Migraines are a neurological condition that affects how the brain processes pain, light, sound, and sensory information. They can cause throbbing head pain, nausea, sensitivity to light or sound, and sometimes visual changes called aura. Girls and women experience migraines far more frequently than boys and men, especially after puberty (Victor et al., 2010). This difference isn’t a coincidence. One of the biggest reasons is estrogen, a hormone that profoundly influences the brain.

How Estrogen Affects the Brain

Estrogen does far more than regulate the menstrual cycle. It also affects mood, sleep, blood vessels, serotonin levels, and how the brain interprets pain. Because of this, even normal hormonal shifts can strongly influence migraine patterns. Research shows that the most important factor is not simply how much estrogen you have, but how quickly those levels rise and fall (MacGregor, 2009; Vetvik & MacGregor, 2017). Many girls begin experiencing migraines soon after puberty begins, and one major reason is that estrogen levels start cycling for the first time.

The most important insight from decades of research is simple: it is usually the change in estrogen, especially a sharp drop, that triggers migraines. This hormonal “swing” is something nearly every menstruating girl experiences.

The Menstrual Cycle and Migraine Patterns

A typical menstrual cycle begins with low estrogen levels during menstruation. Over the next week or so, estrogen steadily rises and reaches its highest point around ovulation. After ovulation, estrogen remains moderately high for a while before dropping sharply right before the next period.

That final drop is one of the strongest migraine triggers known in migraine research (Martin et al., 2006). Scientists call this an estrogen-withdrawal migraine. Early research discovered that when someone has several days of high estrogen and then experiences a sudden decrease, it can reliably bring on a migraine attack (Somerville, 1972). This precise hormonal pattern occurs naturally at the end of every menstrual cycle and explains why so many girls experience migraines either in the days leading up to their period or during the first days of bleeding.

This pattern can also happen when birth control methods are started or stopped, or when cycles are irregular, which is very common in the teenage years.

Where High Estrogen Fits In

Although estrogen drops are the direct trigger, high estrogen levels still play an important role. Elevated estrogen can make the brain more sensitive and can increase cortical excitability (the cerebral cortex activating from a stimulus), which is associated with migraine aura (Hansen et al., 2011). Lifetime high estrogen exposure has also been connected with increased migraine risk in certain populations (Li et al., 2024). For many girls, the high estrogen level during the first part of the cycle creates a situation where the sharp drop later in the cycle is more dramatic.

The truest scientific pattern is: high estrogen followed by a sudden drop makes migraines much more likely. This “set up and trigger” pattern is why both high estrogen and low estrogen matter, but in different ways.

Why Teens Often Experience More Migraines

Before puberty, migraines occur at similar rates across genders. After puberty begins, migraine becomes far more common in girls—two to three times more common, in fact (Victor et al., 2010). Teen years are a period of hormonal instability. Menstrual cycles can be irregular for months or even years, meaning estrogen rises and falls in unpredictable ways. This irregular cycling increases the number of hormonal fluctuations, which increases the likelihood of migraines.

Research shows that menstrual migraine patterns begin very early in adolescence and often become more recognizable and predictable by late teenage years (Morton et al., 2021). Understanding the timing of migraines in relation to the menstrual cycle is one of the most powerful tools for recognizing a hormonally influenced pattern.

Peer-reviewed research confirms several consistent findings. First, estrogen fluctuations, especially the drop before menstruation, are the strongest hormonal triggers for migraine (MacGregor, 2009; Martin et al., 2006). Second, high estrogen can increase the likelihood of aura by making the brain more sensitive to sensory disturbances (Hansen et al., 2011). Third, Somerville’s classic estrogen-withdrawal studies showed that migraine attacks can be brought on simply by withdrawing estrogen after a period of high exposure (Somerville, 1972). Fourth, adolescents experience more migraines in part because their cycles are often irregular, creating more abrupt hormonal changes (Wöber-Bingöl, 2013). Finally, stabilizing estrogen is an effective treatment approach in some individuals (MacGregor et al., 2006).

These insights help explain why migraines are not random for many teens: they follow a biological pattern tied closely to menstrual timing.

What can I do with this?

The most important step is to track your cycle and your symptoms together. Writing down when your period starts and ends, when migraines occur, and any symptoms of aura or sensitivity helps reveal patterns. Even two or three months of tracking often shows whether your migraines cluster around particular cycle days.

Talking with a clinician who understands teen health is essential. If migraines seem connected to your menstrual cycle, treatments may include timing certain medications before the expected estrogen drop, using non-hormonal preventive options, or exploring hormonal stabilization when appropriate. Sharing whether your cycle is irregular, whether you experience aura, or whether symptoms changed after starting birth control helps a clinician design the right plan.

Most importantly, migraines in adolescence are real, valid, and rooted in neurobiology—not weakness, mood, or imagination. Understanding your hormones can help you understand your symptoms.

References

Hansen, J. M., Lipton, R. B., Dodick, D. W., Silberstein, S. D., & Aurora, S. K. (2011). Migraine with aura: Cardiovascular and neurovascular risk. The Lancet Neurology, 10(5), 454–461. https://doi.org/10.1016/S1474-4422(11)70072-5 

Li, C., et al. (2024). Lifetime estrogen exposure and migraine prevalence in postmenopausal women: A population-based cohort study. Neurology, 102(6), e613–e622.

MacGregor, E. A. (2009). Estrogen and attacks of migraine with and without aura. Annals of Neurology, 65(5), 622–626.

MacGregor, E. A., Frith, A., Ellis, J., Aspinall, L., & Hackshaw, A. (2006). Prevention of menstrual attacks of migraine: A double-blind placebo-controlled crossover study. Neurology, 67(12), 2159–2163.

Martin, V. T., Wernke, S., Mandell, K., & Zoma, W. (2006). Medical treatment of menstrual migraine. Obstetrical & Gynecological Survey, 61(10), 677–685.

Morton, S., Davis, J., & Buse, D. (2021). Menstrual migraine in adolescents: Prevalence, disability, and clinical characteristics. Headache, 61(5), 739–748.

Somerville, B. W. (1972). The role of estradiol withdrawal in the precipitation of menstrual migraine. Neurology, 22(4), 355–365.

Vetvik, K. G., & MacGregor, E. A. (2017). Menstrual migraine: A review of epidemiology, mechanisms, and treatment. Nature Reviews Neurology, 13(12), 655–665.

Victor, T. W., Hu, X., Campbell, J., & Buse, D. (2010). Migraine prevalence by age and sex in the United States. Headache, 50(10), 1457–1468.

Wöber-Bingöl, Ç. (2013). Epidemiology of migraine in children and adolescents. Current Pain and Headache Reports, 17(6), 341.