hypertension

Benign intracranial hypertension (pseudotumor cerebri) is caused by the expansion of one or more of the intracranial fluid spaces, such as the vasculature, the extracellular fluid compartment, or the cerebrospinal fluid (CSF) space. Several drugs, such as tetracycline, minocycline, penicillin, gentamicin, oral contraceptives, steroids, indomethacin, thyroid hormone, and lithium carbonate, may be inciting agents.

Other causes

Headache related to meningeal irritation may be caused by infection (meningitis), inflammation (eg, from a tumor), or hemorrhage (eg, from vascular malformation or malignant hypertension).

Epidemiology

Occurrence in the United States

Nearly 40% of all Americans have a significant headache at some time in their lives. Headaches are very common during childhood and become increasingly frequent during adolescence. The prevalence of headache, in general, ranges from 37-51% during the elementary-school years and gradually rises to 57-82% by the high-school years. Frequent or severe headaches, including migraines, were reported over a 12-month period in 17% of a national sample of children and adolescents.[13]

The most frequent type of recurrent headache in childhood is migraine; in adolescents, tension headaches are the most common cause of frequent headache.[14]

Age-related demographics

Throughout the medical literature, estimates of overall frequency of headache in children vary among authors.

Secondary headaches are the ones that are most frequently encountered before age 5 years. Migraine headache can occur as early as a few months of age. (A higher prevalence of migraine seems to exist in city dwellers.) Chronic tension-type headache occurs in 0.9% of 15 year-olds.

In a widely cited study, Bille analyzed a questionnaire of 8993 children aged 7-15 years in the city of Uppsala in Sweden and found that 59% had suffered headache at some time in their life.[15, 16] In a systematic questionnaire of 2941 children, Sillanpaa found the prevalence of headache to be 37% at age 7 years, increasing to 69% by 14 years; migraine accounted for 2.7% and 10.6% of these headaches, respectively.

A meta-analysis found that the prevalence of headache in general was approximately 60% by age 7. Other studies have shown that up to 51% of children aged 7 years and 57-82% of adolescents aged 15 years report recurrent headaches.[17, 18]

A study performed in Taiwan indicated that approximately 85% of children aged 13-15 years have had headache.[19] According to a large survey by Split et al, 75% of children have suffered headaches in general by age 15 years.[20]

Migraine

Starfield screened 2500 children and found that 11% experienced chronic morbidity; among those children, about 20% had headache, with roughly one half of these children having migraine.

According to Sillanpaa, migraine prevalence is around 11% at puberty (age 13 y) but increases over time.[21, 22] Lewis et al, in a meta-analysis of over 25,000 persons, found the incidence of migraine to be 2% by ages 3-7 years; 7% by ages 7-11 years; and 20% by ages 11-15 years. The aforementioned survey by Split et al indicated that 4% of children have migraine by the ages of 7 through 15; by age 15 years, 28% have migraine.[17, 20, 23, 24, 25, 26]

Race- and sex-related demographics

No specific report exists regarding differential incidence of headache by race in children, but migraine frequency in adults in the US declines from whites to African-Americans to Asians.

Approximately 60% of all children with migraines before puberty are male. Thereafter, the relationship is inversed, with 3 times more female than male migraineurs in adulthood. Other headache types are distributed more evenly.

Prognosis

Long-term prognostic studies of pediatric headache are scarce, but Brna et al reported that at 20-year follow-up, 73% of pediatric headache patients in their study continued to suffer from headache.[27] In a follow-up study of 200 patients from a headache clinic over 6 years, 48% of initial migraineurs remained migraine sufferers; 26% became tension-type headache sufferers; and 26% became headache-free.

Similar numbers were observed for initial tension-type headache sufferers but with a slightly higher headache-free rate (41% remained with tension-type headache; 21% developed migraine; and 38% became headache-free).

Headache can cause significant disruption in a child's daily activities, and children with migraine headache are often not appropriately diagnosed and thus go untreated. In a large study looking at the prevalence of migraine headache, 31% of patients reported that they had missed at least 1 day of school or work in the previous 3 months. In this same study, more than half of patients reported that their productivity was reduced by 50%. Some authors believe that children and adolescents with recurrent migraines experience a reduction in their quality of life similar to that of children with cancer.[28]

Primary headache conditions are notorious for their waxing/waning course, and long-term follow-up care is usually necessary. Short-term remissions are not uncommon, but long-term ones are rare. The natural history and prognosis of migraine may follow one of the following 4 clinical patterns[29] :

  • Clinical remission - Some migraine sufferers may become symptom-free over prolonged periods.

  • Partial clinical remission - In others, migraines get less severe over time, resembling common migraine or tension-type headaches.

  • Clinical persistence - The frequency and severity of migraine headache does not improve but does not get worse either.

  • Progression - The frequency and severity of migraine headache gets worse

Early diagnosis and prompt initiation of optimal treatments (abortive and preventative) may lead to better treatment outcomes and prognosis and less disability for children and adolescents with migraine.[30]

Morbidity and mortality

No mortality is associated with primary headaches, and that associated with secondary headaches depends purely on the underlying cause.

However, frequent headaches, as with other chronic pain syndromes, can be psychologically distressing and may have major implications on the life of the growing individual. According to Battistutta et al, chronic tension-type headache is comorbid with psychiatric illnesses such as depression and anxiety disorders, internalization syndrome, and attention deficit and anger-control deficit in adolescents. However the relationship between the psychological condition and the headache syndrome is far from simple and has not yet been resolved. The clinical implication is to attend to the entire symptomatology of the child.[31]

Migraine in general, but especially migraine with aura (any type [typical aura, hemiplegic migraine, basilar migraine]), seems to be associated with a slightly increased risk of ischemic stroke, but overall, the risk remains very low. The stroke risk is further magnified, however, in women, patients younger than 45 years, smokers, and persons using oral contraceptives.[32]

Other conditions comorbid with migraine have been observed, including irritable bowel syndrome, sleep disorders, bruxism, systemic lupus erythematosus, and obesity.[33]

Reports have indicated a higher incidence of ataxia associated with migraine, whether clinical or subclinical during provocation tests. These reports could correlate with white matter lesions on magnetic resonance imaging (MRI), especially in the cerebellum.

Patient Education

Reassure the parents and the patient that the headache process is benign and not progressive. Review with them the headache pattern; associated symptoms such as nausea, dizziness, and photophobia; and the benign nature of the physical examination (including funduscopy).

An imaging study can be reassuring to the family. This simple, but crucial, review will help to alleviate stress and worry, which may contribute to the patient's symptoms and the anxiety of the parents. Realizing that the pain, although unpleasant, is not life-threatening often allows the patient and parents to apply healthier coping strategies.

Parents and patients need to be aware that migraine headaches may be a lifelong condition and that they should expect that the headaches will reappear at some time during the patient’s lifetime, especially during situations of increased stress such as puberty, marriage, or change of job.

Reinforcing good health hygiene is another important educational step; sleep hygiene is particularly required.

For patient education information, see the Headache and Migraine Center, as well as Causes and Treatments of Migraine and Related Headaches; Migraine Headache in Children; Migraine Headaches, Vision Effects; and Migraine and Cluster Headache Medications.

 

Presentation

History

A thorough history should be obtained in any child presenting with headache. The history should describe headache onset, duration, severity, and associated symptoms. A family history of migraines may be helpful in clarifying the diagnosis. A medication history should also be sought.

One study found that a structured interview tool known as the Diagnostic Interview of Headache Syndromes–Child Version (DIHS-C) was reliable and valid for detecting migraine in children and teens in clinical and community settings.[34] The DIHS-C had a sensitivity of 98% and a specificity of 61%.[35] The study authors suggested that this tool can be used in doctors’ offices as an initial history-gathering method administered by a nonphysician, and the treating physician can then use the information obtained.

Although the minority of headaches in children are due to serious underlying pathology, early recognition is paramount for appropriate diagnosis and management. Structural headaches frequently are caused by space-occupying lesions, inflammation, and/or an increase in intracranial pressure. Frequently, neurosurgical intervention is needed.

No single sign or symptom indicates a structural etiology; however, several signs and symptoms warrant further investigation. Headaches due to increased intracranial pressure may be worse in the morning and improve as the day progresses or may be aggravated by sneezing, coughing, or straining. Headaches persistently localized to the occipital region warrant attention (as do any focal neurologic signs or symptoms with or without headache).

Worsening of headache severity and/or frequency (especially with rapid progression) may also suggest an intracranial pathologic process, as may any significant change in a previously diagnosed headache syndrome. Failure of an adequate trial of headache therapy may imply an incorrect diagnosis.

Children with a prior history of epilepsy may have a generalized or focal headache after a seizure. Headaches may also accompany the aura prior to a seizure.

Besides being classified on the basis of associated symptoms, headaches can, as previously mentioned, also be classified according to their temporal pattern, as follows:

  • Acute

  • Acute recurrent (episodic)

  • Chronic nonprogressive

  • Chronic progressive

Acute headache

Acute headache is defined as a recent onset of headache with no prior history of similar episodes. Establishing whether any neurologic symptoms accompany this headache is very important. The differential diagnosis of acute headache includes systemic infection, trauma, CNS infection, and first episode of migraine. Similar headaches that recur as often as several times a month with intervening symptom-free intervals are classified as acute recurrent headaches (usually migraine).

Chronic headache

Nonprogressive

Chronic nonprogressive headaches differ from acute recurrent headaches by their greater frequency and persistence for years with no associated neurologic symptoms or change in headache severity. Chronic nonprogressive headaches may have emotional or behavioral components. A common headache in this category is tension-type headache, but migraine with and without aura can also present this way.

Chronic daily headache (CDH) was first described in adults who reported daily or nearly daily headaches. It was soon recognized that although patients were similar in the number of headaches experienced, the characteristics of their headaches fell on a continuum between migraine and tension-type headache. A similar spectrum has been demonstrated in children. The most common CDH pattern is a progression from episodic migraines to this daily pattern.

Progressive

Chronic progressive headaches occur at least several times a week, but unlike the nonprogressive variety, these headaches increase in frequency and/or severity with time. The changing headache pattern should alert the care provider to the possibility that these headaches are secondary to a structural etiology.

Migraine headache

Symptoms vary according to the type of migraine a patient has. Many children with migraines have a previous history of motion sickness, paroxysmal dizziness, or vertigo. Clinicians should suspect migraine headache in any child who presents with recurrent episodes of incapacitating headaches. Nearly 70% of pediatric patients have a family history of migraine headache.

A possible relationship exists between children who have cyclic vomiting syndrome and migraine headache. A genetic predisposition to develop migraine headaches appears to exist for patients with cyclic vomiting syndrome and their family members. Patients with cyclic vomiting syndrome, their mothers, and grandmothers may have a prevalence of migraine headache that is about twice that of the general population.

Many children with migraine will have some type of premonitory symptoms before the onset of headache. Some of these premonitory symptoms include irritability, fatigue, and changes in facial expression.[36] The recognition of these subtle premonitory symptoms is helpful in the initiation of abortive therapy.

A study by Gelfand et al of 154 infant-mother pairs indicated that infants born to mothers with a history of migraine headaches have a 2.6 times greater risk of developing colic. As a result of this finding, the investigators suggested that migraine may manifest early as colic.[37]

Common differences between pediatric and adult presentation of migraine include, in children, include lack of throbbing, absence of lateralization, and shorter duration of the attack.[1, 38]

Headache triggers

Distinguishing between headache causes and triggers is important, since the latter act merely as precipitants of the headache condition, most often migraine. Factors that precipitate migraine headache include the following:

  • Stress/anxiety

  • Menstruation

  • Oral contraceptives

  • Physical exertion/fatigue

  • Lack of sleep (sleep apnea may also be a primary cause of headache)

  • Glare

  • Hunger

  • Foods/beverages with nitrates, glutamate, caffeine, tyramine, salt

  • Reading/refractive error

  • Cold foods

  • High altitude

  • Drugs such as nitroglycerin, indomethacin, and hydralazine

  • Chemicals, such as tyramine in cheese, chocolate, nuts, and monosodium glutamate

  • Epilepsy - Children with epilepsy are at an increased risk of developing migraine headaches

Migraine with aura

An aura is a sudden and self-limited neurologic dysfunction that generally lasts a few minutes; sometimes several can occur simultaneously or sequentially. The following symptoms can develop:

  • Visual symptoms - Scotomas, phosphenes that look like stars, straight or broken lines (fortification spectra), colors, illusions of shape (micropsias, macropsias, dysmorphopsia), and, rarely, hallucinations (more complex pictures)

  • Sensory symptoms - Paresthesias, rarely dysmorphopsia (impression one's body is deformed)

  • Motor symptoms - Paresis or hemiplegia, especially prominent in familial hemiplegic migraine (FHM)

  • Speech or language disturbance - Dysarthria, aphasia

  • Other cognitive effects - Confusion or amnesia

All of these symptoms have been attributed to cortical dysfunction. In a few instances, the aura supposedly has a brain-stem origin, although it has never been proven (eg, loss of consciousness, ophthalmoparesis, vertigo).

In cases of migraine with aura, the above symptoms precede a sharply defined headache. Adolescent and adult patients who have migraine with aura are thought to be at a higher risk for ischemic stroke, with this risk being magnified among women, patients younger than 45 years, smokers, and persons using oral contraceptives.[32]

Complicated migraine

In complicated migraine, focal or diffuse neurologic deficits may occur with the headache.

Hemiplegic migraine

With hemiplegic or hemisensory migraine, the headache is accompanied by unilateral motor weakness or sensory disturbance (eg, paresthesias) that may persist for several hours after the headache has subsided.

Basilar migraine

With basilar migraine, the pathogenesis involves vasoconstriction of the basilar and posterior cerebral arteries, which is well known to be an epiphenomenon in migraines and is not the cause of the headache. Diplopia, vertigo, tinnitus, or ataxia may also be noted.

Acute confusional states

Acute confusional states refer to an unusual type of migraine headache, characterized by sudden onset of confusion, unresponsiveness, memory disturbances, disorientation, and dysarthria; this type of migraine headache is thought to be more common in boys.

Migraine Disability Assessment Score (MIDAS)

Proper assessment of the patient, besides adequate characterization of migraine attacks, includes an objective determination of the disability imparted by the headache. A helpful adjunct to obtaining the history in such patients is the pediatric adjustment of the migraine disability assessment score (MIDAS), called PedsMIDAS, is an excellent and easy-to-use tool and is recommended by Hershey et al.[33] Quality of life is seriously affected by headaches, especially chronic ones, in children and adolescents, from most standpoints: physical, psychological, and social and role function, as observed by Osterhaus et al and Powers et al.[39, 40]

Tension-type headache

Tension-type headaches are common in children. Differentiating tension headache from migraine headache may be difficult, as many children with migraine headache also complain of neck pain. Distinguishing characteristics of tension headaches include the following:

  • Occurring during times of obvious stress

  • Involving the neck and occiput

  • Continuous pain

  • No nausea, vomiting, or abdominal pain

  • Family history of migraine is less likely

  • In a subgroup of patients with tension headache, some patients have obvious symptoms of depression, such as depressed mood, feelings of worthlessness, anhedonia, or anorexia; in this subgroup, the headaches are relieved when the depression is treated

Cluster headache

In this disorder, headaches occur in groups or clusters. Nasal discharge, congestion, and a watery, red eye are present on the same side of the head as the headache. Pain localizes to one side of the head. Cluster headaches often awaken a patient from sleep and most often occur in middle-aged men. Cluster headaches are rare in children.

Sinus headache

The diagnosis of headache due to sinusitis is suggested by a history of persistent upper respiratory infection (URI) symptoms lasting longer than 10 days. Nasal discharge, congestion, and cough lasting more than 10 days are usually present; fever may be present as well.

Recurrent headaches occur in approximately 15% of children with sinusitis. These patients complain of a throbbing headache that is worse in the morning or that occurs at the same time each day. The pain may vary with changes in head position.

With ethmoid disease, pain may be referred to behind the ipsilateral eye. With frontal sinusitis, pain may occur just above the inner canthi of both eyes.

Acute bacterial sinusitis may present with the following[41] :

  • Persistent symptoms of nasal congestion/discharge and cough lasting more than 10 days without clinical improvement

  • Abrupt onset of severe symptoms/signs of high fever (>39° C), purulent nasal discharge, and facial pain lasting for 3-4 consecutive days

  • Onset of worsening symptoms and signs, such as a new fever, headache, or increased nasal discharge 5-6 days after the onset of a typical viral upper respiratory infection

Head trauma-related headache

Headaches frequently follow closed-head trauma. The headache may appear acutely or may be present for months after the initial injury. Acutely, the patient may complain of headache shortly after the injury, which may worsen and may be accompanied by vomiting, lethargy, or seizures; these may be the earliest symptoms of an intracranial hemorrhage. In chronic cases, headache, dizziness, sleep disturbances, and personality changes may be present for months after the initial injury. Headache is a key feature of the postconcussive syndrome.

Intracranial mass-related headache

Distinguishing intracranial causes from extracranial causes of headache may be difficult. Patients with intracranial masses may complain of pain localized to the region of the mass. However, if a diffuse rise in intracranial pressure exists, the headache may be generalized.

Historical features of intracranial masses include the following:

  • Severe occipital headache

  • Sneezing, coughing, any Valsalva maneuver, or change in head position exacerbates the pain

  • Pain is worse in the morning or awakens the patient from sleep

  • Projectile vomiting without nausea and focal seizures may occur

However, morning headaches and projectile vomiting, once thought to be hallmarks of raised intracranial pressure, may also occur from etiologies other than intracranial masses.

Benign intracranial hypertension

Benign intracranial hypertension (pseudotumor cerebri) produces headaches similar to those occurring in conditions with raised intracranial pressure. In addition to having greater pain in the morning and vomiting, patients may have vision problems (eg, diplopia) or gait abnormalities (eg, ataxia).

Meningeal irritation

Meningeal irritation due to inflammation, infection, or hemorrhage (eg, malignant hypertension, vascular lesions) results in the acute onset of diffuse, severe headache. Neck pain or stiffness and alteration in consciousness may be present.

Medication-overuse headache

Chronic use of medications to treat headaches, such as analgesics or triptans, can result in medication-overuse headache. The International Classification of Headache Disorders (ICHD) has recognized this entity. It is defined as the development of a different type of headache or worsening of a migraine or tension headache, resulting in chronic daily headaches. It develops after use of medications such as analgesics or the triptans on more than 10 days per month or after the use of over-the-counter (OTC) analgesics for more than 15 days per month for 3 months' duration.

Physical Examination

A thorough physical examination often can exclude systemic causes of headache. Attention should be paid to vital signs, especially the presence of fever, elevated blood pressure, or bradycardia. Search the skin for rashes or cutaneous lesions (eg, petechiae, purpura, ash-leaf spots, café-au-lait spots).

A thorough neurologic examination should be performed to assess the level of consciousness and to evaluate cranial nerve dysfunction, hypertonia, hyperreflexia, hemiparesis, or hemiplegia. Also look for nuchal rigidity, and check the head for hematomas or other signs of trauma. Perform funduscopic examination, looking for papilledema or subhyaloid hemorrhage. Other findings can include the following:

  • Migraine headache - Most children with migraine headaches have a normal physical examination without focal deficits; some children with complicated migraine, however, may have focal neurologic abnormalities, such as weakness, third-nerve palsy, or ataxia.

  • Tension headache - The physical examination findings are usually normal, but pain on palpation of the posterior neck muscles may be noted

  • Sinus headache - Physical findings include pale, edematous nasal mucosa; boggy turbinates; clear or yellow nasal discharge; pain on palpation of frontal or maxillary sinuses; and failure of these sinuses to transilluminate

Head injuries

In acute injuries to the head, the child may have an altered level of consciousness, focal neurologic deficits, abnormalities in cranial nerve function (III, VI), and hemiparesis. In chronic injuries, the physical examination findings often are normal.

Intracranial masses

Patients with headaches due to an intracranial mass often have focal neurologic abnormalities, especially if they have had headaches for several months. These abnormalities include papilledema, sixth-nerve palsy, ataxia, spasticity of the lower extremities, and indications of brain dysfunction regarding language, motor control, or vision (depending on the location of the lesion). Early in the course of the mass lesion, the physical examination findings may be normal. Children with intracranial abscesses may have alteration of the level of consciousness only during the acute presentation.

Other diagnostic signs

Other findings in pediatric patients with headache can include the following:

  • Intracranial hypertension - These patients usually have papilledema and occasionally other neurologic deficits (eg, sixth-nerve palsy, ataxia, spasticity of the extremities)

  • Uncomplicated idiopathic epilepsy - These children have normal physical examination findings

  • Seizures - Children with seizures due to metabolic disorders or abnormal brain architecture may have baseline neurologic deficits (eg, hypertonia, hemiparesis).

  • Meningeal irritation - In cases of meningeal irritation, fever (meningitis) or hypertension (malignant hypertension) may be present, as well as altered consciousness, nuchal rigidity, or perivenous hemorrhage of the fundus (subarachnoid hemorrhage secondary to hypertension)

 

DDx

Diagnostic Considerations

To properly manage childhood headache, physicians must understand the common headache patterns and the signs and symptoms that may indicate serious intracranial disease. Treatment of pediatric headaches is complicated by unanswered questions regarding the safety and efficacy of adapting adult pharmacologic therapy to the diverse pediatric population. Problems to be considered include pseudotumor cerebri, Lyme disease, and medication-overuse headache.

One of the common errors would be to simply consider that a neurologic deficit occurring at the time of a throbbing headache with GI symptoms is by definition a migraine with aura. These cases need to be thoroughly characterized and investigated if the description does not fit the classic picture of migraine with aura.

Acute sinusitis can be a cause of headache if associated with the classic purulent discharge and fever and radiologic demonstration of an infection, but chronic sinusitis is not typically considered a cause of headache.

Differential Diagnoses

 

Workup

Approach Considerations

In the case of migraine or tension headache, a thorough history and physical examination is usually all that is needed. Laboratory, radiologic, or encephalographic studies are not useful to confirm the diagnosis of migraine but may help to exclude other causes of headache. For example, electroencephalography may be helpful to exclude seizures in children with acute confusional migraines.

Although imaging studies are not needed for every child who complains of headache, neuroimaging should be performed when the caregiver has any suspicion or concern that the headache may have a structural etiology. Given the broad differential of structural headaches and the imaging choices that are available, many practitioners are unsure which imaging modality will yield the most information in a cost-effective manner.

If a patient has had headaches for a long time (months to years) and the neurologic examination is normal, the likelihood of this patient harboring any serious intracranial pathology is minimal, and, therefore, neuroimaging studies should not be performed routinely.

Electroencephalography is useful to assess the status of an underlying seizure disorder associated with headache.

Laboratory Studies

In cases of headache associated with head trauma or a significant intracranial hemorrhage, a consumptive coagulopathy, such as thrombocytopenia, and prolonged prothrombin and activated partial thromboplastin times may be evident. Thus, a complete blood count (CBC), prothrombin time (PT), and activated partial thromboplastin time (aPTT) may be indicated in such cases.

Check anticonvulsant levels in patients with a headache and a known history of epilepsy because adequate seizure control usually prevents the headache.

Lumbar Puncture

A lumbar puncture may reveal elevated opening pressure, leukocytosis, elevated protein level, and low glucose level. For example, in patients with meningitis, a lumbar puncture may show an elevated opening pressure, white blood cells (WBCs), low glucose level, high protein level, and bacteria on Gram stain.

Lumbar puncture is the most sensitive test in the diagnosis of subarachnoid hemorrhage, demonstrating hemorrhagic cerebrospinal fluid (CSF) that does not clear during the collection of the first and last tubes. Opening pressure may also be elevated.

Imaging Studies

Neuroimaging (eg, computed tomography [CT] scanning, MRI) usually is not indicated for the routine care of patients with headache except possibly in the very young child and if absolutely no family history can be found despite thorough review. However, according to a study of over 700 children by Graf et al, there appears to be an increase in the rate at which neuroimaging for nonacute headache is being ordered by primary care physicians.[42]

If the baseline neurologic examination changes, neuroimaging should be considered. Neuroimaging is also warranted, despite normal baseline examination findings, if a patient’s first seizure is coincident with a headache, to exclude the possibility of an intracranial mass.

Radiography

Diagnosis of sinus headache may be made by sinus radiographs depicting air-fluid levels in the sinuses. However, this test is not sensitive, and false-negative results are common. CT scanning of the sinuses is more sensitive but is usually more expensive.

CT scanning

Any abnormality on physical examination in children with head trauma and headache should prompt radiologic evaluation, such as CT scanning, provided that the child has a protected airway and stable cardiovascular status.

Structural lesions

A CT brain scan with contrast can define most structural lesions. A CT scan without contrast is somewhat more limited in its sensitivity, although it can define hydrocephalus and hemorrhage easily. Routine noncontrast CT should be reserved for more acute situations in which time is crucial and intracranial hemorrhage is suspected.

Intracranial hemorrhage

CT scanning is the best initial study to demonstrate intracranial hemorrhage from malignant hypertension or vascular lesions. However, CT scan findings are positive in only about 90% of patients with subarachnoid hemorrhage, so a lumbar puncture should be performed despite unremarkable CT scan findings in patients thought to have a subarachnoid hemorrhage.

Intracranial hypertension

CT scan findings may be normal or may show slit-like ventricles in patients with benign intracranial hypertension (pseudotumor cerebri). CT scanning is usually needed to exclude other causes of increased intracranial pressure, such as tumors. Intracranial masses are most often diagnosed by means of CT scanning (with contrast to enhance subtle lesions) or MRI.

Sinus headache

In children with sinus headache, CT scanning of the sinuses is sensitive but expensive. Note that there is often mucoperiosteal thickening in the paranasal sinuses of children, so that it is difficult to determine whether the soft tissue changes of the sinuses are due to either bacterial infection or inflammation from other causes, such as viral infection, allergy, or chemical irritation. Thus, CT scanning should not be used to make the diagnosis of sinusitis but, rather, should be obtained only in children in whom antibiotic therapy has not ameliorated symptoms or in whom sinus surgery is being considered after appropriate antibiotic therapy has failed.

MRI

MRI is generally more costly, takes longer, and may require sedation, but its superior imaging capabilities offer detailed structural definition overall. Visualization of the posterior fossa in particular is superior to that achieved with CT scanning. Gadolinium enhances MRI sensitivity of vascular lesions and those that disrupt the blood-brain barrier.

All patients who present with any features of a structural headache should undergo high-quality imaging, preferably an MRI scan with gadolinium enhancement. In less suggestive clinical situations or for parental or patient reassurance, routine MRI or high-quality CT scanning with contrast is sufficient.

 

Treatment

Approach Considerations

Some authors believe that early diagnosis and prompt initiation of optimal treatments (abortive and preventive) lead to better treatment outcome and prognosis and less disability for children and adolescents with migraine.[30] However, much less data are available for the pediatric age group than for adults.[43]

Treatment of a secondary headache is focused on its specific cause, but an additional, symptomatic therapy may be useful as long as the cause has not yet been eradicated. As for a primary headache, always consider a preventative treatment and a symptomatic therapy.

The short-term goals of therapy for migraine and tension-type headache are to relieve pain, alleviate nausea, and promote sleep. The long-term goals are to improve the patient’s quality of life by reducing the frequency and severity of headache episodes. The treatment of chronic daily headache (CDH) combines therapies that are used for tension-type and migraine headache.

Symptomatic treatment

Drugs used in symptomatic treatment should be chosen carefully according to headache type (eg, beta-blockers or cyproheptadine for migraine, amitriptyline for migraine or tension-type headache), frequency (eg, amitriptyline for more frequent/chronic headache), type of symptoms (cyproheptadine if prominent vomiting), adverse-effect profile (eg, no beta-blockers if asthma). It is advisable to include comorbidities in the choice, such as depression and insomnia, which a tricyclic antidepressant helps to control along with migraine.

Multiple levels of symptomatic therapy exist. The current opinion is that rather than using a step-care treatment starting with the least expensive drugs and then stepping up as needed, the stratified care approach is best; up front the patient situation is assessed and the severity and level of care needed is taken into account to decide on the most effective and overall cost-containing treatment.

Adjusting treatment is recommended until the most efficient regimen is found; this regimen would treat all symptoms, including the headache itself but also other complaints such as nausea, vomiting, and photophobia. Self-treatment can lead to medication-overuse headache. Therapy must be monitored by parents.

Treatment of Migraine and Tension-Type Headaches

Triptans may be helpful in the treatment of these headaches, especially if the onset of headache has been recent. Narcotic and nonnarcotic analgesics, sedatives, and antiemetics are helpful adjunctive therapy, but an effort should be made to avoid excessive use of medications, particularly narcotics.

Sleep, darkness, and a quiet room are essential in managing acute migraine and tension-type headache.[44] In addition, encourage scheduled times for meals, bedtime, relaxation, and exercise. Individual treatment decisions should be based on the age of the child and receptiveness to behavioral techniques. Behavioral techniques can be highly effective for migraine and tension-type headaches. More focus is also being directed toward the use of complementary/alternative therapies such as acupuncture.

Acute tension headaches often respond to symptomatic treatments. Ibuprofen and acetaminophen are recommended to relieve headache pain. Avoid narcotics and other potentially addictive medications.

Eliminate identified precipitants; for example, alcohol, drugs, or caffeine may trigger headaches. Encourage appropriate lifestyle changes.

Lifestyle changes

The role of diet in headaches remains controversial. However, if a given food or beverage is associated with headaches, its avoidance has an obvious and significantly positive impact.

A study by Milde-Busch et al linked obesity and physical inactivity to childhood and adolescent headache disorders.[45] A lifestyle that includes physical exercise improves the quality of life of these patients in more than 1 way.

Regular sleep schedules, especially adequate amounts of sleep, have an effect on migraine control. A common tendency exists for teenagers to not sleep enough.

Stress relief

Stress, as a trigger and as a consequence of headache, is a logical target for nonpharmacologic therapy. Patients who are prone to tension headaches should attempt to minimize stress and may benefit from behavioral/relaxation therapy. Psychotherapy is indicated for any patient under significant stress. Consider family therapy in situations that involve divorce or illness of a sibling or when the family unit is a contributing factor.

Relaxation techniques with biofeedback of either cutaneous temperature with a finger probe or muscular contraction with an electromyography (EMG) needle are very helpful as adjunct therapy; they can even prevent headache on their own in the older child, granted that adequate cooperation can be obtained. Recommended treatment is 2-3 times weekly for 4-8 weeks. Usually, a physical therapist, or sometimes a psychologist with cognitive-behavioral skills, performs this therapy.

Regular physical activity can also reduce patient stress levels and is especially useful in cases of tension-type headache.

Abortive therapy

Abortive therapy uses medications to interrupt a headache after its onset. All abortive medications carry a risk of medication-overuse headache with excessive use in patients with frequent headaches.

Triptans

Sumatriptan (Imitrex), a serotonin 5-HT1 receptor agonist that causes vasoconstriction, among other actions, is effective in aborting migraine (about 70% efficacy in adults). It is available as an oral tablet, nasal inhalant, transdermal, or subcutaneous patient autoinjection system (vials for injection). The injected form of sumatriptan works faster than the nasal spray or the oral form. New, needleless parenteral forms of sumatriptan are also available.

Adverse effects of sumatriptan include the following:

  • Tingling

  • Dizziness

  • Warm sensations

  • Chest pain

  • Cardiac arrhythmias

Sumatriptan is absolutely contraindicated for patients with cardiac disease, uncontrolled hypertension, hemiplegic and basilar migraines, or pregnancy.

In children aged 12-17 years, controlled clinical trials with oral sumatriptan failed to show efficacy. This is probably due to high placebo effect observed in pediatric migraine trials. This means that children seem to respond well to placebo, therefore obscuring the response to active medication. Pediatric and adolescent studies indicate efficacy with the nasal spray form of this medication.[46]

Subcutaneous sumatriptan has also been effective, although the manufacturer does not recommend the use of it in patients who are younger than 18 years. In children, the trial subcutaneous dose is 0.1 mg/kg/dose. Current autoinjection sumatriptan is available in 6 mg and 4 mg unit doses.

Several triptans are approved by the US Food and Drug Administration (FDA) to be used as abortive therapy in the treatment of pediatric migraine. A study by Linder et al provided evidence that almotriptan (Axert) is effective and well tolerated in adolescents with migraines; the drug gained FDA approval for this indication shortly after the study.[47] Other triptans that are approved for acute treatment of pediatric migraine include rizatriptan (Maxalt) in children aged 6-17 years[48, 49] and zolmitriptan (Zomig Nasal Spray). In the Spring of 2015 the FDA approved a combination of naproxen sodium and sumatriptan (Treximet) for the acute treatment of migraine with or without aura in pediatric patients 12 years of age and older.[50]

Clinicians usually use almotriptan, rizatriptan for pediatric migraine, and other triptans off-label in their daily clinical practice, even if they are not indicated by the FDA for children. These include, in no specific order, naratriptan (Amerge), eletriptan (Relpax), and frovatriptan (Frova).

Clinical trials of some of these medications in children are currently under way. For years in the author's practice, when children and adolescents have not responded to nonsteroidal anti-inflammatory drugs (NSAIDs) or other over-the-count (OTC) analgesics, he has treated them with triptans, with good results.

Isometheptene and ergotamines

Isometheptene (Midrin) and ergotamines are also available for abortive migraine therapy (Although Midrin was removed from the US market in 2011, a generic form has appeared on the market.). While scientific evidence for their efficacy is lacking, many clinicians have used these medications with success. They are most effective when administered at aura onset or at the start of the headache. Because aura is less common in pediatric migraine and because children may be less able to communicate early symptoms of a headache, administering these abortive therapies at the appropriate time can be difficult.

Ergotamines generally are not used for young children (aged 6 years or younger) and may cause GI upset.

Analgesics

Analgesics such as acetaminophen and NSAIDs can be used as abortive therapy. They seem to be particularly effective in the pediatric population, and they can be obtained without prescription. Less risk of medication-overuse headache (rebound or withdrawal headache) may be seen with long-acting NSAIDs such as naproxen sodium.

Prophylactic therapy

Although consensus does not exist regarding the criteria to start prophylactic treatment, frequency and severity will be the main factors to guide the decision. Consider prophylactic therapy when headaches are frequent enough to interfere with the patient's lifestyle. In deciding to begin prophylactic therapy, consider the risks of long-term drug use against the benefit of potential headache relief. The possibility of pregnancy should also be considered if prophylactic medication is prescribed. As with abortive therapy, several classes of pharmacologic agents are available for prophylactic treatment.

In general, the effect of prophylactic therapy is not immediate, often taking as long as 6-8 weeks before improvement occurs. Providing this information to the patient and his/her parents leads to improved compliance and more realistic goals. Giving an appropriate trial before attempting a new treatment is important.

Migraines are known to remit spontaneously in some patients during childhood. Every 6-12 months, reassess the need for continued prophylaxis. This can be achieved by tapering the medication until either the headaches resume or the patient remains headache-free off therapy.

On the other hand, parents and patients need to be aware that migraine headaches may be a lifelong condition, and they should expect that the headaches will reappear at some time during a patient’s lifetime, especially during situations of increased stress, such as puberty, marriage, or change of job.

Beta-blockers

Beta-blockers are commonly used as prophylactic therapy for childhood migraine; propranolol and nadolol are each effective. Nadolol has the advantage of being longer acting (given once daily). Beta-blockers are contraindicated in patients with asthma or diabetes, and they may cause depression in adolescents. If the patient is an athlete, beta-blockers may interfere with the patient’s performance.

Tricyclic agents and cyproheptadine

Tricyclic agents (amitriptyline, nortriptyline) are frequently used for prophylactic therapy, especially in older children and adolescents. Nortriptyline tends to be less sedating than amitriptyline, but there are no well-conducted scientific trials demonstrating the efficacy of nortriptyline. There is, however, plenty of scientific evidence that amitriptyline is efficacious in migraine prevention. A paper presented at the American Academy of Neurology Annual Meeting in New Orleans (2012) showed that amitriptyline was safe and effective for migraine prevention in children and adolescents.

Cyproheptadine (Periactin), an antihistamine/antiserotonin drug, is also used, especially in younger children. Side effects include sedation, appetite stimulation, and weight gain.

No good scientific evidence supports the use of tricyclic agents or cyproheptadine in the pediatric population, but many clinicians have used these medications with success over decades.

Anticonvulsants

Anticonvulsants such as valproic acid, zonisamide, and topiramate have been used as prophylactic agents with reasonable success. These agents are especially useful when a seizure disorder coexists with migraines. Good scientific evidence exists to support the use of valproic acid and topiramate but is lacking for any other anticonvulsant. In 2014, the FDA approved the use of topiramate for the prevention of headaches in migraine patients aged 12-17 years.

Although some patients on topiramate complain of cognitive changes, the authors' own experience and published data[51] are consistent with the fact that cognitive changes are not common and topiramate is safe and effective in the pediatric population.

Calcium channel blockers

Calcium channel blockers (eg, verapamil) have been used in adults for migraine prophylaxis, but their efficacy in children is variable.

Treatment of Chronic Daily Headache

As previously mentioned, the treatment of CDH combines therapies that are used for tension and migraine headache. The patient should discontinue the use of OTC analgesics and all narcotics. Chronic, intermittent analgesic use may result in medication-overuse headaches. Tricyclic antidepressants appear to be most helpful for treating CDH in children. There are also data on topiramate and CDH.[52, 53, 54]

Psychological, behavioral, and relaxation interventions are also beneficial. Consider using these techniques concomitantly with tricyclic antidepressants. When the CDH pattern includes well-defined migraine attacks, abortive therapy may provide symptomatic relief. Late in 2012, the National Institutes of Health funded a study called CHAMP (CHildhood and Adolescent Migraine Prevention); the study was terminated early after interim analysis showed no significant difference in responder rates between subjects who received amitriptyline, topiramate, or placebo, and the occurrence of adverse events in patients who received study drug. However, neurologists continue to utilize these medications, as they have anecdotal observations of benefit.[55]

Treatment of Other Headaches

Sinusitis

The treatment of sinusitis includes appropriate antibiotic coverage, as well as the use of analgesics (eg, NSAIDs, acetaminophen) and nasal decongestants. Analgesics are also useful for chronic, postconcussive headaches, but there is the risk of medication-overuse headaches if analgesics are used 10 or more days per month.

Intracranial hemorrhage

In the event of an intracranial hemorrhage or an intracranial mass causing headache, appropriate airway management, with the goal of adequate oxygenation and hyperventilation to reduce cerebral blood flow and lower intracranial pressure, is the immediate goal. Subsequent surgery is necessary to evacuate the lesion.

To alleviate the increased intracranial pressure associated with intracranial hypertension (pseudotumor cerebri), a lumbar puncture is used to reduce the volume of CSF. Carbonic anhydrase inhibitors decrease the production of CSF.

Meningeal inflammation

The treatment goal for meningeal inflammation is treatment of the underlying cause, such as malignant hypertension (antihypertensives), infection (antibiotics), or subarachnoid hemorrhage (surgical evacuation of intracranial hemorrhage; nimodipine can be used to reduce vasospasm).

Inpatient Care

Inpatient care is provided for individuals with CDH after outpatient treatment has failed. It usually is intended to initiate prophylaxis while intravenous (IV) symptomatic therapy is being administered and, sometimes, IV fluids in case of severe nausea and vomiting. Also, status migrainosus can justify a brief hospital stay for symptomatic treatment.

Headaches of unclear etiology that are severe and worsening, as well as worrisome symptoms and signs, also can justify hospitalization in certain cases.

Diet

Much has been written concerning food items that can trigger headaches, especially migraine. However, there is a high degree of variability, and good scientific explanations for correlations between food and headache is rare. Moreover, causative items most often contain multiple potential triggers.

Avoid food triggers, such as old, fermented cheese; citrus fruits; and monosodium glutamate (found not only in Chinese food but also, widely, in commercial preparations). In addition, caffeine excess and especially caffeine withdrawal can precipitate migrainous headaches. With regard to the association between migraine and chocolate, the possibility exists that this is far more frequently a consequence of sugar craving, part of migraine premonitory symptoms, than a trigger.

Consultations

The primary care physician can manage a significant portion of pediatric headaches and can reserve neurologic referral for complicated headache patterns, headaches refractory to treatment, and headaches with a suspected structural etiology.

Consultation with a surgeon is appropriate for headache caused by mass lesions, intracranial hemorrhage, or abscess.

Chronic recurrent headaches should be referred to either a pediatric neurologist or a neurosurgeon, depending on the cause.

Note that an ophthalmologic consultation frequently is requested to evaluate for refractive abnormalities; although this scenario is possible, an excessive tendency exists to attribute headaches to this problem.

 

Medication

Medication Summary

If the diagnosis for a patient with headache is not a surgical condition that requires immediate operative treatment, the emphasis of headache therapy should be to provide analgesia and to treat the headache’s underlying cause. In patients with migraine, tension-type, or posttraumatic headache, the goals of therapy are to relieve pain, alleviate nausea, and promote sleep.

Pharmacologic treatment of migraine may be abortive or prophylactic. Abortive agents include the following:

  • Selective agonists for serotonin 5-HT1 receptors - These include sumatriptan, naratriptan, zolmitriptan, rizatriptan, almotriptan, frovatriptan, and eletriptan

  • Ergotamines

  • Analgesics such as acetaminophen and NSAIDs

Prophylactic agents include the following:

  • Beta-blockers - Propranolol and nadolol

  • Tricyclics - Amitriptyline

  • Antiepileptic drugs - Valproic acid, topiramate, and zonisamide

  • Verapamil

Abortive therapies should be used selectively. If possible, they should be used no more than 4 days in a month, per month, according to Termine et al, but they should be used early on in the course of the attack.[56]

Prophylactic agents can and should be used for daily headache, and they can be considered for over 4 attacks per month for more than 2 months. This has to be addressed clearly with the parents, since it requires a level of commitment.

It must be emphasized that the placebo effect for headache treatment in children is very high, reaching 55% for prophylactic agents and 69% for abortive ones.[57, 58]

Additional agents

Drugs exist that can be considered individually but cannot be recommended on a routine basis because either (1) they have not been studied specifically or used regularly in the pediatric population, or (2) they are not available in the United States. These medications are migraine preventatives; they include flunarizine, a calcium channel blocker; gabapentin; riboflavin; and metoprolol . (This list is not comprehensive.)

Analgesics, Other

Class Summary

Analgesics are indicated for the treatment of mild to moderate pain and headache. They are the mainstays of headache treatment. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients in pain.

Aspirin (Bayer Aspirin, Ecotrin, Tri-Buffered Aspirin)

Aspirin is used to treat mild to moderate pain. It inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2.

Acetaminophen (Tylenol, FeverAll, Acephen, Little Fevers, Mapap)

Acetaminophen is the drug of choice for pain in patients with documented hypersensitivity to aspirin or NSAIDs, upper GI disease, or current oral anticoagulant use.

It can be used for symptomatic relief in migraine and tension-type headaches, although its efficacy in relieving tension-type headache is modest. Acetaminophen is fairly effective in migraine attack termination, especially when it is combined with an antiemetic.

Combinations with pseudoephedrine (Sudafed) or caffeine (Excedrin Migraine) can be considered but should not be used regularly short of a risk of rebound withdrawal headache.

Acetaminophen 15 mg/kg was slightly less effective than ibuprofen 10 mg/kg at 2 hours, but was equally effective at 1 hour, in a randomized, controlled trial by Hamalainen et al. There were no serious adverse events.[58]

Morphine (Duramorph, Avinza, Kadian, MS Contin, Oramorph)

Morphine is the drug of choice for analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. It is the most potent of the opiate agonists and is useful for the acute management of headache due to migraine. Various IV doses are used and are commonly titrated until the desired effect is obtained. Its use is cautioned in conditions with raised intracranial pressure. Opiates should be used with a great deal of caution in the pediatric population.

Sedative/Hypnotics

Class Summary

Chloral hydrate promotes sleep in children with migraine headache.

Chloral hydrate (Somnote)

Chloral hydrate is a CNS depressant. Its mechanism of action is unknown.

Serotonin 5-HT-Receptor Agonists

Class Summary

The pathophysiology of vasoconstrictors is uncertain. A reduction in regional cerebral blood flow during the aura and early headache phases of migraine has been demonstrated.

Therapeutic activity of the serotonin 5-HT1 receptor agonists (ie, triptans) in migraine is most likely attributed to agonist effects at 5-HT1B/1D receptors. These specific receptor subtypes act on the extracerebral, intracranial blood vessels that become dilated during a migraine attack and on nerve terminals in the trigeminal system. Almotriptan (Axert) and zolmitriptan (Zomig Nasal Spray) have been approved by the FDA for use in adolescents aged 12-17 years, and rizatriptan has received FDA approval for migraine relief in children aged 6-17 years.[48, 49]

The profile of naratriptan is different from all other triptans, as it has a long half-life with a slow onset and prolonged duration of action. Differences between the other drugs (eg, oral sumatriptan, zolmitriptan, rizatriptan, almotriptan, frovatriptan, eletriptan) are modest. Rizatriptan is available in orally disintegrating tablets and zolmitriptan as a nasal spray that are convenient for the pediatric patient.

The American Academy of Neurology quality standards subcommittee and the practice committee of the Child Neurology Society have provided guidelines for treating migraine headaches in children and adolescents.[43]

Naproxen/sumatriptan (Treximet)

This combination product indicated for the acute treatment of migraine attacks with or without aura in adolescents aged 12 y or older. Naproxen inhibits synthesis of prostaglandins in body tissues by inhibiting at least 2 cyclooxygenase (COX) isoenzymes, COX-1 and COX-2; may inhibit chemotaxis, alter lymphocyte activity, and decreases proinflammatory cytokine activity. Sumatriptan is a selective 5-HT1B and 5-HT1D receptor agonist in cranial arteries. It elicits vasoconstrictive and anti-inflammatory effects. It is associated with antidromic neuronal transmission and is used for relief of migraine headache.

Rizatriptan (Maxalt, Maxalt-MLT)

Rizatriptan is a selective agonist for serotonin 5-HT1 receptors in cranial arteries and suppresses the inflammation associated with migraine headaches. It has a high affinity for 5-HT1D and 5-HT1B receptor subtypes. Rizatriptan has been approved by the FDA for migraine relief in children aged 6-17 years.[48, 49]

A randomized, controlled trial by Winner et al found the drug to be no better than placebo in adolescents. However, an open-label, long-term investigation by Visser et al seemed to indicate a small advantage over standard care (pain relief at 2 hours 77% for 5 mg ,vs 64 % for placebo).[59, 60]

Another open-label, long-term study (mean duration, 292 days), by Hewitt et al, also found rizatriptan to be effective in pediatric patients, as well as generally safe for and well tolerated during acute, long-term migraine treatment, with a consistent treatment effect revealed over time. The study included 606 migraineurs aged 12-17 years who were treated with rizatriptan, with 583 patients (weighing 40 kg or more) given 10 mg doses and 23 patients (weighing less than 40 kg) given 5 mg doses.[61]

Almotriptan (Axert)

Almotriptan is used to treat acute migraine. It is a selective 5-HT1B/1D/1F receptor agonist that causes cranial vessel constriction, inhibition of neuropeptide release, and reduced pain transmission in trigeminal pathways. Almotriptan has received FDA approval to be used in children aged 12-17 years.

Zolmitriptan (Zomig Nasal Spray)

Zolmitriptan is used for the symptomatic relief of headache. It is a selective serotonin (5-HT1) receptor agonist in cranial arteries. This agent elicits vasoconstriction and reduces inflammation associated with antidromic neuronal transmission in chronic headache. Zolmitriptan has a high affinity for 5-HT1D and 5-HT1B receptor subtypes and can reduce the severity of headache within 15 minutes. The intranasal spray is approved by the FDA for use in adolescents aged >12 y; however, the oral dosage forms are not approved for use in children or adolescents.

Naratriptan (Amerge)

Naratriptan is a selective 5-HT1 agonist with a long half-life and a high affinity for the 5-HT1D receptor subtype. The drug has a duration of action of up to 24 hours, with a low rate of headache recurrence. It is useful for patients with slow-onset, prolonged migraine, such as menstrual migraine. Naratriptan has had no formal FDA approval for use in headache relief for children.

Frovatriptan (Frova)

Frovatriptan is a selective 5-HT1 agonist with a long half-life (26-30 h). It has a high affinity for 5-HT1D and 5-HT1B receptor subtypes. Its duration of action is as long as 24 hours, with a low rate of headache recurrence. Frovatriptan is useful for patients with slow-onset, prolonged migraine, such as menstrual migraine. It has had no formal FDA approval for use in headache relief for children.

Eletriptan (Relpax)

Eletriptan is a selective serotonin agonist. It specifically acts at 5-HT1B/1D/1F receptors on intracranial blood vessels and sensory nerve endings to relieve pain associated with acute migraine. As of now, it has had no formal FDA approval for use in headache relief for children.

Antiemetic Agents

Class Summary

Antiemetics are useful in the treatment of symptomatic nausea. Interestingly, sometimes the GI symptoms of migraine, as opposed to the pain, are at the forefront of the clinical picture and require the most attention. This can significantly differ from the management of adults with migraine. Delayed gastric peristalsis can hinder medication absorption.[59]

Promethazine (Phenergan, Promethegan, Phenadoz)

Promethazine blocks the postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to the brain-stem reticular system. It has antiemetic and antihistaminic actions that alleviate nausea and vomiting and promote sleep. Because of its antidopamine action, promethazine also has a direct antimigraine effect. It is usually well tolerated.

Metoclopramide (Reglan, Metozolv ODT)

Metoclopramide promotes gastric emptying and has antiemetic effects, which are useful for treating the nausea and vomiting associated with migraine.

Beta-Blockers

Class Summary

Beta-blockers are effective in migraine prophylactic therapy, possibly by blocking vasodilators, decreasing platelet adhesiveness and aggregation, stabilizing membranes, or increasing the release of oxygen to tissues.

Propranolol (Inderal, InnoPran XL)

Taken long-term, beta-blockers such as propranolol are frequently effective in reducing the number and severity of attacks. When administering this medication, start with the lowest dose and increase the dose gradually (usually at monthly intervals) to allow each dose level to exert its maximum effect. The ideal dosage will reduce the heart rate by about 20%.

Propranolol is extensively used in migraine prevention in adults and children. Its mechanism of action in migraine prevention is supposed to be a reduction of central noradrenergic activity.

Timolol

Timolol is FDA approved for migraine prophylaxis, although there is less scientific evidence of efficacy for timolol than for propranolol.

Metoprolol (Lopressor, Toprol XL)

Metoprolol is not FDA approved for migraine prevention. It achieves efficacy in prophylactic therapy presumably by blocking vasodilators, decreasing platelet adhesiveness and aggregation, stabilizing membranes, or increasing the release of oxygen to tissues.

Nadolol (Corgard)

Nadolol is not FDA approved for migraine prevention. It achieves efficacy in prophylactic therapy presumably by blocking vasodilators, decreasing platelet adhesiveness and aggregation, stabilizing membranes, or increasing the release of oxygen to tissues.

Atenolol (Tenormin)

Atenolol is not FDA approved for migraine prevention. It achieves efficacy in prophylactic therapy presumably by blocking vasodilators, decreasing platelet adhesiveness and aggregation, stabilizing membranes, or increasing the release of oxygen to tissues.

Tricyclic Antidepressants

Class Summary

In low doses, tricyclic antidepressants (eg, amitriptyline) are useful in preventing migraines, particularly in patients with cyclic vomiting syndrome. They appear to exert their antimigraine effect independent of their effect on depression.

Amitriptyline

Amitriptyline has efficacy for migraine prophylaxis that is independent of its antidepressant effect. Its mechanism of action is unknown, but it inhibits the activity of such diverse agents as histamine, 5-HT, and acetylcholine. Its mechanism of action may also be central serotonin enhancement, but this has never been proven. When amitriptyline is administered at a low dose, it may be particularly effective against cyclic vomiting of childhood. The drug also has been used for long-term prophylactic treatment of chronic tension-type headache. It cannot be formally recommended for individuals under 12 years.

Doxepin

Doxepin has efficacy for migraine prophylaxis that is independent of its antidepressant effect. Its mechanism of action is unknown, but it increases the concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by the presynaptic neuronal membrane. It also inhibits histamine and acetylcholine activity.

Anticonvulsants

Class Summary

When given in doses lower than those generally used for preventing seizures, valproic acid and topiramate usually have antimigraine activity; divalproex sodium (which contains valproic acid) and topiramate have been approved by the FDA for migraine prophylaxis.

Divalproex sodium (Depakote)

Divalproex sodium is a stable coordination compound composed of sodium valproate and valproic acid in a 1:1 molar relationship; it has been approved by the FDA for prevention of migraine in children older than 12 years. It is likely that all forms of valproic acid have similar efficacy. Preparations that can be used include 250 mg tablets, 125 mg sprinkle capsules, and 250 mg/5 mL liquid formulations (US preparations). The mechanism of action in migraine is unknown, but it is reported to act through the inhibitory neurotransmitter gamma-aminobutyric acid in the treatment of epilepsy.

Valproic acid (Stavzor)

Valproic acid has been approved by the FDA for the prevention of migraine in children older than 12 years. The mechanism of action in migraine is unknown, but it is reported to act through the inhibitory neurotransmitter gamma-aminobutyric acid in the treatment of epilepsy.

Gabapentin (Neurontin, Gralise)

Gabapentin is used for migraine headache prophylaxis.

Topiramate (Topamax)

Migraine prophylaxis in adults is a labeled indication for topiramate. Although studies of the use of the drug in adolescents and children are under way, in 2014 the FDA approved the use of topiramate for the prevention of headaches in migraine patients aged 12-17 years. Topiramate is sedating and causes cognitive slowing if the dose is advanced rapidly or the starting dose is high.

Calcium Channel Blockers

Class Summary

Migraine prophylaxis has been reported with various calcium channel blockers, including verapamil, nifedipine, and others. The calcium channel blocker with the highest evidence of efficacy is flunarizine, which is not available in the United States. Results are not entirely predictable, and the dosage must be individualized. Some patients experience exacerbation of migraine with these agents.

Verapamil (Calan, Calan SR, Covera-HS, Verelan)

Verapamil relaxes smooth muscles and increases oxygen delivery during vasospasms. It is used in children for migraine with aura and for basilar migraine. Verapamil has not been FDA approved for use in migraine.

Antihistamines

Class Summary

Cyproheptadine is occasionally useful for migraine prophylaxis, probably because of its serotonergic (as opposed to antihistaminic) effects. Other antihistamines generally are not useful for migraine prophylaxis.

Cyproheptadine

Cyproheptadine is an antihistamine that has been used for migraine prevention in children more than it has in adults. It is usually well tolerated. The mechanism by which cyproheptadine acts has not been clarified; hypotheses include antihistaminic and anti-5-HT2 effects. There is no solid scientific evidence that this medication has any value in migraine prevention, but it is used by many physicians.

Corticosteroids

Class Summary

Steroid therapy may decrease intracranial pressure in benign intracranial hypertension.

Prednisone

Prednisolone is not used as often as it once was, but it should still be part of the armamentarium. It should be emphasized that the treatment of benign intracranial hypertension ought to be left to a neurology/neurosurgery specialist. Prednisolone should be part of an integrated treatment approach that includes decompressive procedures.

Carbonic Anhydrase Inhibitors

Class Summary

These agents are used for the treatment of idiopathic intracranial hypertension.

Acetazolamide (Diamox)

Acetazolamide decreases the production of CSF and has diuretic effects. It has not been formally recommended for pediatric use and should be reserved for consultation.

Ergot Derivatives

Class Summary

Ergot derivatives are not approved for children and off-label use requires close monitoring. The risk ergotism (intense vasoconstriction) may result and is typically associated with overdosage or prolonged use. Causes constriction of peripheral and central vasculature.

Dihydroergotamine (Migranal, D.H.E. 45)

Ergot derivatives include ergotamine and dihydroergotamine. Ergotamine comes only in oral form and has significant adverse effects, including vomiting, which makes it far less suitable than other drugs for the treatment of migraine.

Dihydroergotamine is used parenterally for severe migraine attacks in the adult patient and can be considered in some instances in children.

Ergotamine (Ergomar)

Ergotamine is an alpha-adrenergic and serotonin (5-HT1) antagonist and partial agonist (depending on the receptor site). It causes constriction of peripheral and cranial blood vessels. This agent works best when it is used in the early stages of migraine. Significant nausea and vomiting have been associated with its use.

 

Questions & Answers

Overview

How prevalent is pediatric headache?

What is included in the clinical history of pediatric headache?

What are the types of pediatric migraine headache?

What the signs and symptoms of pediatric tension headache?

What the types of pediatric headache?

What is included in the physical exam to evaluate pediatric headache?

What is included in the workup of pediatric headache?

When are lab tests indicated in the workup of pediatric headache?

Which imaging studies are performed in the workup of pediatric headache?

Which types of therapies are used in the treatment of pediatric headache?

How are medications selected for the treatment of pediatric headache symptoms?

What are the nonpharmacologic treatments for pediatric headache?

What is included in abortive therapy for pediatric headache?

Which medications are used in prophylactic therapy for the treatment of pediatric headache?

Which therapies are used in the treatment of pediatric chronic daily headache (CDH)?

What are the variants of pediatric migraine?

What is pediatric headache?

What is pediatric migraine headache?

What is pediatric tension-type headache?

What is the IHS classification for pediatric headache?

What are the diagnostic criteria for pediatric migraine without aura?

What are the diagnostic criteria for pediatric migraine with aura?

What is the classification of pediatric headache by temporal pattern?

How does pediatric headache affect quality of life?

What causes pediatric headache?

What is the pathogenesis of pediatric migraine headache?

What is the role of cortical spreading depression in the pathogenesis of pediatric migraine headache?

What is the role of genetics in the etiology of pediatric migraine headache?

What causes pediatric migrainelike headache?

What causes pediatric tension-type headache?

What is pediatric posttraumatic headache?

What causes pediatric sinus headache?

What causes benign intracranial hypertension in pediatric headache?

What are causes meningeal irritation in pediatric headache?

What is the prevalence of pediatric headache in the US?

How does the prevalence of pediatric headache vary by age?

Which age groups have the highest prevalence of pediatric migraine headache?

What are the racial predilections of pediatric headache?

What are the sexual predilections of pediatric headache?

What is the prognosis of pediatric headache?

What is the morbidity and mortality associated with pediatric headache?

What is included in patient education about pediatric headache?

Presentation

What is the focus of the clinical history to evaluate pediatric headache?

What is the temporal pattern classification of pediatric headache?

Which clinical history findings are characteristic of acute pediatric headache?

Which clinical history findings are characteristic of nonprogressive chronic pediatric headache?

Which clinical history findings are characteristic of progressive chronic pediatric headache?

Which clinical history findings are characteristic of pediatric migraine headache?

What are the precipitating factors in pediatric migraine headache?

What are the signs and symptoms of pediatric migraine with aura?

What are the signs and symptoms of complicated pediatric migraine headache?

What are the signs and symptoms of hemiplegic pediatric migraine headache?

What are the signs and symptoms of basilar pediatric migraine headache?

What are the signs and symptoms of acute confusional states in pediatric headache?

What is the migraine disability assessment score (MIDAS) for the evaluation of pediatric headache?

Which clinical history findings are characteristic of tension-type pediatric headaches?

Which clinical history findings are characteristic of pediatric cluster headaches?

Which clinical history findings are characteristic of pediatric sinus headaches?

Which clinical history findings are characteristic of head trauma-related pediatric headaches?

Which clinical history findings are characteristic of intracranial mass-related pediatric headaches?

Which clinical history findings are characteristic of benign intracranial hypertension -caused pediatric headache?

Which clinical history findings are characteristic of meningeal irritation in pediatric headache?

Which clinical history findings are characteristic of medication-overuse pediatric headaches?

What is included in the physical exam to evaluate pediatric headache?

Which physical findings are characteristic of head-trauma-caused pediatric headache?

Which physical findings are characteristic of intracranial masses in pediatric headache?

Which physical findings are characteristic of intracranial hypertension in pediatric headache?

Which physical findings are characteristic of seizures in pediatric headache?

Which physical findings are characteristic of meningeal irritation in pediatric headache?

DDX

Which conditions are included in the differential diagnoses of pediatric headache?

What are the differential diagnoses for Pediatric Headache?

Workup

How is pediatric headache diagnosed?

What is the role of lab tests in the workup of pediatric headache?

What is the role of lumbar puncture in the workup of pediatric headache?

What is the role of neuroimaging in the workup of pediatric headache?

What is the role of radiography in the workup of pediatric headache?

What is the role of CT scanning in the workup of pediatric headache?

Which CT findings are characteristic of structural lesions in pediatric headache?

Which CT findings are characteristic of intracranial hemorrhage in pediatric headache?

Which CT findings are characteristic of intracranial hypertension in pediatric headache?

Which CT findings are characteristic of pediatric sinus headache?

What is the role of MRI in the workup of pediatric headache?

Treatment

How is pediatric headache treated?

How are pediatric headache symptoms treated?

How are migraine and tension-type pediatric headaches treated?

What is the role of lifestyle changes in the treatment of migraine and tension-type pediatric headache?

What techniques are used to relieve stress in the treatment of pediatric headache?

What is the role of abortive therapy in the treatment of pediatric headache?

What is the role of sumatriptan (Imitrex) in the treatment of pediatric headache?

What are the possible adverse effects and contraindications of sumatriptan (Imitrex) for the treatment of pediatric headache?

What is the efficacy of triptans for the treatment of pediatric headache?

What is the role of isometheptene (Midrin) and ergotamines in the treatment of pediatric headache?

What is the role of analgesics in the treatment of pediatric headache?

What is the role of prophylactic therapy in the treatment of pediatric headache?

What is the role of beta-blockers in the treatment of pediatric headache?

What is the role of tricyclic agents and cyproheptadine in the treatment of pediatric headache?

What is the role of anticonvulsants in the treatment of pediatric headache?

What is the role of calcium channel blockers in the treatment of pediatric headache?

How is pediatric chronic daily headache (CDH) treated?

How is sinusitis treated in pediatric headache?

How is intracranial hemorrhage treated in pediatric headache?

How is meningeal inflammation treated in pediatric headache?

What is included in the inpatient care for pediatric headache?

Which dietary modification are used in the treatment of treatment of pediatric headache?

Which specialist consultations are beneficial to patients with pediatric headache?

Medications

What is the role of medications in the treatment of pediatric headache?

Which medications are used for abortive treatment of pediatric migraine headache?

Which medications are used for prophylaxis in the treatment of pediatric migraine headache?

Which medications are sometimes used in the prevention of pediatric migraine headache?

Which medications in the drug class Ergot Derivatives are used in the treatment of Pediatric Headache?

Which medications in the drug class Carbonic Anhydrase Inhibitors are used in the treatment of Pediatric Headache?

Which medications in the drug class Corticosteroids are used in the treatment of Pediatric Headache?

Which medications in the drug class Antihistamines are used in the treatment of Pediatric Headache?

Which medications in the drug class Calcium Channel Blockers are used in the treatment of Pediatric Headache?

Which medications in the drug class Anticonvulsants are used in the treatment of Pediatric Headache?

Which medications in the drug class Tricyclic Antidepressants are used in the treatment of Pediatric Headache?

Which medications in the drug class Beta-Blockers are used in the treatment of Pediatric Headache?

Which medications in the drug class Antiemetic Agents are used in the treatment of Pediatric Headache?

Which medications in the drug class Serotonin 5-HT-Receptor Agonists are used in the treatment of Pediatric Headache?

Which medications in the drug class Sedative/Hypnotics are used in the treatment of Pediatric Headache?

Which medications in the drug class Analgesics, Other are used in the treatment of Pediatric Headache?