Neurology
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Changes in estrogen levels at menarche, menstruation, pregnancy, and menopause may trigger or change the prevalence of migraine. The fall in estrogen that occurs with menstruation is the trigger for menstrual migraine, whereas the sustained high estrogen levels during pregnancy frequently result in headache relief. Estrogen produces changes in prostaglandins, hypothalmic opioids, and prolactin secretion, which may in part account for genesis of headache. The treatment of menstrual migraine and migraine associated with menopause and the use of oral contraceptives is discussed, focusing on standard headache treatment and hormonal manipulation.
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Recent evidence suggests that migraine may not be due to vasoconstriction followed by reactive vasodilation, and tension-type headache may not be due to excess muscle contraction. The prodromes of migraine may have a hypothalamic origin, and the aura and changes in cognition may have a cortical neuronal origin. The pain of migraine and tension-type headache may be generated centrally or enhanced or generated by neurogenic inflammation. Drugs used to treat headache frequently interact with serotonin receptor subtypes: abortive drugs at the 5-HT1 receptor and preventive drugs at the 5-HT2 receptor.