Hemicrania

• headache disorders are classified by the ICHD-III as (1)
  • primary headache disorders:
    • migraine
    • tension type headache
    • cluster headache and other trigeminal autonomic cephalgias
    • 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 (2,4)
  • 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 (2)
    • prevalence peaks in the fourth and fifth decades of life and decreases substantially in later decades (4)
  • 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 (2)
  • 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 (4)
  • migraine onset may occur at any time but typically begins in late childhood, early adolescence, or mid-adulthood (4)
  • migraine is more common in preadolescent boys than girls but later becomes 3 times more common in women than men (4)
• 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
  
  
• pathophysiology of migraine (3)
  • 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 trigemino-vascular 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

References:

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