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Sex hormones and migraine are closely interlinked. Women report higher levels of migraine symptoms during periods of sex hormone fluctuation, particularly during puberty, pregnancy, and perimenopause. Ovarian steroids, such as estrogen and progesterone, exert complex effects on the peripheral and central nervous systems, including pain, a variety of special sensory and autonomic functions, and affective processing. A panel of basic scientists, when challenged to explain what was known about how sex hormones affect the nervous system, focused on two hormones: estrogen and oxytocin.
Estrogen plays a complicated role in migraine disease. Both drops and fluctuations in estrogen are associated with migraine symptoms, but its effect varies between individuals because of different receptors, metabolites, and interactions with other hormones. The dominant understanding of how crucial estrogen is in protecting individuals from migraine symptoms is what happens when estrogen levels decline: the estrogen withdrawal hypothesis. This hypothesis theorizes that drops in plasma estrogen trigger migraine attacks and neuroinflammation, eventually leading to chronic sensitization [29]. There are several possible mechanisms to explain his theory. One explanation is that estrogen suppresses pain by binding to estrogen receptor alpha (ER alpha) and estrogen receptor beta (ER beta), which are primarily associated with cell nuclei in the trigeminal ganglia. Activation of these nuclear receptors regulates inflammatory genes that ultimately suppresses cell excitability [30].
Prolactin (PRL) is a hormone that is responsible for lactation, breast development, and hundreds of other actions needed to maintain homeostasis. PRL is chemically related to growth hormones and placental lactogen hormones. In an animal model, high levels of prolactin increased meningeal trigeminal pain sensitivity by only affecting CGRP in female rodents [74].