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נעשו כמובן הרבה מחקרים אך אין ממש מסקנות חד משמעותיות. J Womens Health Gend Based Med 1999 Sep;8(7):919-31 Menstrual migraine. Silberstein SD. Jefferson Headache Center and Department of Neurology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania 19107, USA. Migraine in women is influenced by hormonal changes throughout the life cycle: menarche, menstruation, oral contraceptive use, pregnancy, menopause, and hormonal replacement therapy (HRT). Based on clinical experience, the frequency of menstrual migraine has been reported to be as high as 60%-70%. Most women have increased headache and migraine attacks (usually without aura) at the time of menses. Attacks occurring only with menstruation, even if infrequent, are called true menstrual migraine. Attacks occurring both at menstruation and at other times of the month could be called "menstrually triggered migraine." Menstrual migraine occurs at the time of the greatest fluctuation in estrogen levels. Estrogen withdrawal is probably the trigger for migraine attacks in susceptible women. Drugs that are proven effective or commonly used for the acute treatment of menstrual migraine include nonsteroidal anti-inflammatory drugs (NSAIDs), dihydroergotamine, the triptans, and the combination of aspirin, acetaminophen, and caffeine. The goal of standard continuous preventive therapy is to reduce the frequency, duration, and intensity of attacks. Preventive therapy may eliminate all headaches except those associated with menses. Women already using prophylactic medication who continue to have menstrual migraine can increase the dose of their medication prior to their menses. Women who do not use preventive medicine or have migraine exclusively with their menses can be treated perimenstrually with short-term prophylaxis. If severe menstrual migraine cannot be controlled by acute and preventive treatment, hormonal therapy may be indicated. Funct Neurol 2000;15 Suppl 3:143-53 Migraine associated with menstruation. MacGregor A. City of London Migraine Clinic and St Bartholomew's Hospital, London, UK. Many women report increased frequency of migraine in association with menstruation. The term 'menstrual' migraine is often used despite lack of an agreed definition. The International Headache Society has classified most headaches but not 'menstrual' migraine. A proposed definition is based on the finding that the prevalence of migraine increases on day 1 +/- 2 of the menstrual cycle. Attacks occurring at this time of the cycle are typically without aura. Effective acute therapy is the mainstay of management for menstrual and non-menstrual attacks although there is some evidence that attacks linked to menstruation are less responsive to treatment compared with migraine at other times of the cycle. If several attacks occur throughout the cycle, standard prophylactic agents should be used. Women with exclusive 'menstrual' migraine may benefit from perimenstrual prophylaxis but this should only be instigated once the association between migraine and menstruation has been confirmed with prospective records kept for a minimum of three cycles. NSAIDs are the treatment of choice in reducing migraine associated with menorrhagia and/or dysmenorrhoea, otherwise perimenstrual oestrogen supplements using percutaneous or transdermal oestrogens are recommended. Combined oral contraceptives are useful for women requiring contraception although there is a tendency for attacks to occur during the pill-free interval. If these are contraindicated, depot progestogen is an alternative as it also inhibits ovulation and can improve migraine, provided amenorrhoea is achieved. Oral progestogen-only contraception has little place in the management of 'menstrual' migraine as it does not inhibit ovulation and is often associated with a disrupted menstrual cycle. Some women consulting with menstrual migraine are menopausal and may be considering hormone replacement therapy. Studies suggest that non-oral routes of delivery of oestrogen, which provide stable levels, are more likely to improve migraine than oral oestrogens, which produce variable day-to-day levels. Too low a dose of oestrogen is ineffective at controlling symptoms but too high a dose, particularly if coupled with surges of endogenous oestrogen, can trigger migraine aura. Once the route and dose has been optimised, continuous oestrogens can control migraine as well as menopausal symptoms. Additional progestogen, necessary for unhysterectomised women, can exacerbate migraine. To minimise this, progesterone derivatives or non-oral routes of delivery are recommended, with continuous regimens used where possible.