Hormonal instability during perimenopause can worsen migraine frequency and predictability. Migraine without aura often improves after menopause, whereas migraine with aura tends to persist and increases ischemic stroke risk. Midlife comorbidities—vasomotor symptoms, sleep disturbance, mood disorders, and metabolic disease—further complicate management.

Hormone therapy has variable effects. Oral estrogen, particularly at higher doses, may worsen migraine and elevate vascular risk, especially in women with aura. In contrast, low-dose transdermal estrogen appears safer and better tolerated. Continuous progestogen regimens may reduce withdrawal-related attacks. Non-hormonal options such as SSRIs, SNRIs, gabapentin, and clonidine are useful for both migraine and vasomotor symptoms.

Traditional migraine therapies (triptans, NSAIDs, beta-blockers, topiramate, antidepressants) remain central but require tailoring to vascular and metabolic health. Newer agents—including CGRP monoclonal antibodies, gepants, and ditans—offer effective, non-vasoconstrictive options, especially when cardiovascular risk is present.

Migraine during the menopausal transition reflects the interplay between hormonal dynamics and systemic health. Management requires balancing efficacy with vascular and metabolic safety while incorporating patient preferences. Evidence gaps include the lack of trials stratified by menopausal stage or migraine subtype. Multidisciplinary, menopause-informed care and prospective studies are needed to optimize outcomes in this population.