More than a Headache: Understanding Migraine in Women

As we mark Migraine and Headache Awareness Month, it’s essential to spotlight a condition that affects one in five women - often silently, chronically, and with devastating impact. Migraine is not "just a headache"; it's the second leading cause of years lived with disability (YLDs) worldwide, and disproportionately burdens women, especially during their reproductive years (Steiner et al., 2020). 

“It’s not just the pain - it’s the planning around it, the guilt of missing work or family time, and the fear of not being believed.”

— Rania, 38, living with chronic migraine since her teens

In recognition of this, we’re highlighting key insights from a 2025 review by Dr. Mona Ghadiri-Sani, exploring how hormonal biology, clinical presentation, and therapeutic strategies intersect in women’s experience of migraine.

Epidemiology: A Gendered Burden

Migraine affects 14% of the global population, but women are 2–3 times more likely to be affected than men. This disparity becomes pronounced after puberty and peaks during reproductive years (15–49), where up to 17% of women meet diagnostic criteria for migraine (Vetvik & MacGregor, 2017).

Key Stats:

• Chronic migraine (≥15 headache days/month) is more common in women

• Women experience longer, more disabling attacks, higher recurrence rates, and greater medication use

• Comorbid conditions such as depression, anxiety, epilepsy, vascular disease, and chronic pain are more prevalent (Ghadiri-Sani, 2025).

Pathophysiology: The Role of CGRP and Sensory Processing

Migraine is increasingly understood as a disorder of sensory processing, initiated via activation of the trigeminovascular system. This activation leads to the release of calcitonin gene-related peptide (CGRP), a potent vasodilator and inflammatory neuropeptide, which drives pain and associated symptoms (Goadsby et al., 2017).

There are 4 key phases of migraines:

• Prodrome: Mood changes, food cravings

• Aura (25% of patients): Visual/sensory disturbances caused by cortical spreading depression (CSD), a wave of neuronal and glial depolarisation followed by suppression of brain activity that spreads across the cortex

• Migraine Attack/Headache: Typically unilateral, throbbing, aggravated by activity, with nausea, photophobia, phonophobia

• Postdrome: Fatigue, cognitive slowing

Hormones and Migraine: The Oestrogen Effect

Hormonal fluctuations (particularly in oestrogen) modulate migraine patterns in women. Oestrogen exerts effects across multiple neural systems, including serotonergic, dopaminergic, glutamatergic, and GABAergic pathways, and directly influences trigeminal sensory neurons.

Oestrogen plays a dual role in migraines:

• High oestrogen states (e.g., pregnancy, combined oral contraceptive use) → ↑ migraine with aura

• Oestrogen withdrawal (e.g., menstruation, postpartum) → ↑ migraine without aura

In animal models, oestradiol (the main oestrogen hormone found in women) increases CGRP expression, while progesterone and testosterone show antinociceptive and anti-inflammatory properties (Martin & Behbehani, 2006; Vetvik & MacGregor, 2017). Functional MRI studies have also shown women with migraine have increased activation in pain-affective circuits like the insula and amygdala compared to men (Ghadiri-Sani, 2025). 

Migraine Across the Lifespan

Menstrual Migraine

This type of migraine occurs in the perimenstrual window (days -2 to +3 of menstruation), tends to be more severe, prolonged, and disabling, and is often less responsive to standard treatment (Sacco et al., 2012). There are a few evidence-based treatments:

Acute: NSAIDs, triptans, mefenamic acid (Al-Waili, 2000)

Preventative:

• CGRP monoclonal antibodies show marked reduction in attack frequency, intensity, and duration (Silvestro et al., 2021; Jiang & Huang, 2022)

• Hormonal therapies (e.g., continuous low-dose combined oral contraceptives which contain both oestrogen and progestin, or oestrogen supplementation) may help stabilise hormone levels and reduce migraine frequency. These should be used with caution in women with aura due to an increased risk of ischemic stroke (Massiou & MacGregor, 2000; Kemmeren et al., 2001).

Pregnancy and Postpartum

Pregnancy offers a unique hormonal environment that can significantly influence migraine activity. For many women (particularly those with migraine without aura), symptoms often improve or remit during pregnancy, especially in the second and third trimesters, when oestrogen levels rise steadily and stabilise. Studies report a noticeable reduction in migraine frequency and severity during this time (in up to 89% of patients) (Granella et al., 2003). Treating migraine during pregnancy is often complex due to safety concerns for the fetus. The goal is to balance effective symptom control with minimisation of fetal exposure to pharmacologic agents.

In contrast, the postpartum period is often marked by a sharp decline in oestrogen, sleep deprivation, stress, and changes in routine - all of which can reactivate or worsen migraine symptoms. Many women report their most severe migraines occurring in the days to weeks following delivery. Women who continue to experience active migraine during pregnancy and postpartum also experience increased associated risks, such as preeclampsia, stroke, or thromboembolism (Bushnell et al., 2009). 

Perimenopause and Menopause

The menopausal transition, or perimenopause, is a time of significant hormonal fluctuation, particularly in oestrogen and progesterone levels, which can lead to a resurgence or worsening of migraine in many women. These fluctuations are often erratic and unpredictable, and migraines during this time are frequently described as more intense, frequent, and refractory to treatment. For many, especially those with a history of menstrual migraine, this period can represent a particularly challenging phase of disease burden.

In contrast, post-menopause (when oestrogen levels stabilise at consistently low levels) is often associated with spontaneous improvement or remission of migraine symptoms (Wang et al., 2003). However, this is not universal, and the trajectory can vary depending on migraine type, baseline hormonal sensitivity, surgical history, and comorbidities.

Surgical vs. Natural Menopause

Women who undergo surgical menopause (e.g., bilateral oophorectomy) often report worse migraine outcomes compared to those who experience natural menopause. The abrupt cessation of ovarian hormone production in surgical menopause results in a sudden drop in oestrogen, which can trigger severe and persistent migraines. In contrast, natural menopause involves a more gradual decline, allowing for a period of hormonal adaptation.

Racial and Socioeconomic Disparities in Migraine Diagnosis and Treatment

Migraine disproportionately affects women, but within this population, women of color and those from lower-income backgrounds face additional and well-documented disparities.

Black and Hispanic women are 25–37% less likely than white women to receive a migraine diagnosis, despite comparable symptom profiles (Buse et al., 2013). Access to care is uneven, with lower-income patients less likely to see specialists and more reliant on emergency departments (Minen et al., 2016).

"Every time I went to the ER, they told me it was just stress or dehydration. It took years before anyone even said the word ‘migraine’."

- Carmen, 42, Afro-Latina woman with undiagnosed chronic migraine for over a decade

High-cost therapies such as CGRP monoclonal antibodies and gepants are underutilised in these groups due to insurance barriers, provider bias, and lack of communication about newer options (Robbins et al., 2022). Undiagnosed or inadequately treated migraine contributes to higher ED visits, missed work, mental health comorbidities, and reduced quality of life (Steiner et al., 2020).

Addressing these disparities requires systemic reforms, including expanding access, ensuring provider training on bias and equity, and increasing the inclusion of underrepresented groups in migraine research.

Final Thoughts

As we shine a spotlight on Migraine Awareness Month, we must continue to emphasise that migraine is a biologically complex, hormonally modulated, and debilitating neurological disorder - particularly for women. Understanding the role of oestrogen, tailoring treatment across life stages, and integrating both pharmacological and nonpharmacological strategies are key to improving outcomes.

Let’s advocate for gender-aware research, equitable access to emerging treatments, and greater awareness - because every woman deserves to be migraine free.  

References

Steiner TJ, Stovner LJ, Jensen R, Uluduz D, Katsarava Z. Migraine remains second among the world’s causes of disability, and first among young women: findings from GBD 2019. J Headache Pain. 2020;21(1):17.

Vetvik KG, MacGregor EA. Sex differences in the epidemiology, clinical features, and pathophysiology of migraine. Lancet Neurol. 2017;16(1):76–87.

Ghadiri-Sani, M. (2025). Migraine in women: A review. Current Opinion in Neurology, 00(0), 1–6. https://doi.org/10.1097/WCO.0000000000001372

Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S. Pathophysiology of migraine: a disorder of sensory processing. Physiol Rev. 2017;97(2):553–622.

Martin VT, Behbehani M. Ovarian hormones and migraine headache: understanding mechanisms and pathogenesis. Headache. 2006;46(Suppl 1): S3–S23.

Sacco S, Ricci S, Degan D, Carolei A. Migraine in women: the role of hormones and their impact on vascular diseases. J Headache Pain. 2012;13(3):177–189.

Al-Waili NS. Treatment of menstrual migraine with prostaglandin synthesis inhibitor mefenamic acid: double-blind study with placebo. Eur J Med Res. 2000;5(4):176–182.

Silvestro M, Orologio I, Bonavita S, et al. Effectiveness and safety of CGRP-mAbs in menstrual related migraine: a real-world experience. Pain Ther. 2021;10(2):1203–1214.

Jiang Y, Huang ZL. Recent advances in targeting calcitonin gene-related peptide for the treatment of menstrual migraine. Medicine (Baltimore). 2022;101(39): e29361.

Massiou H, MacGregor EA. Evolution and treatment of migraine with oral contraceptives. Cephalalgia. 2000;20(2):170–174.

Kemmeren JM, Algra A, Grobbee DE. Third generation oral contraceptives and risk of venous thrombosis: meta-analysis. BMJ. 2001;323(7305):131–134.

Granella F, Sances G, Pucci E, et al. Course of migraine during pregnancy and postpartum: a prospective study. Cephalalgia. 2003;23(3):197–205.

Bushnell CD, Jamison M, James AH. Migraine during pregnancy linked to stroke and vascular diseases: US population-based case–control study. BMJ. 2009;338: b664.

Wang SJ, Fuh JL, Lu SR, et al. Migraine prevalence during menopausal transition. Headache. 2003;43(5):470–478. 

Buse, D. C., Loder, E. W., Gorman, J. A., & Lipton, R. B. (2013). Sex differences in the burden of migraine: Results from the American Migraine Prevalence and Prevention (AMPP) Study. Headache, 53(4), 673–692.

Minen, M. T., Tanev, K., Friedman, B. W., & Norris, E. (2016). Evaluation and treatment of migraine in the emergency department: A review. Headache, 54(7), 1131–1145.

Robbins, M. S., Starling, A. J., Pradhan, A. A., et al. (2022). Barriers to equitable access to CGRP-targeted treatments for migraine: A narrative review. Neurology: Clinical Practice, 12(1), 35–43.

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This article was written by Neave Smith and edited by Julia Dabrowska, with graphics produced by Neave Smith. If you enjoyed this article, be the first to be notified about new posts by signing up to become a WiNUK member (top right of this page)! Interested in writing for WiNUK yourself? Contact us through the blog page and the editors will be in touch.