Increases or decreases in estrogen levels can trigger headaches, including migraines. Changes in estrogen levels can result from biologic processes (eg, menstruation, pregnancy, or menopause) or from use of hormones (eg, hormone-containing contraceptives, in vitro fertilization). Migraine is the headache type most affected by estrogen.
The pathophysiology of migraine is likely multifactorial. It is thought to be related to changes in neural networks involved in pain connectivity. Briefly, activation of central pain pathways stimulates the trigeminovascular system causing associated release of vascular inflammatory substances, such as calcitonin gene-related peptide (CGRP), cytokines, and prostaglandins. Estrogen has been shown to modulate this pathway in multiple complex ways, altering these vascular inflammatory substances.
Female physiology is one of the most common risk factors for migraine development. Migraine is up to three times more prevalent in females than males. Before puberty, the prevalence of migraine is similar for females and males. Migraine prevalence in females starts to climb in early adolescence (which coincides with the onset of menses), peaks during the 20s and 30s, and decreases following menopause. Observational studies of females with migraine have reported approximately 18 to 25 percent note a relationship between menses and migraine.
Patients with any type of estrogen-associated migraine have multiple treatment options, including nonpharmacologic lifestyle changes for migraine prevention, targeted treatment for acute symptoms, preventative therapy as needed (mini prophylaxis), or continuous prophylaxis. Please make an appointment with a MCHN provider to discuss.
–Alice Wong, NP