Headache: Migraine

Introduction

• Description: Migraine headaches are recurrent severe headaches that last for 4–72 hours and are accompanied by neurologic, gastrointestinal, and autonomic changes. These may or may not be preceded by a characteristic aura.

• Prevalence: Migraine headaches affect 15%–20% of women in the reproductive age. Approximately 10% of tension headache sufferers also have migraine headaches.

• Predominant Age: Migraine headaches—ages 25–55 years (peak, 30–49 years), first attack generally between adolescence and 20 years.

• Genetics: Migraines are three times more common in women than in men. Of migraine sufferers, 89% have a family history of headache. Several genes have been implicated, including the KCNK18 gene (encodes for TRESK, a two-pore domain potassium channel) and the CSNK1D (encodes casein kinase I isoform delta), but confirmed associations are lacking.

Etiology and Pathogenesis

• Causes: Neuronal dysfunction leads to a sequence of changes intracranially and extracranially that results in migraine (including the four phases; prodromal symptoms, aura, headache, and postdrome). Migraine aura and headache are related to a cortical spreading depression (self-propagating wave of neuronal and glial depolarization that spreads over the cerebral cortex). This depolarization results in the aura of migraine, activation of trigeminal nerve afferents, and altered blood-brain barrier permeability. Activation of trigeminal afferents causes sterile inflammatory changes in the pain-sensitive meninges, resulting in headache. Stimulation of the trigeminal ganglion also causes release of vasoactive neuropeptides (substance P, calcitonin gene-related peptide [CGRP], neurokinin A) resulting in vasodilation and protein extravasation. Neuronal sensitization occurs, amplifying nociception. The CGRP (a 37–amino acid neuropeptide) plays a key role in mediating trigeminovascular pain transmission and vasodilation. A strong relationship with female sex hormones is suspected.

• Risk Factors: More common in upper-income patients (1.6 times); 60%–70% of women note a link with menstruation (14% of women have migraine headaches only during menses). Precipitating factors: emotional stress (80%), some foods, stress relief (let down), missed meals, sleep disturbances.

Signs and Symptoms

• May be preceded by prodrome (75%) or aura lasting <1 hour (25%)

• May begin with dull ache

• Unilateral pain (30%–40%, may switch sides from attack to attack)

• Pulsating quality (60%), rapid onset

• Moderate to severe intensity

• Made worse by activity

• Frequently accompanied by nausea (90%), vomiting (60%), photophobia (80%), phonophobia, blurred vision, scalp tenderness and neck stiffness, restlessness, irritability, nasal congestion, facial edema

• Menstrual migraine is characterized by onset between 1 day before and 4 days after menstruation (first day is most common). This pattern is observed in 15% of patients.

Diagnostic Approach