Update on Migraine Management

Lisa Larkin, MD, FACP, NCMP, IF


Menopause. 2022;29(5):606-608. 

In This Article

Pathophysiology and Diagnostic Criteria

Diagnosis of episodic migraine (EM), with or without aura, requires a history of five unilateral, pulsating, moderate to severe headaches, lasting between 4 and 72 hours, that are worse with exercise and associated with nausea and vomiting or photophobia or phonophobia.[2] Twenty-five percent of persons with EM have EM with aura—a constellation of visual, auditory, or somatosensory symptoms that precede the headache.

Migraine frequency in women is affected by reproductive hormone changes. The headaches often start at puberty, improve during pregnancy, worsen during perimenopause, and often improve after menopause. Seven percent of premenopausal women with migraine have pure menstrual migraine (PMM), and headaches occur only during the perimenstrual period. Seventy percent of women with EM have menstrual-related migraines (MRM), with headaches occurring not only around the menses but also at other times not associated with menses. It is the decline in estrogen levels that triggers migraine in women with PMM and MRM; onset is typically 2 to 3 days before onset of menses through day 2 today 3 of the menstrual cycle. Compared with EM, PMM and MRM are less associated with aura, tend to be more severe, last longer, and are more refractory to abortive treatment.

For decades, migraine was thought to be related to vascular dysregulation in the central nervous system (CNS). We now understand migraine through a model that involves the activation of the trigeminal vascular system (TGVS) in the CNS. In this model, a modulating trigger (such as lack of sleep or hormone changes) leads to activation of the TGVS and release of calcitonin gene-related peptide (CGRP), a 37 amino acid peptide with a half-life of 5 minutes that regulates pain transmission.[3] Its levels increase during a migraine attack, and infusion of CGRP induces migraine.