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treatment & management

Migraines During Childhood & Adolescence

© Janet McKenzie
© Janet McKenzie

Dancing With Migraine Disease As A Youth

By Michael John Coleman

I still remember clearly the first time a Migraine disrupted my life, I was just six years old and in the first grade. I looked sick enough that the teacher asked me to put my head down on my desk. I still recall looking through the tall classroom windows, with the blinds drawn all the way up and dark battleship-gray fluffy-bellied clouds looming as part of an approaching autumn thunderstorm. Unbeknown to me at the time was that atmospheric pressure changes, induced by weather fronts, was a major Migraine trigger, a fact I will learn later in life. I marveled as the clouds seamed to hover over one side of the playground, and the bright and painful afternoon sunlight on the opposite side of a baseball field, a chiaroscuro effect.

"USDA Roadside View"
© Michael John Coleman 1978

Purchase an artist hand signed giclee print of this original image and all proceeds will be donated to MAGNUM!

To this day, dramatic skies play a dominant roll in the landscapes I produce as an artist. The pain of my Migraines throughout my life has been like being tortured by invisible terrorists. An acute severe Migraine is difficult to explain to a non-suffer. Put it this way; after enduring the so-called 'headaches,' you don't fear other things, such as dentists and bullies. But you do fear having to explain to your childhood friends why you don't want to go out to play basketball. Better to play in pain than say "I have a headache", as that just invites bullying because kids just don't understand what they have not experienced.

Growing up didn’t make things any easier as Migraines became more aggressive as I entered puberty. However, I learned tricks to cope socially. In a Washington, DC suburb high school I had some great friends, only a few knew I had sick headaches (as they where often called 'back in the day'). The pain was horrible, the flickering Florissant lights in the classrooms felt like I was being hit on the head with each flutter. No one else understood, so many teachers opened the blinds on sunny days, and within 15 minutes, the glaring sunlight would beckon the Migraine's aura, as it would come dancing into my line of sight. Never painful the aura, but it was like Alice's Cheshirecat, as it loved taunting me, letting me know I was not going to make it through the class.

The nausea would come next. That sick feeling in your gut wanted to make me vomit, but not in front of my classmates. The pounding would start, like being hit by a baseball bat every 30 or 40 seconds. It was amazing that I passed my classes! The pain would get so bad that I would grab a clump of my hair and pull as hard as I could to distract myself from the pain. I felt like I was going to rip a patch of scalp from my head, but luckily for me I still have all my hair. I would suffer wave after wave of nausea, and I felt as if I could just vomit, I would feel so much better. But never in the classroom in front of the healthy kids, no never that.

Never that because sick people are weak in the eyes of a high school child, and weakness makes you a target of abuse.Luckily for me it was the 70's and illegal drugs where cool, so I would make a B-line to the boys room when the bell rang. I looked like I had been up all night, in a cold sweat, and would kick the door open and head right for a toilet.

Often the pain was so bad I would be shaking, and in the spirit of Ragan in the Exorcist spew projectile vomit across the bathroom floor. Not a pretty sight. Others would walk in behind me and as I sat on the floor throwing up into a toilet I could often here my peers comment, "Hey, Coleman's so wasted, he's cool man!" Like I said, lucky for me, it was the 70's, so I was "in" and never did I let them know I was really severely ill. After severe vomiting, I feel a bit better, at least for a short while, until about half way through my next class the fun would begin again.

I had many friends back then that never had experienced head-pain of any type, and I still know many people like that today, that never understand suffering. Or oddly enough, never even figure out I am in violent pain so often. It's amazing me as an adult today to know so many good and decent people who don't have a clue what person in pain deals with.

As an adult, the pain and suffering I have lived though is freighting, and what is more freighting is knowing that there are millions of others who face this and lose millions of days, weeks, and even years of their lives to Migraine disease. It is only through good disease education, good treatment, proper treatment, and fighting to reclaim my life back that I feel alive today. It amazes me that I still marvel at those dramatic summer thunderclouds with all their beauty, knowing that the barometric pressure change they bring with them may make me horribly ill. But at least know there are things I can do to fight back.

Above is an excerpt from interview with MAGNUM Founder and Executive Director Michael John Coleman discussing his childhood experiences with Migraine disease. If you are a young person visiting the site, his childhood experiences may sound familiar to you. We hope you feel better knowing that you are not alone. However, if you are not getting medical care now, please make sure you sit down with you parents ask for help. You don’t have to try to ‘live with’ this horrible disease. Understanding your illness as well as working with your parents and a good doctor you will soon be enjoying more of your life!

Parents, below you will find an excerpt from MAGNUM advisor Dr. Randy W. Evans, with co-author Dr. Nina T. Mathew, two leading Migraine and headache disorder experts. The excerpt is from their recent book ‘Handbook of Headache,’ published at the respected publisher Lippincott-Williams & Wilkins. Take a few minutes to read the excerpts from Chapter 7 -- Headaches During Childhood and Adolescence:

From Handbook of Headache; Chapter 7-- Headaches During Childhood and Adolescence by Randolph W. Evans, MD, advisor to MAGNUM.

Excerpt from Evans RW, Mathew NT, Handbook of Headache, Lippincott-Williams & Wilkins, Philadelphia, 2000, pp 139-149, 2000, with permission.

To purchase this book directly from the publishers click here or visit: http://lww.com/cgi-bin/wwonline.storefront to view other selections available direct from this pubilsher.


     Headaches are common in children and teenagers. By age 7, 40% of children have had headaches with 2.5% having frequent non-Migraine types and 1.4% Migraine(i). By age 15, 75% have had headaches: 15.7% with frequent tension type, 5.3% with Migraines, and 54% with infrequent non-Migraine headaches.

     The evaluation of the child with headaches is similar to the basic approach in adults described in Chapter 1. A complete history is essential. Information from parents and other family members or caregivers, especially for younger children, is vital. In some adolescents, it is helpful to obtain the history from the child without family members present and then from family members. A psychosocial history is also important. For recurring or chronic headaches, what is the impact of the headaches on the child's life? Has school been missed, homework not done, or other activities curtailed? Because of the frequent familial nature of Migraine, family history is also important. When you ask the parents about their own headaches, often you will diagnose their Migraines for the first time. A general physical and neurological examination are also necessary. General indications for diagnostic testing are discussed in Chapter 1 with table 7 giving general indications for neuroimaging and table 8 focusing on indications in children.

     This chapter covers the following topics: Migraine, episodic tension type headaches, chronic non-progressive headaches, acute headaches, and chronic progressive headaches. Cluster headaches, the subject of Chapter 4, are not separately discussed since the onset is usually over the age of 20 and they are rare in children. Some other causes of secondary headaches in children and adolescents such as posttraumatic, ophthalmologic causes, and pseudotumor cerebri are also reviewed in other chapters.



Introduction.(ii) A variety of Migraine types can occur in children and teenagers. Individuals may have just one type or can have different types. In addition to obtaining the usual history about possible triggers, it is also helpful to ask about a history of motion sickness or sleepwalking which occur much more often in Migraineurs. Motion sickness is reported by 45% of children with Migraine and 5% of controls.(iii) Somnambulism (sleepwalking) occurs in 28% of children with Migraine and 5% of controls.(iv)

Epidemiology. The onset of Migraine frequently occurs during childhood: 20% before the age of 10 and 45% before the age of 20. Until puberty, the prevalence of Migraine is the same in boys and girls. After puberty, the ratio of females to males is 3:1. The peak of new cases of Migraine, the incidence, occurs during childhood (Table 1).(v) The onset of Migraine with aura is earlier than Migraine without aura. Migraine also begins earlier in males than females. By age 15, 5% of children have had Migraines. Of these, about 1.5% have Migraine with aura. The risk of a child developing Migraine is 70% when both parents have Migraine and 45% when one parent is affected.

Table 1. The peak incidence of Migraine with and without aura in males and females
Gender Aura Incidence (per 1000 person-years) Peak age (years)
Male With 6.6 5
Male Without 10 10-11
Females With 14.1 12-13
Females Without 18.9 14-17




Clinical manifestations.

Migraine without aura. As in adults, Migraine without aura is the most common type. However, childhood Migraine can be somewhat different. The duration of headache is often much shorter, lasting as short as 1 hour. Pediatric Migraine is more often bilateral, frontal and temporal, rather than unilateral (35% vs 60% in adults). Finally, there is a higher incidence of light or noise sensitivity alone compared to adults. To reflect these differences, there is a proposed revision of the IHS classification (Table 2).(iv)

Table 2. Proposed Diagnostic Criteria (revised IHS Classification) for Pediatric Migraine
Migraine without aura
A. At least 5 attacks fulfilling B-D
B. Headache attack lasting 1 to 48 hours

C. Headache has at leas 2 of the following:

  1. Bilateral (frontal/temporal) or unilateral location
  2. Pulsating quality
  3. Moderate to severe intensity
  4. Aggravation by routine physical activity

D. During headache, at least 1 of the following:

  1. Nausea and/or vomiting
  2. Photophobia and/or phonophobia
Migraine with aura
A. At least 2 attacks fulfilling B

B. At least 3 of the following:

  1. One or more fully reversible aura symptoms indicating focal cortical and/or brain stem dysfunction
  2. At least 1 aura developing gradually over more than 4 minutes, or 2 or more symptoms occurring in succession.
  3. No auras lasting more than 60 minutes.
  4. Headache follows less than 60 minutes (Headache usually lasts 1 hour to 48 hours).

Migraine with aura. About 20% of children will report the gradual onset of a visual aura before or during the onset of the headache. Descriptions include spots, colors, dots, or lights which are usually in both eyes but about 7% of the time in one eye. The aura usually lasts less than 30 minutes. There can even be distortion of vision where objects may appear larger and smaller ("Alice in Wonderland" syndrome). Table 2 provides criteria for diagnosis.

     Rarely, benign occipital epilepsy can mimic Migraine with aura in children and adolescents. Visual symptoms such as amaurosis, phosphenes (flashes of light), illusions, and visual hallucinations, may be followed by usually hemiclonic movements. Other types of seizure activity can occur such as simple partial, complex partial, and partial with secondary generalization. Headache, nausea, vomiting, and vertigo can be pre and postictal symptoms. The EEG usually shows occipital discharges.

Familial hemiplegic Migraine.(vii) This rare variant is Migraine with aura including hemiplegia or hemiparesis. At least one first degree relative has Migraine with at least one hemiparetic attack. The inheritance is autosomal dominant on chromosome 19. The gene defect is a mutation in a brain-specific P/Q calcium channel subunit.

     Attacks may occur on the same or different side from prior episodes. The face, arm, and leg typically become paretic with a slow spreading progression. There may be an associated alteration in consciousness ranging from confusion to coma. When the dominant hemisphere is involved, aphasia may also be present. Episodes may be triggered by minor head trauma and can also occur without associated headache. The headache can be ipsilateral to the paresis in one third of cases. The hemiparesis may last from less than one hour to days or weeks. Complete recovery usually occurs. Triptans and DHE should not be used during the neurologic deficit because of the potential for vasoconstriction and stroke. Beta blocker medications might be avoided because of anecdotal reports of Migraine induced stroke. Verapamil and valproic acid can be used as preventative agents.

     Depending upon the availability of a family history, the evaluation is similar to that of stroke in the young and may include MRI with MRA and sometimes MRV, blood studies (CBC with platelets, anticardiolipin antibodies, lupus anticoagulant, antithrombin III, protein S and C, Factor V mutation, and others depending upon the clinical context) and cardiac evaluation such as 2D echocardiography. There are numerous causes of hemiparesis and headache including partial seizures, congenital heart disease, acquired heart disease, infectious/inflammatory disease (e.g. HIV and varicella encephalitis), systemic vascular dysfunction (e.g. venous sinus thrombosis and hypertension), vascular disorders (e.g. carotid artery dissection, homocystinuria, MELAS syndrome, and connective tissue disorders), hematologic disorders (e.g hemoglobinopathies, disseminated intravascular coagulation, and antiphospholipid antibody syndrome), cerebrovascular malformations (arteriovenous malformations, aneurysms, and Sturge-Weber syndrome), and head trauma.


Basilar Migraine.(vii) Migraine with aura symptoms originating from the brain stem or from both occipital lobes is known as basilar Migraine (Table 3). The aura of basilar Migraine usually lasts from 5 to 60 minutes but can last up to 3 days. Visual symptoms, including blurred vision, teichopsia (shimmering colored lights accompanied by blanks spots in the visual field), scintillating scotoma, graying of vision, or total loss of vision, may start in one visual field and then spread to become bilateral. Diplopia may be present in up to 16% of cases. Vertigo (which can be present with tinnitus), dysarthria, gait ataxia, and paresthesias (usually bilateral but may alternate sides with a hemidistribution) may be present alone or in various combinations. In 50% of cases, bilateral motor weakness occurs. Impairment of consciousness often occurs including obtundation, amnesia, syncope, and rarely prolonged coma.

     A severe throbbing headache is present in 96% of cases, usually with a bilateral occipital location. Nausea and vomiting typically occur with light and noise sensitivity occurring in up to 50%.

     The differential diagnosis and diagnostic evaluation is similar to that in hemiplegic Migraine. Partial seizures, especially of occipital and temporal lobe origin, can have features similar to basilar Migraine. An EEG study may be considered as part of the evaluation. EEG abnormalities are found in less than 20% of cases. Children and adolescents may have interictal occipital spike-slow wave or spike-wave activity.

     Basilar Migraine is an uncommon disorder. The onset is typically before the age of 30 (although the first attack can occasionally occur in those over age 50) with a 3:1 female preponderance following puberty as other forms of Migraine. The age of onset peaks during adolescence. Children may also have this Migraine type. Those with basilar Migraine may also have other types of Migraine although the basilar type is the predominant one in 75% of cases.

     The frequency of basilar Migraine decreases as patients enter their twenties and thirties. Stroke is a rare complication. As with other forms of Migraine, triggers should be avoided if possible. Although analgesics or non-steroidal anti-inflammatory drugs can be used for the pain, triptans, ergotamine, and DHE should not be used at all because of the potential for vasoconstriction and stroke. Beta-blockers should be avoided because of the potential for stroke but verapamil and valproic acid can be tried as preventative agents.

Table 3. IHS diagnostic criteria for basilar Migraine (Migraine with aura symptoms clearly originating from the brain stem or from both occipital lobes)
A. Fulfills criteria for Migraine with aura

B. Two or more aura symptoms of the following types

  • Visual symptoms in both the temporal and nasal fields of both eyes
  • Dysarthria
  • Vertigo
  • Tinnitus
  • Decreased hearing
  • Double vision
  • Ataxia
  • Bilateral paresthesias
  • Bilateral paresis
  • Decreased level of consciousness

Ophthalmoplegic Migraine. These patients present complaining of Migraine headache and diplopia. This is a rare condition with onset often during adolescence although it may occur during infancy.

     As the intensity of an ipsilateral severe headache subsides after a day or more, paresis of one or more of cranial nerves III, IV, and VI occurs. The 3rd cranial nerve is involved in about 80% of cases, initially with ptosis and then oculomotor paresis which is usually complete but may be partial. Dilation of the pupil, mydriasis, is present in more than 50% of cases. Recovery of nerve function may occur in a week to 4 to 6 weeks. Recovery may be incomplete after multiple attacks.

     The diagnosis is made by excluding as appropriate conditions such as Tolosa-Hunt syndrome (granulomatous inflammation in the cavernous sinus), parasellar lesions, diabetic cranial neuropathy, collagen vascular disease, and orbital pseudotumor (an idiopathic infiltration of orbital structures with chronic inflammatory cells). MRI with MRA is usually adequate although a cerebral arteriogram may be necessary in some cases.

Benign paroxysmal vertigo of childhood.(ix) The onset is usually between 2 and 5 years of age but can start before the age of 1 or as late as the age of 12. Unprovoked stereotypical episodes of true vertigo (with a sensation of movement as described by verbal children) last for seconds or minutes but occasionally can last for hours. The child becomes pale, cannot maintain an upright posture, and wishes to remain absolutely still. There is no complaint of headache or alteration of consciousness although nausea or other abdominal discomfort may follow the vertigo. Because the episodes are so brief, treatment is not usually needed.

     As the child becomes older, the episodes of vertigo may be associated with Migraine headache or may become less severe and disappear. Other types of Migraine may then occur in 21% of these patients.(x)

     Other causes of vertigo in children should be considered. A single prolonged episode could be due to infection of the labyrinth or vestibular nerve. Partial seizures can also produce true vertigo.

Abdominal Migraine (cyclical vomiting). Criteria suggested for abdominal Migraine include the following: a family history of Migraine; a history of Migraine with or without aura in the patient; recurrent identical attacks of abdominal pain; no abdominal symptoms between attacks; onset of attacks of abdominal pain in early childhood or early adult life (before the age of 40), mainly in females; episodes lasting from 1 to several hours; and pain usually located in the upper abdomen.(xi) The episodes may be associated with nausea and vomiting and pallor or flushing. The prevalence peaks at ages 5 to 9 years. As with all Migraine types, this is a diagnosis of exclusion. If there is alteration of consciousness, a seizure disorder should be considered. Other disorders in the differential diagnosis include urogenital disorders , ornithine transcarbamylase deficiency, peptic ulcer disease, cholecystitis, Meckel's diverticulum, partial duodenal obstruction, gastroesophageal reflux, Crohn's disease, and irritable bowel syndrome. Drugs used for Migraine prevention and symptomatic treatment may be helpful.

Confusional Migraine. This is Migraine with a headache, which can be minimal, associated with a confusional state which can last from 10 minutes to 2 days. The patient may be agitated and have impaired memory. There may be inattention, distractibility, and difficulty maintaining coherent speech or action. The diagnosis is made by excluding, as appropriate, the numerous causes of an acute encephalopathy including partial complex seizures, metabolic disorders, infection, and subarachnoid hemorrhage. "Footballer's" Migraine. As discussed in chapter 6, acute minor head trauma can trigger Migraine in children and adolescents. In a study of children with a mean age of 7.4 years who had mild head injuries, a history of motion sickness, Migraines, and a family history of Migraine are highly predictive of vomiting after a mild head injury.(xii)

MELAS syndrome. Mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes, a rare disorder, can present as episodic Migraine early in the course of the disease. The following features must be present: strokelike episodes before age 40 years; encephalopathy with seizures, dementia, or both; and evidence of a mitochondrial myopathy with lactic acidosis, ragged-red fibers, or both. At least two of the following should be present: normal early development, recurrent headache, or recurrent vomiting. The majority of patients have exercise intolerance, limb weakness, short stature, hearing loss, and elevated CSF protein.

     The cause of 90% of cases is an A-to-G point mutation in the mitochondrial gene encoding for tRNA[Leu(UUR)] at nucleotide position 223243. The other 10% are due to seven other mitochondrial DNA point mutations. All children of mothers with MELAS are affected because of maternal transmission of mitochondrial DNA.


Management. Non-medication approaches. Identification and avoidance of Migraine triggers is important. Missing meals, stress, and sleep deprivation can be particularly important triggers. Elimination of caffeinated beverages can be helpful in some cases. Biofeedback, stress management, and progressive relaxation training may be beneficial.(xiii) Education about Migraine for the patient and parents or caretakers is well worthwhile.

Pharmacologic treatments. Acute or symptomatic and preventative type medications are available. Many of the recommendations in this section are anecdotal because of the lack of well-designed studies of treatment of childhood and adolescent Migraine.

Acute headaches (Table 4).(xiv)Aspirin should be avoided before the age of 15 because of the potential for Reye's syndrome. Headaches in children ages 6 and younger are typically brief and resolve with acetaminophen and/or sleep. For children over age 6, acetaminophen alone (10-15 mg/kg) or with the addition of pseudoephedrine (30 mg tablet) may be effective.

     Other options include the following: non-steroidal anti-inflammatory drugs such as ibuprofen (10 mg/kg), naproxen sodium (10 mg/kg);(xv) isometheptene mucate 65 mg, dichloralphenazone 100 mg, and acetaminophen 325 mg (Midrin®,1 capsule); butalbital 50 mg, acetaminophen 325 mg, and caffeine 40 mg (Fioricet®,6-9 years, 1/2 tablet; 9-12 years, 3/4 tablet, and more than 12 years, 1 tablet).
     Children with significant nausea and/or vomiting may benefit from the use of metoclopramide 0.2 mg/kg orally or promethazine 0.5 mg/kg orally or suppository. Some children and adolescents will additionally benefit from a combination of codeine and acetaminophen or acetaminophen, butalbital, and caffeine.

     Total weekly doses of symptomatic medications and caffeine should be carefully monitored because of the potential for causing rebound headaches. There are restrictions on the use of certain acute and preventative medications in hemiplegic and basilar Migraine as detailed above.

     There are additional treatments available for severe Migraines in children and adolescents ages 6 and over not responsive to these medications. In a study of 50 children ages 6-18, Linder administered sumatriptan (Imitrex®) subcutaneously (dose of 0.06 mg/kg) and reported efficacy in 78%.(xvi) In responders, the Migraine recurrence rate was 6%. Adverse events, usually transient and mild, occur in 80%.

     Oral triptans such as sumatriptan (Imitrex®, 25 to 50 mg),(xvii) are often effective in adolescents ages 12 and over. Sumatriptan nasal spray (5 mg or 20 mg depending on size of the patient, efficacy, and adverse events) can also be effective. Anecdotally, triptans may be effective in children over the age of 6. Side effects of triptans are discussed in chapter 2. Triptans are not FDA approved for use in those under age 18.

Table 4. Symptomatic treatment for Migraine in children and adolescents
Acetaminophen 10-15 mg/kg po
Pseudoephedrine HCL 30 mg po
Ibuprofen 10 mg/kg po
Naproxen sodium 10 mg/kg po
Butalbital 50 mg,acetaminophen 325 mg,caffeine 40 mg
  • 6-9 yrs,1/2 tablet
  • 9-12 yrs, 3/4 tablet
  • >12 yrs, 1 tablet
Isometheptene mucate, dichloralphenazone 100 mg, and acetaminophen 325 mg
  • 6-12 yrs, 1 capsule
  • >12 yrs,1-2 capsules
  • 0.06 mg/kg SC
  • 25-50 mg po
  • 5 or 20 mg NS
DHE IV (see Table 6)

     Alternatively, as in adults, children and adolescents with prolonged Migraine often respond to an inpatient protocol of an antiemetic, metoclopramide, and DHE (Table 5), as reported by Linder.(xviii) The oral metoclopramide and IV DHE can be given every 6 hours for a maximum of 8 doses. When the headache ceases, one additional dose can be given. The dose of DHE may be increased by 0.05 mg/dose up to the point where the patient has mild abdominal discomfort. The protocol should be continued at the dose prior to the onset of the abdominal discomfort. Triptans and DHE should not be given within less than 24 hours of each other.

Table 6. Dosing of metoclopramide and DHE for severe intractable Migraine.
Age, years Metoclopramide* DHE
  mg/kg/dose mg/dose
6-9 0.2 mg/kg 0.1 mg/dose
9-12 0.2 mg/kg 0.15 mg/dose
12-16 0.2 mg/kg 0.2 mg/dose

*Administered orally 30 minutes prior to administration of IV DHE. Maximum dose of 20 mg.

These medications can have significant side effects. If metoclopramide causes an extrapyramidal syndrome, diphenhydramine can be given (1 mg/kg, maximum dose of 50 mg) orally, IM, or IV. Metoclopramide can also cause nausea and vomiting. For subsequent DHE doses, ondansetron 0.15 mg/kg IV 30 minutes prior to the DHE dose can be given as an alternative, if necessary, to prevent nausea and vomiting which can be a side effect of DHE or part of the Migraine. Side effects of DHE include a flushed feeling, tingling in the extremities, leg cramping, and a transient increase in headache. DHE is not FDA approved for use in those under age 18.


Preventative medications (Table 6).(xix)Preventative medications should be considered for children and adolescents with frequent Migraines not well-responsive to symptomatic medications or which significantly interfere with school or home activities. In general, preventative medications are started at low doses and slowly increased.

     Beta blockers such as propranol may be effective. The initial dose for children age 8 or older is 10 mg bid which can be increased, depending upon response, by 10 mg per week or slower to a maximum of 20 mg tid for children under 14 years and adult doses (Table 6) for those 14 years and over. Those on higher does of propranolol can be switched to or started on the long acting preparation. Among the numerous possible side effects, beta blockers can occasionally exacerbate asthma, cause hypotension, and cause depression. Propranolol given to diabetic children on insulin can mask symptoms of hypoglycemia. Congestive heart failure, atrioventricular conduction defects, and renal insufficiency are also contraindications to use. In some patients, nadolol or atenolol may be better tolerated with less side effects such as depression or asthenia than propranolol.

Table 6. Preventative medications for Migraine in children and adolescents
Medication Dosage
Propanolol < 14 yrs, initial dose 10 mg po bid May increase by 10 mg/day/each week to 20 mg tid maximum >14 yrs, initial dose 20 mg po bid. May increase by 20 mg/day each week up to 240 mg/day. Equivalent long acting doses may be used.
Cyproheptadine HCl _6 years, 4 mg po hs. May be slowly increased to 12 mg po hs or 8 mg po hs and 4 mg po q.am
Amitriptyline or nortriptline 10 mg po hs. May be increased every 2 weeks to 50 mg po hs <12 yrs and 100 mg po hs >12 y
Divalproex sodium >10 yrs, 125-250 mg po hs, slowly increase to 500-1000 mg in 2 divided doses

     Cyproheptadine (Periactin®), an antihistamine, can also be an effective preventative medication at doses from 4 to 12 mg as a single dose at bedtime or in divided doses such as morning and evening for children 6 years and older. (e.g. starting at 4 mg hs and, depending on effect, slowly increasing after several weeks to 8 mg hs, and later, if necessary, to 12 mg hs or 8 mg hs and 4 mg in the morning). The dose for children under 6 years is 1 mg hs and slowly increasing to 2 mg hs and 2 mg in the morning. Common side effects include weight gain and drowsiness. Cyproheptadine may be the preventative of first choice for those with frequent Migraines and atopic allergies or sinus disease.

     Tricyclic antidepressants, such as amitriptyline (Elavil®) and nortriptyline (Pamelor®), can also be used. For children over 8 years, the starting dose of either is 10 mg per day at bedtime. Depending upon the response and side effects, the total daily dose can be increased by 10 mg every 1 to 2 weeks or slower. Effective daily dosage is typically 50 mg or less in younger children and 100 mg or less in adolescents. Common side effects include sedation, weight gain, and dry mouth. Nortriptyline is less sedating than amitriptyline. The tricylics are often the preventative of choice for those with frequent Migraine and tension type headaches, chronic daily headaches, or associated depression or sleep disturbance. If a tricyclic is not effective, a trial of trazadone (1 mg/kg a day divided into 3 doses) might be considered.(xx)

     Valproic acid may also be effective for Migraine prevention in children and adolescents. Divalproex sodium (Depakote®), the enteric coated form, is commonly used to minimize gastrointestinal side effects. According to data from adult studies, there may be efficacy for Migraine prevention at doses lower than those used for epilepsy. A starting dose of about 125-250 mg given at bedtime may be used and then slowly increased at 2 week intervals or slower. The total daily effective dose, given at bedtime and in the morning, is often 500 mg/day or less in younger children and 500-1000 mg/day in adolescents. This total daily dose may be less than that used for the treatment of epilepsy. There are numerous side effects, as described in Chapter 2, most commonly weight gain, tremor, hair loss, and nausea. Tremor and hair loss are fully reversible after discontinuing the medication. If nausea is persistent, the sprinkle formulation may be better tolerated. This drug can be the one of choice for those with epilepsy and Migraines.

     The rare complication of fatal hepatotoxicity almost always occurs in children under the age of 10. (This complication has been reported for children taking the medication for epilepsy. The risk for those on polytherapy is 1:8307 and on monotherapy, 1:16,317.) Therefore, divalproex sodium should be avoided in children under age 10 unless routine medications have failed, in which case it should be used as monotherapy.(xxi)

Prognosis. Migraine with onset before age 7 more commonly remits in boys than in girls. By age 22, 50% of men and 60% of women still have Migraine. In persons with severe Migraine beginning between the ages of 7 and 15, 20% are Migraine free by age 25 and 50% continue to have Migraines into their fifties and sixties.(xxii)



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iiKandt RS. Childhood Migraine. In Gilman S, Goldstein GW, Waxman SG, editors. Neurobase, San Diego, Arbor Publishing, 1st 1999 ed.

iiiJan MMS. History of motion sickness is predictive of childhood Migraine. J Paediatr Child Health 1998;34:483-484.

ivGiroud M, Nivelon JL, Dumas R. [Somnambulism and Migraine in chidren. A non-fortuitous association]. Arch Fr Pediatr 1987;44:263-265.

vStewart WF, Linet MS, Celentano DD, Van Natta M, Ziegler D. Age and sex-specific incidence rates of Migraine with and without visual aura. Am J Epidemiol 1993:34:1111-1120.

viWinner P, Wasiewski W, Gladstein J, Linder S. Multicenter prospective evaluation of proposed pediatric Migraine revisions to the IHS criteria. Headache 1997;37:545-548.

viiWelch KMA. Hemiplegic Migraine. In Gilman S, Goldstein GW, Waxman SG (eds). Neurobase. San Diego, Arbor Publishing, 1st 1999 ed.

viiiWelch KMA. Basilar Migraine. In Gilman S, Goldstein GW, Waxman SG (eds). Neurobase. San Diego, Arbor Publishing, 1st 1999 ed.

ixDavidoff RA. Benign paroxysmal vertigo of childhood. In Gilman S, Goldstein GW, Waxman SG (eds). Neurobase. San Diego, Arbor Publishing, 1st 1999 ed.

xLindskog U, Ödkvist L, Noaksson L, Wallquist J. Benign paroxysmal vertigo in childhood: a long-term follow-up. Headache 1999;39:33-37.

xiLundberg PO. Abdominal Migraine. Triangle 1978;17:81-84.

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xviiiLinder S. Treatment of childhood headache with dihydroergotamine mesylate. Headache 1994;34:578-580.

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Handbook of Headache
by Randolph W. Evans, & Ninan T. Mathew,
Lippincott Williams & Wilkins
ISBN: 0-7817-1877-5

Information offered at this Web site by either a lay person or a health professional should not be interpreted as giving a diagnosis or a treatment recommendation. These can only be provided by a physician who has had an opportunity to interact with a patient in person and at length, with access to the patient's previous records and appropriate follow-up.