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A 35-year-old woman presented to the office to discuss her migraines. She has episodic unilateral throbbing headaches accompanied by nausea, photophobia, and phonophobia. She used to have a migraine about every 3 months, but is now having one almost every 2 weeks. As this frequency interferes with her life, prophylactic therapy is discussed. She accepts, and her migraine frequency decreases dramatically.


More than 77% of adults experience headaches during their lifetime. Headaches are either primary (migraine, tension-type, trigeminal autonomic cephalgias, or other primary) or secondary (headaches attributed to another cause, including headache medication overuse). The presence or absence of red flags is useful to distinguish dangerous causes of secondary headaches. The most common primary headaches are tension-type and migraine; cluster headache is the most common trigeminal autonomic cephalgia. Medication overuse can complicate headache therapy. Treatment and prognosis depend on type of headache.


  • Lifetime prevalence estimated to be greater than 77% in adults.1

  • Fifty-three percent of adults (61% of women and 45% of men), and 53% of children have had a headache in the past year.1 Elderly adults have a lower rate of headaches, with 36% reporting a headache in the past year.

  • Episodic tension-type headache (TTH) prevalence is 62.6% in adults and 15.9% in children.1

  • Chronic (>15 days per month) TTH has a prevalence of 3.3% in adults and 0.9% in children.1

  • Migraine has a prevalence of 14.7% in adults (8% in men, 17.6% in women) and 9.2% in children.1

  • Medication overuse contributes to daily headache in approximately 1% of adults in the general population.1

  • Cluster headache has a lifetime prevalence of 0.2% to 0.3%.1


  • TTH etiology is uncertain, but likely caused by activation of peripheral afferent neurons in head and neck muscles.2

  • Migraine headache is thought to be caused by genetically influenced neuronal hypersensitivity and anatomic alterations that contribute to extreme sensitivity to changes in homeostasis, which is experienced as recurrent headaches.3 Nociceptive input from the meningeal vessels is abnormally modulated in the dorsal raphe nucleus, locus coeruleus, and nucleus raphe magnus. This activation can be seen on positron emission tomography (PET) scan during an acute attack (Figure 239-1).

  • Trigeminal autonomic cephalgias (TACs), which include cluster headaches, are caused by trigeminal activation with hypothalamic involvement, but the inciting mechanism is unknown.4

FIGURE 239-1

Imaging has helped clarify the etiology of migraine disorder. This positron emission tomography image shows activation in the dorsolateral pons, which includes the noradrenergic locus coeruleus, an area that modulates nociceptive input from the meningeal vessels. (Reproduced with permission from Longo D, Fauci A, Kasper D, et al: Harrison's Principles of Internal Medicine, 18th ed. New York, NY: McGraw-Hill Education; 2011.)

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