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Approaching the appropriate pharmacotherapy of menstrual migraine

Migraine is now the leading cause of disability in people aged under 50 [1]. It is three times more common in women who go from the beginning of fertility to menopause or immediately after it. The menstrual migraine (MM) subset lasts more than the usual 72 hours and shows a higher acute drug resistance [2]. Additionally, MM preventative treatment is a serious obstacle for the clinician; giving nonsteroidal antiinflammatory drugs (NSAIDs) or triptans as mini-prophylaxis, might limit acute therapeutic options during the menstrual period [3]. The presence of premenstrual syndrome worsens the already complex clinical picture where short-term prophylaxis with triptans, NSAIDs, dihydroergotamine or magnesium shows unsatisfactory results. In cases of medium-high frequency migraine, including MM, therapeutic choices are different offering triptans, NSAIDs and other analgesics as acute treatment. Short-term prophylaxis is based on the same acute drugs plus dihydroergotamine, magnesium and estrogen supplementation, while long-term prophylaxis foresees topiramate, combined hormonal contraceptives, progestogen-only contraception and also phytoestrogens [2,4]. During pregnancy, migraine crises reduce their intensity and frequency in the vast majority of women, returning to previous levels after childbirth [5,6]. The trigeminovascular system in migraine cross-reacts with the local expression of female sex hormones which may modulate calcitonin gene related peptide receptors. Recent preliminary evidence has shown an association between the NRP1 gene and MM, but genomic risk scores showed a weak predictivity for migraine without aura, excluding in any case a diagnostic or prognostic value [7].