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Query: UMLS:C0018681 (headache)
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The normal female life cycle is associated with a number of hormonal milestones: menarche, pregnancy, contraceptive use, menopause, and the use of replacement sex hormones. All these events and interventions alter the levels and cycling of sex hormones and may cause a change in the prevalence or intensity of headache. The menstrual cycle is the result of a carefully orchestrated sequence of interactions among the hypothalamus, pituitary, ovary, and endometrium, with the sex hormones acting as modulators and effectors at each level. Oestrogen and progestins have potent effects on central serotonergic and opioid neurons, modulating both neuronal activity and receptor density. The primary trigger of menstrual migraine appears to be the withdrawal of oestrogen rather than the maintenance of sustained high or low oestrogen levels. However, changes in the sustained oestrogen levels with pregnancy (increased) and menopause (decreased) appear to affect headaches. Headaches that occur with premenstrual syndrome appear to be centrally generated, involving the inherent rhythm of CNS neurons, including perhaps the serotonergic pain-modulating systems.
Cephalalgia 2000 Apr
PMID:Physiology of the menstrual cycle. 1099 66

The normal female life cycle is associated with a number of hormonal milestones: menarche, pregnancy, contraceptive use, menopause, and the use of replacement sex hormones. Menarche marks the onset of menses and cyclic changes in hormone levels. Pregnancy is associated with rising noncyclic levels of sex hormones, and menopause with declining noncyclic levels. Hormonal contraceptive use during the reproductive years and hormone replacement in menopause are therapeutic hormonal interventions that alter the levels and cycling of sex hormones. These events and interventions may cause a change in the prevalence or intensity of headache. The menstrual cycle is the result of a carefully orchestrated sequence of interactions between the hypothalamus, pituitary, ovary, and endometrium, with the sex hormones acting as modulators and effectors at each level. Estrogen and progestins have potent effects on central serotonergic and opioid neurons, modulating both neuronal activity and receptor density. The primary trigger of Menstrually-related migraine (MM) appears to be the withdrawal of estrogen rather than the maintenance of sustained high or low estrogen levels. However, changes in the sustained estrogen levels with pregnancy (increased) and menopause (decreased) appear to affect headaches. Headaches associated with OC use or menopausal hormonal replacement therapy may be related, in part, to periodic discontinuation of oral sex hormone preparations. The treatment of migraine associated with changes in sex hormone levels is frequently difficult and the patients are often refractory to therapy. Based on what is known of the pathophysiology of migraine, we have attempted to provide a logical approach to the treatment of headaches that are associated with menses, menopause, and OCs using abortive and preventive medications and hormonal manipulations. Considerable evidence suggests a link between estrogen and progesterone, the female sex hormones, and migraine. (Silberstein and Merriam, 1997; Lipton and Stewart, 1993; Epstein et al., 1975; Goldstein and Chen, 1982; Selby and Lance, 1960) Although no gender difference is apparent in prepubertal children, with migraine occurring equally in 4p. 100 of boys and girls, (Goldstein and Chen, 1982, Waters and O'Connor, 1971) migraine occurs more frequently in adult women (18p. 100) than in men (6p. 100). (Lipton and Stewart, 1993) Migraine develops most frequently in the second decade, with the peak incidence occurring with adolescence. (Selby and Lance, 1960; Epstein et al., 1975) Menstrually-related migraine (MM) begins at menarche in 33p. 100 of affected women (Epstein et al. , 1975). MM occurs mainly at the time of menses in many migrainous women, and exclusively with menses (true menstrual migraine [TMM]) in some (Epstein et al., 1975). Menstrual migraine can be associated with other somatic complaints arising before and often persisting into menses, such as nausea, backache, breast tenderness, and cramps and like them appears to be the result of falling sex hormone levels (Silberstein and Merriam, 1997; American Psychiatric Association, 1994). In addition, premenstrual migraine can be associated with premenstrual dysphoric disorder (PDD), also called "premenstrual syndrome" (PMS), which is distinct from the physical symptoms of the perimenstrual period and is probably not directly driven by declining progesterone levels (Mortola, 1998). Migraine occurring during (rather than prior to) menstruation is usually not associated with PMS (Silberstein and Merriam, 1997). Migraine may worsen during the first trimester of pregnancy and, although many women become headache-free during the last two trimesters, 25p. 100 have no change in their migraine (Silberstein, 1997). MM typically improves with pregnancy, perhaps due to sustained high estrogen levels (Silberstein, 1997). Hormonal replacement with estrogens can exacerbate migraine and oral contraceptives (OCs) can change its character and frequency
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PMID:Sex hormones and headache. 1113 45

Slightly less than half of women with migraine report that menstruation is an important trigger of headache episodes. However, it is rare that menstruation is the only trigger for a patient and its importance as a trigger may be over- emphasized. Accurate diagnosis requires a prospectively kept diary of information showing a consistent and mechanistically valid temporal correlation between migraine attacks and menstrual periods. Abnormal central nervous system response to normal fluctuations in hormones is the likely underlying cause of menstrual migraine. Patients with menstrual migraine do not generally have hormonal abnormalities. Currently available abortive therapy works well for menstrual-related migraine attacks. For the small subset of women for whom this is not the case, and whose menstrual periods and associated headaches are predictable, pre-emptive treatment of the expected headache with scheduled perimenstrual use of a number of agents can be helpful. A hormonal trigger for migraine headache does not mean that treatment must also be hormonal in nature. Choice of therapy depends on the frequency of menstrual migraine, predictability of menstrual periods, patient preference, and cost. For the small group of women with refractory menstrual migraine, hormonal therapy can be tried, with the understanding that the quality of evidence for these interventions is low and their risk to benefit ratios not established. The perimenstrual use of triptan medications is currently being investigated for the treatment of menstrual migraine. Preliminary results are inconclusive, and until further evidence regarding the efficacy, safety, practicality, and cost effectiveness of this approach is available, their routine use in this manner for menstrual migraine is not recommended.
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PMID:Menstrual Migraine. 1118 Jul 56

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.
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PMID:Migraine associated with menstruation. 1120 Jul 85

Chronic headache fluctuates in response to changes in hormonal levels. Headache generally improves with rising estrogen levels, and worsens with falling levels. Headache should, therefore, predictably improve with pregnancy and worsen postpartum. Several retrospective studies have confirmed this pattern. In this study, 49 pregnant women with chronic headache (18 with migraine, 16 with tension-type, and 15 with combined migraine and tension-type) were followed prospectively. Headache activity was recorded daily throughout pregnancy and for 3 months postpartum. Overall, there was a 30% improvement in headache between the second and third trimesters for the entire sample. This was not statistically significant. Headache improved significantly for 41% of the women, with a slightly greater tendency for headache to improve in women with migraine compared to those with tension-type or combined migraine and tension-type headaches. Headache activity was not influenced by history of menstrual migraine, history of headache change with prior pregnancies, parity, or breast-feeding. In general, women reporting headache at the end of their first trimester continued to report headache throughout pregnancy and postpartum.
Headache 1999 Oct
PMID:Longitudinal prospective study of headache during pregnancy and postpartum. 1127 58

Migraine and tension headaches are among the most common diagnoses in women's health. Secondary causes of headache such as brain tumor, subarachnoid hemorrhage, and meningitis are uncommon but must not be missed. A careful history and physical examination, use of diagnostic criteria, and certain facts about the serious causes of headache are the keys to diagnosis and treatment. Neuroimaging should be limited to patients displaying signs or symptoms of a secondary headache cause. Menstrual migraine can be managed similarly to nonmenstrual migraine.
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PMID:Diagnosis and management of headache. 1143 Jan 73

We assessed the prevalence of menstrual migraine and its restrictions on daily activities in a representative Dutch population sample of 1181 Dutch women, aged 13-55 years. Further, we evaluated the potential role of oral contraceptives, and how menstrual migraine is treated. More than half suffered from menstrual complaints, a substantial proportion reported headache or migraine as a frequent problem. Use of oral contraceptives seemed to reduce the occurrence of menstrual complaints, but not the occurrence of headache and migraine. In our study, the prevalence of menstrual migraine (3%) is lower than in the literature, most probably because we did not use a selected group of patients but a population-based sample of ordinary women. It was confirmed that attacks of menstrual migraine are more severe, of longer duration, and more resistant to treatment than migraine attacks at other times of the month.
Cephalalgia 2003 May
PMID:Menstrual migraine in a representative Dutch population sample: prevalence, disability and treatment. 1271 49

A menstrual migraine occurs in approximately 7-10 % of women suffering from migraine. The migraine occurs from 2 days before until 3 days after the end of the menstrual period. The choice of treatment depends on the duration of the attack, which ranges from 3 to 7 days. An attack of up to 3 days duration should be treated with acetylsalicylic acid, ergotamine tartrate or naproxen, each in combination with an antiemetic (domperidone, metoclopramide). If there is no response, sumatriptan can be administered orally (25-100 mg) or subcutaneously (6 mg). In the attacks continue for more than 3 days, short-term prophylaxis with naproxen or the application of an estrogen-containing patch is indicated. Neither ovulation inhibitors nor traditional migraine prophylaxis has an influence on menstrual migraine. Patients should keep a headache diary. Short-term prophylaxis with ergotamine tartrate or tamoxifen is obsolete.
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PMID:[Medical therapy for menstrual migraine]. 1279 61

The 45(th) Annual Scientific Meeting of the American Headache Society focused on new areas of headache research: revised diagnostic criteria, increased the understanding of the pathogenesis of migraine and expansion of identified physiological changes in migraine beyond head pain to include cognitive, sleep and vestibular disturbances. A preview of the new International Headache Society criteria described changes in diagnostic categories, including special criteria for research. New definitions to categorise chronic daily headache, menstrual migraine and secondary headaches were the main highlights of the modified criteria. In addition, novel data on activation within trigeminovascular pathways expand the understanding of the pathogenesis of migraine. Identification of the ability of treatment to impact activation and sensitisation of peripheral and central neurons results in: an explanation for initial headache worsening and neck/chest tightness that commonly occur with triptans, a better understanding of the mechanisms of triptans, and a strong recommendation for early triptan intervention (within 20 min of headache onset). Application of matrix metalloproteinase models to migraine helps explain the ability of medications to cross the blood-brain barrier during a migraine episode, as well as describe possible ischaemia with repeated migraine (e.g., white matter abnormalities seen on magnetic resonance scanning). Improved classification of headache disorders, along with increased understanding of the physiology of migraine and mechanism of action of common treatments, should enhance future development and evaluation of effective headache therapy.
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PMID:45(th) Annual Scientific Meeting of the American Headache Society June 19 -22, 2003, Chicago, IL, USA. 1294 91

This pilot study investigated the effect of menstrual cycle phase (late luteal and mid-follicular) on cerebral perfusion changes during photic stimulation in both controls (n = 5) and true menstrual migraine patients (n = 5). No significant differences in resting baseline perfusion were observed between the two groups during either phase of the menstrual cycle. During the late luteal phase, changes in perfusion within the occipital lobe due to photic stimulation were similar for both groups. However, during the mid-follicular phase, occipital perfusion during visual stimulation decreased for controls but significantly increased for true menstrual migraine patients (P < 0.05). A two way repeated measures anova also demonstrated a significant difference between menstrual migraine patients and controls for photic activation (P < 0.05).
Cephalalgia 2003 Nov
PMID:Perfusion changes with photic stimulation during two phases of the menstrual cycle: a pilot study comparing controls and true menstrual migraine patients. 1461 33


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