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
Reference:
(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
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