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  • headache disorders are classified by the ICHD-III as (1)
    • primary headache disorders:
      • migraine
      • tension type headache
      • cluster headache and other trigeminal autonomic cephalagias
      • other primary headache disorders
    • secondary headache disorders
      • these include a new headache occurring with another lesion capable of causing it.( e.g., headache attributed to intracranial tumour)
  • migraine is a common disabling primary headache disorder
    • migraine is the second most prevalent neurologic disorder (after tension-type headache), with a female-to-male ratio of 3:1 and an estimated 1-year prevalence of approximately 15% in the general population (4,6)
    • prevalence peaks between the ages of 35 and 39 years, and about 75% of affected persons report the onset of migraine before the age of 35 years (4)
      • prevalence peaks in the fourth and fifth decades of life and decreases substantially in later decades (6)
    • since the disorder tends to remit with older age, an onset of migraine after the age of 50 years should arouse suspicion of a secondary headache disorder (4)
    • a person has a 50% chance of having migraine if 1 of their parents has it and a 75% chance if both parents have it (6)
    • migraine onset may occur at any time but typically begins in late childhood, early adolescence, or mid-adulthood (6)
    • migraine is more common in preadolescent boys than girls but later becomes 3 times more common in women than men (6)
  • migraine is a syndrome characterised by:
    • periodic headaches with complete resolution between attacks
    • an attack may be composed of the following stages:
      • prodrome
      • aura
      • headache
      • resolution
    • the frequency of attacks is variable:
      • as high as several per week
      • as low as several per lifetime
    • a prodrome is a vague change in mood or appetite
    • an aura is a clear neurological symptom:
      • visual disturbance
      • motor or sensory disturbance
  • in children, migraine is a diagnosis of exclusion (3)

  • pathophysiology of migraine (5)
    • is complex, with clinical and laboratory evidence suggesting that vulnerability to migraine can be genetic or acquired
      • individual migraine attacks may be triggered by a disruption of homeostatic function resulting in a cascade of effects including:
        • activation of a neuronal phenomenon known as cortical spreading depression,
        • central and peripheral sensitization,
        • triggering of the trigeminovascular pathway
          • this pathway results in release of vasodilatory, pro-inflammatory, or pain producing neuropeptides such as calcitonin gene related peptide (CGRP), a target for pharmacotherapy
      • chronic migraine is associated with a change in nociception threshold, sensitization, and structural brain changes such as cortical thinning


  • (1)Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition. Cephalalgia 2018; 38: 1-211
  • (2) Drug and Therapeutics Bulletin (1998); 36(6):41-4.
  • (3) Drug and Therapeutics Bulletin (2004); 42 (4): 25-8.
  • (4) Ashina M. Migraine. N Engl J Med 2020;383:1866-76. DOI: 10.1056/NEJMra1915327
  • (5) Hovaguimian A, Roth J. Management of chronic migraine BMJ 2022; 379 :e067670 doi:10.1136/bmj-2021-067670
  • (6) Niushen Zhang, Matthew S. Robbins. Migraine. Ann Intern Med. [Epub 10 January 2023]. doi:10.7326/AITC202301170

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