Updated: Feb 3, 2008
Headache is a common reason for children to seek medical care. Headaches in children may be due to numerous causes, such as migraine and its variants, intracranial masses, or sinusitis. This article discusses the important and common causes of headache in the pediatric population.
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.
The pathophysiology of migraine headache is multifactorial. The onset of a migraine headache is thought to be mediated by cortical spreading depression (CSD), which is due to 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 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 also stimulates the release of several different neurotransmitters that lead to cerebral vasodilatation and activation of CNS nociceptors.
Nearly 40% of Americans have a significant headache at some time. Children frequently complain of headache. Headaches are very common during childhood and become increasing more 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. Before puberty, reports indicate that boys are more frequently affected than girls, but, following the onset of puberty, headaches are reportedly more frequent in girls.
Headache can cause significant disruption in a child's daily activities. For example, 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 one 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%.
A thorough history should be obtained in any child presenting to the ED with a 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.
A thorough physical examination often can exclude systemic causes of headache.
| Encephalitis | Meningitis |
| Epidural and Subdural Infections | Neoplasms, Brain |
| Epidural Hematoma | Pediatrics, Meningitis and Encephalitis |
| Headache, Cluster | Subarachnoid Hemorrhage |
| Headache, Migraine | Subdural Hematoma |
| Headache, Tension | Toxicity, Vitamin |
| Hypertensive Emergencies |
Pseudotumor cerebri
Lyme disease
Medication overuse headache (MOH)
If the diagnosis is not a surgical condition that requires immediate operative treatment, the emphasis of medical therapy should be to provide analgesia and to treat the underlying cause of headache. In patients with migraine, tension, and posttraumatic headache, the goals of therapy are to relieve pain, alleviate nausea, and promote sleep. Vasoconstrictive agents may also be helpful, especially if the onset of the migraine headache is recent.
These agents are indicated for the treatment of mild to moderate pain and headache. They are the mainstays of headache treatment.
Treats mild to moderate pain. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.
325-650 mg PO q4-6h prn pain; not to exceed 4 g/d
10-15 mg/kg/dose PO q4h prn pain; not to exceed 60-80 mg/kg/d
Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; because of association of aspirin with Reye syndrome, do not to use in children (<16 y) with flu
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in severe anemia, history of blood coagulation defects, or current anticoagulant use
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, upper GI disease, or current oral anticoagulant use.
325-650 mg PO/PR q4-6h prn; not to exceed 4 g/d
10-15 mg/kg/dose PO/PR q4-6h prn; not to exceed 2.6 g/d
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; liver failure; G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses exceeding recommended maximum dose
NSAID that is DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h prn pain; not to exceed 3.2 g/d
5-10 mg/kg/dose PO q4-6h prn pain; not to exceed 2.4 g/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
DOC for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone. 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 desired effect obtained. Its use is cautioned in conditions with raised intracranial pressure.
2.5-20 mg/dose IV q2-6h prn
0.05-0.1 mg/kg/dose IV q1h prn
Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Documented hypersensitivity; hypotension; potentially compromised airway where establishing rapid airway control would be difficult; increased intracranial pressure; severe renal or hepatic failure
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
This agent promotes sleep in children with migraine headache.
CNS depressant. Mechanism of action unknown.
500-1000 mg PO/PR; not to exceed 2 g/d
25-50 mg/kg/dose PO qd or bid prn; not to exceed 2 g/24 h in 2 divided doses
May potentiate effects of CNS depressants, warfarin, and alcohol
Documented hypersensitivity; severe cardiac, renal, or hepatic insufficiency; history of porphyria; allergy to tartrazine dye
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
CNS depression, additive with other CNS depressants; SVT and ventricular arrhythmias have been reported during toxic doses; minimal respiratory depressant effects (isolated case reports in the literature); adverse reactions include drowsiness, hypothermia, dysarthria, ataxia, excitability, and generalized weakness; other adverse effects include rash, nausea, vomiting, severe abdominal pain, cardiac arrhythmia, confusion, hallucinations, and, rarely, convulsions
Although the pathophysiology is uncertain, abnormalities of the cerebral vasculature, causing vasoconstriction, and then vasodilation, is the most often cited mechanism for migraine. A reduction in regional cerebral blood flow during the aura and early headache phases of migraine has been demonstrated. This is the rationale behind the use of vasoconstrictive agents in the treatment of migraine. Therapeutic activity of the serotonin 5-HT1 receptor agonists (ie, triptans) in migraine is most likely attributed to agonist effects at 5-HT 1B/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. Triptans have not been FDA approved for children younger than 18 years.
A recent report of the American Academy of Neurology quality standards subcommittee and the practice committee of the child neurology society has provided guidelines for treating migraine headaches in children and adolescents.1
Alpha-adrenergic and serotonin (5HT1) antagonist and partial agonist (depending on receptor site). Causes constriction of peripheral and cranial blood vessels. Useful in classic and common migraine headache. Works best if used in early stages of migraine. Significant nausea and vomiting has been associated with its use.
Oral: 2 tab PO at onset of attack and 1 tab q30min prn; not to exceed 6 tab per attack or 10 tab/wk
Sublingual: 1 tab SL at first sign of the attack and 1 tab q30min; not to exceed 3 tab/24 h or 5 tab/wk
1-2 mg SL at time of attack, repeat q30min; not to exceed 3 doses/d
Increases effects of heparin and toxicity of nitroglycerin, propranolol, erythromycin, and clarithromycin
Documented hypersensitivity; hepatic or renal disease; peptic ulcer disease; sepsis; peripheral vascular disease; pregnancy; hypertension; PVD; not to be prescribed for hemiplegic migraine
X - Contraindicated; benefit does not outweigh risk
Strong uterine stimulant actions; avoid using prolonged regimens because of danger of causing gangrene or dependency; commonly causes nausea and vomiting
Selective agonist for serotonin 5-HT1 receptors (probably 5HT1D) in cranial arteries and suppresses inflammation associated with migraine headaches. Useful in common and classic migraine during early stages of headache.
As of now, has had no formal approval for use in headache relief for children. However, accumulating evidence from several clinical studies indicates efficacy and safety in that population, and many child neurologists are beginning to use triptans in children. The decision to choose these drugs might be best reserved for consultation.
Oral: 25 mg PO at migraine onset; if satisfactory response not observed in 2 h, an additional dose (not to exceed 100 mg) may be administered; administer an additional dose q2h if headache returns; not to exceed cumulative daily dose of 200 mg; individualize initial dose, may use 25, 50, or 100 mg; weigh possible benefit of higher dose with potential for risk of adverse effects
Injection: 6 mg SC; if satisfactory response not observed in 1 h, an additional 6 mg injection may be administered, not to exceed 2 injections/d
Intranasal: 5, 10, or 20 mg may be administered in one nostril; may administer 10 mg dose by administering a single 5 mg dose in each nostril; if satisfactory response not observed in 2 h, additional dose may be administered, not to exceed 40 mg/d
Not established; data limited, clinical trials have shown the nasal spray (5-20 mg) effective to treat acute migraine in adolescents
Toxicity increases when administered concomitantly with ergot-containing drugs, selective serotonin reuptake inhibitors, and MAOIs
Documented hypersensitivity; ischemic heart disease; uncontrolled hypertension
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hypertensive crisis, coronary artery vasospasm, cardiac arrest, peripheral ischemia, and bloody diarrhea may occur rarely when administering medication; adverse effects include hot flashes, nausea, vomiting, and drowsiness
For symptomatic relief. Selective serotonin (5HT1) receptor agonist in cranial arteries; elicits vasoconstriction and reduce inflammation associated with antidromic neuronal transmission in CH. High affinity for 5-HT 1D and 5-HT 1B receptor subtypes.
Can reduce severity of headache within 15 min of SC injection. As of now, has had no formal approval for use in headache relief for children. However, accumulating evidence from several clinical studies indicates efficacy and safety in that population, and many child neurologists are beginning to use them in children. The decision to choose these drugs might be best reserved for consultation.
2.5 mg or 5 mg PO; repeat dose after 2 h prn; not to exceed 10 mg/d; may give dose lower than 2.5 mg by breaking scored tab in half
Oral disintegrating tablets: 2.5 mg dissolved on tongue once; may repeat dose after 2 h, not to exceed 10 mg/24 h
Intranasal: 5 mg administered in 1 nostril at migraine onset; may repeat once after 2 h if needed; not to exceed 10 mg/d
Not established
Toxicity increases when administered concomitantly with ergot-containing drugs, selective serotonin reuptake inhibitors, and MAOIs
Documented hypersensitivity; ischemic heart disease and uncontrolled hypertension; do not administer within 24 h of taking another serotonin agonist or ergotamine or within 2 wk of taking an MAOI
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hypertensive crisis, coronary artery vasospasm, cardiac arrest, peripheral ischemia, bloody diarrhea, and death may occur when administering this medication
Selective 5-HT1 agonist with a long half-life. High affinity for 5-HT 1D receptor subtype. Duration of action up to 24 h with low headache recurrence rate. Useful for patients with slow-onset prolonged migraine, such as menstrual migraine.
As of now, has had no formal approval for use in headache relief for children. However, accumulating evidence from several clinical studies indicates efficacy and safety in that population, and many child neurologists are beginning to use them in children. The decision to choose these drugs might be best reserved for consultation.
1-2.5 mg PO at migraine onset; may repeat once after 4 h; not to exceed 5 mg/d
Not established
Oral contraceptives may significantly increase serum concentrations and prolonged vasospastic reactions may occur, avoid concurrent use within 24 h of each other; toxicity may increase when administered concomitantly with ergot-containing drugs, selective serotonin reuptake inhibitors, and MAOIs
Documented hypersensitivity; ischemic heart disease; uncontrolled hypertension; cerebrovascular or peripheral vascular syndromes; severe renal impairment (CrCl <15 mL/min); severe hepatic impairment (Child-Pugh grade C)
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Chest, jaw, or neck tightness may occur after 5-HT1 agonist administration; atypical sensations over precordium (pain, tightness, pressure, heaviness) may occur (rarely associated with arrhythmias or ischemic ECG changes); evaluate patients with signs or symptoms suggestive of angina for presence of CAD or predisposition to Prinzmetal angina before receiving additional doses; monitor ECG if dosing resumed and similar symptoms recur
Selective agonist for serotonin 5-HT1 receptors in cranial arteries and suppresses the inflammation associated with migraine headaches. High affinity for 5-HT 1D and 5-HT 1B receptor subtypes.
As of now, has had no formal approval for use in headache relief for children. However, accumulating evidence from several clinical studies indicates efficacy and safety in that population, and many child neurologists are beginning to use them in children. The decision to choose these drugs might be best reserved for consultation.
5-10 mg PO at migraine onset; may repeat dose after 2 h prn; not to exceed 30 mg/d
Oral disintegrating tab: 5-10 mg PO dissolved on tongue at migraine onset; may repeat dose after 2 h prn; not to exceed 30 mg/d
Not established
Toxicity increases when administered concomitantly with ergot-containing drugs, selective serotonin reuptake inhibitors, and MAOIs
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hypertensive crisis, coronary artery vasospasm, cardiac arrest, peripheral ischemia, bloody diarrhea, and death may occur when administering this medication
Used to treat acute migraine. Selective 5-HT1B/1D/1F receptor agonist. Results in cranial vessel constriction, inhibition of neuropeptide release, and reduced pain transmission in trigeminal pathways.
As of now, has had no formal approval for use in headache relief for children. However, accumulating evidence from several clinical studies indicates efficacy and safety in that population, and many child neurologists are beginning to use them in children. The decision to choose these drugs might be best reserved for consultation.
6.25-12.5 mg PO at onset of migraine; may repeat once, not to exceed 25 mg/d
<18 years: Not established
>18 years: Administer as in adults
Toxicity may increase when used within 24 h of ergotamines or other 5-HT agonists; coadministration with SSRIs may cause weakness, hyperreflexia, or incoordination; CYP3A4 inhibitors (eg, ketoconazole, itraconazole, ritonavir, erythromycin) may increase plasma concentration and subsequent toxicity
Documented hypersensitivity; hemiplegic or basilar migraine; ischemic heart disease; uncontrolled hypertension
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Decrease dose and do not exceed 12.5 mg/d in renal or hepatic impairment
Selective 5-HT1 agonist with long half-life. High affinity for 5-HT 1D and 5-HT 1B receptor subtypes. Has duration of action as long as 24 h with low headache recurrence rate. Useful for patients with slow-onset, prolonged migraine, such as menstrual migraine. Has long half-life (ie, 26-30 h), thus decreases recurrence of migraine within 24 h after treatment.
As of now, has had no formal approval for use in headache relief for children. However, accumulating evidence from several clinical studies indicates efficacy and safety in that population, and many child neurologists are beginning to use them in children. The decision to choose these drugs might be best reserved for consultation.
2.5 mg PO once at onset of migraine attack; may repeat at intervals of 2 h prn; not to exceed 7.5 mg/d
<18 years: Not established
>18 years: Administer as in adults
Toxicity may increase when used within 24 h of ergotamines or other 5-HT agonists; coadministration with SSRIs may cause weakness, hyperreflexia, or incoordination
Documented hypersensitivity; hemiplegic or basilar migraine; ischemic heart disease; uncontrolled hypertension
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hypertensive crisis, coronary artery vasospasm, cardiac arrest, peripheral ischemia, bloody diarrhea, and death may occur
Selective serotonin agonist. 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, has had no formal approval for use in headache relief for children. However, accumulating evidence from several clinical studies indicates efficacy and safety in that population, and many child neurologists are beginning to use them in children. The decision to choose these drugs might be best reserved for consultation.
20-40 mg/dose PO at onset of migraine; if initial dose ineffective, may repeat dose once after 2 h; not to exceed 80 mg/d
<18 years: Not established
>18 years: Administer as in adults
Potent CYP3A4 inhibitors (eg, ketoconazole, itraconazole, nefazodone, troleandomycin, clarithromycin, ritonavir, nelfinavir) may increase toxicity; concurrent administration with ergot-containing drugs may increase vasospastic reactions
Documented hypersensitivity; severe hepatic impairment; age >65 y; administration within 72 h of potent CYP3A4 inhibitors
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Patients with known or suspected coronary artery disease may have increased risk of myocardial ischemia, infarction, or other cardiac or cerebrovascular events (5-HT1 agonists may cause coronary vasospasm)
These agents are useful in the treatment of symptomatic nausea.
Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system. Antiemetic and antihistaminic actions that alleviate nausea and vomiting and promote sleep.
12.5 mg PO/PR tid and 25 mg hs
25 mg IV/IM; repeat prn in 2 h; switch to PO as soon as possible
<2 years: Contraindicated
>2 years: 0.25-0.5 mg/kg/dose PO/IV/IM q6h
May have additive effects when used concurrently with other CNS depressants or anticonvulsants; coadministration with epinephrine may cause hypotension
Documented hypersensitivity; children <2 y (incidences of death due to respiratory depression)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cardiovascular disease, impaired liver function, seizures, sleep apnea, and asthma
Metoclopramide promotes gastric emptying and has antiemetic effects, which are useful to treat the nausea and vomiting associated with migraine.
5-10 mg PO/IV/IM tid
0.1 mg/kg/dose PO/IV q6h prn
Anticholinergics may antagonize effects of metoclopramide; opiate analgesics may increase metoclopramide toxicity in CNS
Documented hypersensitivity; pheochromocytoma; GI hemorrhage, obstruction, or perforation; history of seizure disorders
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adverse reactions include drowsiness, diarrhea, and hypotension; caution in history of mental illness and Parkinson disease (acute dystonic reactions are more common at higher doses); caution in seizure history
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headache, migraine, migraine headache, tension headache, sinus headache, sinusitis, head trauma, intracranial mass, benign intracranial hypertension, pseudotumor cerebri, epilepsy, meningeal irritation, headache causes, headaches in teenagers, basilar migraine, cyclic vomiting syndrome, CVS, ophthalmoplegic migraine, cluster headache, medication overuse headache, MOH, hemiplegic migraine, hemisensory migraine, common migraine, classic migraine, complicated migraine
Kirsten A Bechtel, MD, Associate Professor, Department of Pediatrics, Yale University School of Medicine; Attending Physician, Department of Pediatric Emergency Medicine, Yale-New Haven Children's Hospital
Kirsten A Bechtel, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.
William G Gossman, MD, Associate Clinical Professor of Emergency Medicine, Creighton University School of Medicine; Consulting Staff, Department of Emergency Medicine, Creighton University Medical Center
William G Gossman, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Wayne Wolfram, MD, MPH, Clinical Associate Professor, Departments of Pediatrics, Children's Hospital and University of Cincinnati
Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.
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