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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study was conducted on 1300 women suffering from migraine without aura referred to the Headache Centers of Parma and Pavia from 1984 to 1990. All the data concerning their reproductive life, and the modifications induced by it on the course of headache were obtained from record-charts. Migraine frequently started at menarche (10.7%); in 60% of cases the migraine attacks occurred mostly or exclusively in the perimenstrual period, in 67% of cases disappeared during pregnancy, and in 24.1% significantly (P < 0.0001) worsened with "pill" intake. This study also designated a migraine subgroup which is more influenced by changes in sexual hormones, i.e. migraine with onset at menarche. This form of migraine shows more frequently a menstrual periodicity, and usually improves during pregnancy. Furthermore, menstrual migraine patients show social and cultural characteristics with distinguish them from other women.
Headache
PMID:Migraine without aura and reproductive life events: a clinical epidemiological study in 1300 women. 898 94

Stages of the reproductive cycle--menarche, menstruation, pregnancy, and menopause--are linked to changes in estrogen and progestin levels. Menarche begins menses and cyclic fluctuations in hormone levels. Sex hormone levels rise with pregnancy and fall with menopause. Use of oral contraceptives (OCs) during the childbearing years and hormone replacement during menopause modifies the levels and cycling of sex hormones. Reproductive events and therapeutic intervention may alter the frequency or severity of headaches. Sex hormones modulate and affect the hypothalamus, pituitary, ovary, and endometrium, resulting in a sequence of interactions which comprise the menstrual cycle. For example, estrogen and progestin have strong effects on central serotonergic and opioid neurons, regulating neuronal activity and receptor density. They also alter the endometrium and stimulate production of prostaglandins and other peptides. Research indicates that withdrawal of estrogen, not the maintenance of sustained high or low estrogen levels, primarily triggers menstrual migraine. Changes in the sustained estrogen levels with pregnancy and menopause also cause changes in headaches. Periodic discontinuation of oral preparations of sex hormones may contribute to headaches associated with OC use and hormonal replacement therapy. A possible mechanism for estrogen-induced headaches is a disparity between the ovarian cycles of estrogen and progestin and the intrinsic pulse of central nervous system estrogen-sensitive neurons, including perhaps the serotonergic pain-modulating systems. This mechanisms may explain the rise in headaches in some women who use OCs or are pregnant while other women, e.g., those with menstrually related headache, will have fewer headaches under the same conditions. Migraine headaches linked to sex hormone level fluctuations often do not respond to treatment. Based on the mechanism theory, treatment for such migraines should include both estrogen supplements and inhibition of estrogen synthesis, e.g., ergotamine and derivatives.
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PMID:Sex hormones and headache. 849 7

A leading patient complaint is headaches which tend to occur more often in women than men. Nonvascular headache is the most common and is caused by tension or muscle contraction. Oral contraceptives (OCs) do not affect nonvascular headaches. They can also be safely used in women who experience common migraines whose symptoms do not become more severe or frequent during OC use. On the other hand, women who have classic migraine (headache accompanied by focal neurologic symptoms) or common migraine with symptoms becoming more severe or frequent during OC use should discontinue OC use. Instead, they should use a barrier method or the IUD. Estradiol treatment appears to be effective in treating menstrual migraine. Since the data are inconclusive about the effect of OCs on young women who have experienced a stroke or transient ischemic attacks, it would be best for them to use a barrier method. Most antiepileptic drugs (phenobarbital, phenytoin, paramethadione, and carbamazepine) cause enzyme induction which may be linked to decreased levels of estrogen and increases in irregular bleeding, thereby increasing the likelihood of an epileptic OC user becoming pregnant. Possible contraceptive failure exposes a developing fetus to the teratogenic properties of the antiepileptic drugs. Thus, physicians should prescribe OCs with 50 mcg of ethinyl estradiol rather than 35 mcg ethinyl estradiol. Epileptic women can also use Depo-Provera, because it is not only effective in preventing pregnancy but reduces seizure frequency. It is important for any contraceptive method chosen for epileptic women to be effective because pregnancy intensifies seizures which in turn can damage the mother and/or fetus and cause neonatal distress.
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PMID:Contraceptive methods for women with neurologic disorders. 851 48

In order to understand the possible 5-hydroxytryptamine (5HT) anomalies in migraine, particularly in the period before the headache attack, we compared the levels of 5HT, its stable metabolite 5-hydroxyindoleacetic acid (5HIAA) and platelet monoaminoxidase (MAO) activity in patients with menstrual migraine with those of healthy female controls. In every subject, blood samples were drawn during both follicular and late luteal phases of the menstrual cycle. In controls, platelet 5HT levels remained stable, whereas 5HIAA levels and MAO activity were higher in the luteal than in the follicular phase, suggesting an increased catabolism of 5HT which occurs physiologically just before menses. In menstrual migraine 5HIAA levels and MAO activity showed similar changes with higher values in the luteal than in the follicular phase. The luteal phase values were significantly higher than those of controls. Also, and in contrast to controls, 5HT levels decreased in the luteal phase. These data suggest that 5HT availability is reduced in menstrual migraine, possibly due to an increased catabolism and/or to a reduced synthesis, and hence predisposes patients to migraine attacks.
Cephalalgia 1996 Oct
PMID:Platelet serotonin pathway in menstrual migraine. 890 47

Previous studies have reported the existence of an arginine/nitric oxide (NO) pathway and the involvement of a Ca2+, NADPH-dependent nitric oxide synthase enzyme (NOS) in the generation of NO in human platelets. In the present research, we determined the rate of production of NO and cGMP in the cytosol of platelets stimulated by collagen in 20 females with menstrual migraine (MM), (age range 24-40 years), assessed in the follicular and luteal phases, interictally and ictally in the latter period. The same patients were also assessed at mid-cycle. At the same time, the variations in the collagen response of platelets were evaluated. Moreover, these parameters were determined in the same periods in 20 age-matched control females and in 20 females affected by non-menstrually related migraine (nMM). The collagen-stimulated production of NO in the cytosol of the platelet cytosol was significantly higher in migraine patients with MM than in the control subjects. In MM patients, the increase was greater in the luteal phase of the cycle than during the follicular phase (p < 0.005). A rise in NO production in platelets was also present, although to a lesser extent, in females affected by nMM compared to the healthy females, but this rise was most evident at ovulation (p < 0.001). A slight but significant increase was also observed at mid-cycle in control women, but this increase did not reach the values determined in the migraine groups (p < 0.02). NO production in platelets stimulated by collagen was significantly increased during attacks with respect to the interictal period in both patient groups. Similar variations were observed in the production of cGMP in MM and nMM patients. The increase in NO production was accompanied by a decrease in platelet aggregation in the migraine groups compared with the control group; this decrease was most evident at mid-cycle in nMM patients and in the luteal phase in MM patients. These data suggest an activation of the L-arginine/ NO pathway in MM and nMM patients which could explain the modifications in the platelet response to collagen evidenced in migraine-free periods and during attacks. The activation of this pathway is more accentuated in the luteal phase in MM patients, and this could be the cause of the increased susceptibility to migraine attacks in perimenstrual and menstrual periods in these patients.
Cephalalgia 1996 Nov
PMID:Variations in the platelet arginine/nitric oxide pathway during the ovarian cycle in females affected by menstrual migraine. 893 90

This investigation assessed the effects of an open, prospective trial of adjunctive continuous bromocriptine therapy on the frequency of refractory, disabling menstrual migraine. It compared continuous bromocriptine with previously optimal baseline therapy and cyclic perimenstrual bromocriptine use. The subjects were 24 women with disabling migraines that occurred exclusively or at least 50% of the time within 3 days before or after the onset of menstruation despite treatment. We added bromocriptine 2.5 mg three times a day to their existing regimen and compared menstrual migraine frequency during the first year with the year prior to bromocriptine. Eighteen of the 24 women experienced a 25% or greater decline in migraine frequency. Migraine frequency declined by 72% overall (p < 0.01). Three women did not tolerate bromocriptine, and three did not benefit. None of the women had a 10% or greater increase in headaches. Continuous bromocriptine therapy was also significantly more effective than intermittent bromocriptine use (p < 0.05). Continuous bromocriptine therapy appears to benefit menstrual migraine.
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PMID:Continuous bromocriptine therapy in menstrual migraine. 900 2

This study examined the prevalence of menstrually related headache and the relationship between the menstrual cycle and stress in a group of young women migraineurs sampled from a general population. Participants (N = 20) meeting International Headache Society criteria for migraine with or migraine without sure and not meeting criteria for menstrual migraine, provided daily headache activity, perceived stress, cognitive appraisal, and coping strategy data during two menstrual cycles. Multiple regression was used to analyze these data following a time-series approach in which the phases of the menstrual cycle were used as predictors of variation in each participant's headache, stress, appraisal, and coping data. Analyses revealed that fewer participants than expected showed significant relationships between their menstrual cycle and their headache activity (20%). However, for these women the amount of variation explained by the menstrual cycle was substantial. We suggest that, though some women's migraines vary with their menstrual cycle, the number of women substantially affected may be much smaller than has been estimated in the literature. Relationships between the menstrual cycle and the stress process were also found; however, inconsistencies between this and a previous study in our laboratory suggest that the nature of this relationship may vary across women migraineurs.
Headache 1997 Apr
PMID:The menstrual cycle and migraine: a time-series analysis of 20 women migraineurs. 915 Jun 19

Migraine headache is a common condition in women and frequently occurs in relation to the menstrual cycle. This article reviews the neuroendocrine etiology of menstrual migraine, its possible relationship to premenstrual syndrome, and recent developments in treatment strategies for these often refractory headaches.
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PMID:Menstrual migraines: etiology, treatment, and relationship to premenstrual syndrome. 926 97

We measured reactivity to a stress paradigm during the premenstrual period in 19 women affected by Menstrually Related Disorders (MRD) and in 11 normal controls. Eight had premenstrual syndrome diagnosed by the Menstrual Distress Questionnaire and 11 suffered menstrual migraine, diagnosed according to International Headache Society criteria. Subjects were observed during two menstrual cycles and submitted to a psychocognitive test (Stroop Color Word) during the luteal phase. In both groups the stimulation by Stroop C-W was present for systolic blood pressure (SBP) (F = 18.14, p = 0.000), diastolic blood pressure (DBP) (F = 9.56, p = 0.000), and heart rate (F = 12.80, p = 0.000). Moreover, an interaction of response by group was present for DBP (2.58, p = 0.04); DBP values were higher in MRD subjects. Also baseline DBP values were higher in MRD with respect to controls. Area under the curve (AUC) subtracted from baseline for the SBP, DBP and heart rate did not differ between groups. In conclusion, MRD subjects facing a cognitive stress had normal cardiovascular response. However, patients had increased arousal of cardiovascular measures before and after testing. The significant differences during stress of testing were dissociated from those of experimental stress stimulation. MRD subjects may have less ability to cope with novelty than healthy volunteers.
Cephalalgia 1997 Dec
PMID:Cardiovascular response to cognitive stress in subjects with menstrually related disorders. 949 69

We review the role of several biochemical and hormonal factors in menstrual migraine pathogenesis: ovarian hormones, aldosterone circadian rhythm, nocturnal urinary melatonin excretion, sympathetic autonomic system, prolactin levels and dopaminergic function, endogenous opioid tonus, platelet activity and arachidonic acid metabolites. In particular, we focus on certain aspects of platelet function and prostaglandin metabolism, taking into consideration the different behavior of platelet sensitivity to prostacyclin, intraplatelet 5HT, peripheral plasma concentrations of 6-keto-PGF1alpha and PGE2 in menstrual migraine sufferers and in control subjects during the menstrual cycle. A comprehensive view of the data suggests that a complex impairment of PG and 5HT metabolism, and of platelet function, may play a significant role in the pathogenesis of menstrual migraine. However, it is not yet clear whether these alterations are primary or secondary to neuroendocrine disorders.
Cephalalgia 1997 Dec
PMID:Pathophysiological aspects of menstrual migraine. 949 76


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