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Migraine Headaches

  1. Definition:
    2004 International Headache Society criteria
    Pediatric migraine without aura

    Pediatric migraine with aura
    Aura represents transient, focal somatosensory phenomena such as visual scotomata or distortions, dysesthesias, hemiparesis, or aphasia.

    1. At least five attacks fulfilling criteria B-E.
    2. Headache attacks lasting 1 - 72 hours.
    3. Headache has at least two of the following characteristics:
      1. Unilateral location, may be bilateral, frontotemporal (not occipital)
      2. Pulsing quality
      3. Moderate or severe pain intensity
      4. Aggravation by or causing avoidance of routine physical activity
    4. During the headache, at least one of the following:
      1. Nausea and/or vomiting
      2. Photophobia and phonophobia, which may be inferred from behavior
    5. Not attributed to another disorder
    6. At least two attacks fulfilling the criteria below
    7. At least three of the following:
      1. One or more fully reversible aura symptoms
      2. At least one aura symptom develops over 4 or more minutes, or two or more symptoms occur in succession
      3. No aura last more than 60 minutes
      4. Headache follows aura with a free interval of less than 60 minutes
    8. At least one of the following
      1. History, physical, and neurologic examinations do not support an organic disorder
      2. If organic disorder is suggested from the above, it is ruled out by appropriate investigations.
      3. If organic disorder is present, migraine headaches do not occur in close temporal relation to the disorder.
  2. Prevalence of migraine headaches through childhood

    By age (years)  3-77-1115
    Prevalence1.2-3.2%  4-11%  8-23%
    Gender ratioM>FM=F


  3. Pathophysiology
    Pathophysiology of migraines begins with an inherited vulnerability of a hyperexcitable cerebral cortex. Stimuli trigger episodes of cortical spreading depression (CSD). CSD represents a slowly propagating wave (2-6mm/min) of neuronal depolarization. CSD initiates vascular dilation with extravasation of plasma proteins from dural vessels and leads to neurogenic inflammation. At this stage virtually any stimulation is perceived as painful (allodynia).
  4. Clinical manifestations
    Triggers include stress, fatigue, hunger, certain foods, head injuries, changes in weather, exercise and menses.

    Aura signs and symptoms include blurred vision, light distortions, numbness or tingling around the mouth or fingers, difficulty speaking and unilateral weakness. Auras occur in 50% of children with migraine headaches.

    Headache is described as intense, throbbing, or pulsating, but can be dull pressure type pain. Pain is typically unilateral and frontal in location, but children can have bi-frontal or bi-temporal pain. Associated signs and symptoms include nausea, vomiting, photophobia, phonophobia, tremors, vertigo, and abdominal pain.
  5. Treatment
    • Two main treatment strategies: acute pain relief and preventing future attacks. Treatment regimens address 3 major mechanism in the pathogenesis of migraine:
    • Mild to moderate pain (interferes but does not prevent routine activities), no nausea /vomiting
    • Mild to moderate pain with nausea/vomiting
    • Severe pain (prevents routine activities), no nausea/vomiting
    • Severe pain with nausea/vomiting

      (A) effective per blinded, randomized clinical trials (RCT)
      (B) probably effective per prospective matched group cohort studies or less rigid RCT
      (U) unproven

      • dopaminergic hypersensitivity
      • inflammation
      • 5-hydroxytryptamine (5-HT) metabolism
      • acetaminophen 15mg/kg po, max 1000mg (B), and/or:
      • ibuprofen 10mg/kg po, max 600mg (A), and:
      • sumatriptan 10mg intra-nasal, 6 to 11 years of age (A); 20mg intra-nasal, 12 or greater years of age (A)
      • ketorolac 30-60mg IM or IV (A), and:
      • prochlorperazine (compazine) 5 to 10mg IV or IM (U), and:
      • sumatriptan 10mg intra-nasal, 6 to 11 years of age (A); 20mg intra-nasal, 12 or greater years of age (A)
      • same as A (mild to moderate pain, no nausea/vomiting), and:
      • dexamethasone 10 to 20mg po (U)
      • Same as B (mild to moderate pain with nausea/vomiting), and:
      • dexamethasone 10 to 20mg IV or IM (U)
  6. Preventive treatment

    1. Pharmacological agents (all unproven effectiveness)
      Note: Flunarizine (calcium channel blocker) is probably effective for preventive therapy but is not available in the United States.

      1. antihistamine (cyproheptadine)
      2. antihypertensive (propranolol and clonidine)
      3. antidepressant (amitriptyline and trazodone)
      4. anticonvulsant (valproic acid, topiramate, levetiracetam)
      5. calcium channel blockers (nimodipine)
    2. Non-pharmacological treatment
      1. identify and avoid triggers
      2. biobehavorial
        • biofeedback
        • relaxation therapy
        • cognitive therapy/stress management
      3. dietary measures
        • avoid dietary triggers
        • caffeine moderation
    3. Analgesic Rebound Headache

      Definition: recurrent headaches associated with daily to near daily analgesic (acetaminophen and/or ibuprofen) use. Consider this diagnosis in children with migraines.

      Treatment: discontinue daily analgesic use.


  • Bulloch B, Tenenbein M. Emergency Department Management of Pediatric Migraine. Ped Emerg Care. 2000;16:196-201.
  • Lewis DW. Toward the Definition of Childhood Migraine. Curr Opin Pediatr 2004;16:628-636.
  • Winner P, Rothner AD, Saper J, et al. A Randomized, Double-Blind, Placebo-Controlled Study of Sumatriptan Nasal Spray in the Treatment of Acute Migraine in Adolescents (12-17years). Pediatrics 2000;106:989-997.
  • Lewis D, Ashwal S, Hershey A, et al. Practice Parameter: Pharmacological Treatment of Migraine Headache in Children and Adolescents. Neurology 2004;63:2215-2224.
  • Vasconcellos E, Pina-Garza JE, Millan EJ et al. Analgesic Rebound Headache in Children and Adolescents. J Child Neurol 1998; 13:443-447.

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