Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women tend to suffer more often from migraine than men (19% vs. 9%). Further menstruation is associated with attacks in 60% of women who have migraine. Moreover 14% of women with migraine suffer from attacks only with menses. Migraine may be linked to late luteal phase dysphoric disorder and dysmenorrhea. these conditions occur when the greatest fluctuation of estrogen levels occur. These fluctuations indeed cause prostaglandin levels to rise, prolactin release to intensify, and central nervous system opioid dysregulation to occur. In fact, several studies show that decreasing levels of estrogen activate menstrual migraine. Further estrogens and progesterone trigger synthesis of endometrial prostaglandins. In fact, prostaglandins regulate descending norepinephrine pain control systems in the brain, thus increased levels of prostaglandins decreases the pain threshold. In addition, falling levels of estrogens produce dopamine receptor hypersensitivity. Dopamine antagonists cause increased prolactin release throughout the luteal phase in all women and during the entire menstrual cycle in women with menstrual migraine. Physicians can treat menstrual migraine with various nonsteroidal antiinflammatory drugs, simple or combination analgesics, ergotamine, or hormonal therapy when other treatments fail. They should be aware that diuretics and pyridoxine are ineffective in treating menstrual migraine. Several replacement therapies to treat menopausal women with migraine exist. these include adding androgens, reducing estrogen dosage, converting to continuous dosing, and converting to parenteral dosing. Some data show an increase in or severity of migraine among oral contraceptive (OC) users, but other studies find no difference in headache among OC and placebo users. In fact, OCs may exacerbate, improve, or not change the frequency or severity of headaches.
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PMID:The role of sex hormones in headache. 155 90

The effects of oral Magnesium (Mg) pyrrolidone carboxylic acid were evaluated in 20 patients affected by menstrual migraine, in a double-blind, placebo controlled study. After a two cycles run-in period, the treatment (360 mg/day of Mg or placebo) started on the 15th day of the cycle and continued till the next menses, for two months. Oral Mg was then supplemented in an open design for the next two months. At the 2nd month, the Pain Total Index was decreased by both Placebo and Mg, with patients receiving active drug showing the lowest values (P less than 0.03). The number of days with headache was reduced only in the patients on active drug. Mg treatment also improved premenstrual complaints, as demonstrated by the significant reduction of Menstrual Distress Questionnaire (MDQ) scores. The reduction of PTI and MDQ scores was observed also at the 4th month of treatment, when Mg was supplemented in all the patients. Intracellular Mg++ levels in patients with menstrual migraine were reduced compared to controls. During oral Mg treatment, the Mg++ content of Lymphocytes (LC) and Polymorphonucleated cells (PMN) significantly increased, while no changes in plasma or Red Blood Cells were found. An inverse correlation between PTI and Mg++ content in PMN was demonstrated. These data point to magnesium supplementation as a further means for menstrual migraine prophylaxis, and support the possibility that a lower migraine threshold could be related to magnesium deficiency.
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PMID:Magnesium prophylaxis of menstrual migraine: effects on intracellular magnesium. 186 Jul 87

To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma beta-endorphin (beta-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 micrograms iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both beta-EP (F = 5.86, p less than 0.002) and cortisol (F = 4.43, p less than 0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for beta-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased beta-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal beta-EP levels measured in the premenstrual period were lower than those observed in the follicular phase (p less than 0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity.
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PMID:Opioid control of the hypothalamus-pituitary-adrenal axis cyclically fails in menstrual migraine. 231 51

This paper summarizes what has been learned over the years about the role of eicosanoids in the pathogenesis of primary dysmenorrhea, endometriosis and menstrual migraine. The role of prostaglandins (PGs) in the pathogenesis of primary dysmenorrhea is inferred from four main observations: firstly, the clinical symptoms of primary dysmenorrhea are similar to those induced by the administration of PGF2 alpha and PGE2 for the induction of labour; secondly, the increased production of PGs by the endometrium during the luteal and menstrual phases of ovulatory cycles is consistent with the occurrence of primary dysmenorrhea mainly in ovulatory cycles; thirdly, the concentrations of PGF2 alpha and PGE2 in the endometrium and menstrual fluid of dysmenorrheic women are significantly higher than in controls; fourthly, certain PG inhibitors have been proved to be effective in the treatment of dysmenorrhea. The change in PG production can explain the major symptoms of primary dysmenorrhea, including the increased uterine contractility, uterine ischemia and the lowering of the pain threshold to chemical and physical stimuli in the pelvic nerve terminals. Moreover, recent experimental data suggest that leukotrienes (LTs) might be among the alternative pathogenetic causes of primary dysmenorrhea. The data which support a relationship between eicosanoids and endometriosis are as follows: endometriotic tissue produces PGs; the peritoneal fluid concentration of PGF2 alpha increases significantly after the induction of endometriosis in laboratory animals; the concentration of PGs in peritoneal fluid of some patients with endometriosis is greater than in controls and, finally, the number and activation of pelvic macrophages which are able to synthesize eicosanoids increase in patients with endometriosis. Possible roles for eicosanoids in the pathogenesis of infertility and secondary dysmenorrhea induced by endometriosis have been suggested. Eicosanoids are probably also involved in the pathogenesis of menstrual migraine. Different types of PGs might play a role both in the initial vasoconstriction during the prodromal phase of migraine and in the vasodilation and sensitization to pain typical of the pain phase.
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PMID:Eicosanoids in primary dysmenorrhea, endometriosis and menstrual migraine. 265 74

Eighteen patients suffering from true menstrual migraine and 12 control subjects were studied. We evaluated in different phases of the menstrual cycle and during the migraine crisis the peripheral plasma concentrations of 6-keto-PGF1 alpha (the stable metabolite of PGI2), thromboxane B2 (the stable metabolite of thromboxane A2), PGF2 alpha and PGE2. The mean values of 6-keto-PGF1 alpha in menstrual migraine sufferers are lower than in normal women throughout the whole cycle. The difference between the trends observed in the two groups is statistically significant (p less than 0.05). The plasma levels of TXB2 and of PGF2 alpha are similar in the two groups investigated, both in basal conditions and during the attack. The plasma concentrations of PGE2 are slightly lower in migraineurs in basal conditions than in normals. However, during the crisis they increase significantly (p less than 0.05). In conclusion, among all the parameters considered, PGE2 seems to play the most important role during the pain phase of the attack. The results of the present study suggest that a deficit of PGI2, one of the most important protecting agents against ischemia, might be a typical feature of menstrual migraine and might cause in these patients a vascular hypersensitivity to different ischemic stimuli.
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PMID:Relevance of prostaglandins in true menstrual migraine. 271 74

We present the results of treatment with subcutaneous sumatriptan in migraine attacks. The study comprised forty-two patients suffering from migraine both with and without aura, with migraine attacks not susceptible to analgesics, non-steroid anti-inflammatory drugs (NSAID), ergotics or else intolerance to the same. Two groups were independently analyzed, one consisting of ten patients who had menstrual migraine continually for twelve months, the other consisting of thirty-two patients suffering from migraine with and without aura for six months. We assessed the effectiveness of the drug (reduction in the intensity and duration of the attack, action, speed, recurrence) and tolerance (adverse effects). The effectiveness of sumatriptan in relieving headache was 75.9% (80% in the case of the menstrual migraine group and 71.8% in the case of the migraine with and without aura group). This effectiveness was maintained in a similar fashion by analyzing independently the first and last months of treatment. Adverse effects were noted in 38.7% of patients treated (40% for the menstrual migraine group, 37.5% for those with migraine with and without aura). The most frequent effects were pain at the point of injection, a feeling of general tiredness, nausea and a sensation of tension in the neck or chest. These effects were largely slight and short lived. No serious adverse effects were reported. A long term analysis carried out on the menstrual migraine group shows the efficacy of sumatriptan is kept up, with improved tolerance of the drug and a decrease in the number of negative side effects noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Subcutaneous sumatriptan in the treatment of migraine attacks. An analysis of its long term efficaciousness and tolerance]. 749 33

In a controlled double-blind clinical trial, 30 patients aged 18 to 45 years, with menstrual migraine, were randomly assigned to 2 parallel treatment groups of 15 patients each. One group received granular nimesulide 100mg 3 times daily and the other group received placebo. Each treatment was given for 10 days, starting from the onset of migraine symptoms, and was repeated for the 2 following menstrual cycles. The overall assessment of efficacy in the 2 groups was based on hourly self-evaluation of pain during each study day. In patients treated with nimesulide, pain intensity and duration were significantly reduced compared with placebo (p = 0.0001) during all the menstrual cycles in the study.
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PMID:Nimesulide in the treatment of menstrual migraine. 750 54

Female hormones are linked to migraine. Women who have had menstrual migraine and migraine onset at menarche tend to experience no migraine during pregnancy. Not all migraines improve during pregnancy, however. Some women experience migraine for the first time during pregnancy. Migraine developing during pregnancy may indicate an underlying structural or functional disorder, e.g., cerebral aneurysms. Headaches caused by cerebral arteriovenous malformations often present as migraine with aura. Cerebral venous thrombosis (common during pregnancy and the puerperium) may manifest with migraine-like visual disturbance and headache. Idiopathic intracranial hypertension or intracranial hypertension secondary to cerebral venous thrombosis or coincidental brain mass can manifest as a continuous and increasing headache. Physicians need to intensively evaluate such cases to achieve an accurate diagnosis. Spinal procedures linked to delivery can cause a low pressure headache. Oral contraceptive use is linked to migraine. Decreasing estrogen levels appear to precipitate migraine. Estradiol and progesterone therapy for menstrual migraine maintains high estrogen levels during the menstrual epoch, which generally prevents migraine. High but stable estrogen levels prevent migraine. Thus, migraines who do not suffer from migraine during pregnancy benefit from high estrogen levels. Pregnant women with migraine should not take drugs unless the frequency and severity of migraine is life threatening to the mother or fetus. Acetaminophen can be used to relieve pain. Meperidine suppositories can relieve severe pain. Pregnant women should not use aspirin, nonsteroidal anti-inflammatory drugs, or vasoconstrictors. Fluid replacement and acceptable antiemetic drugs can treat dehydration and vomiting. Behavioral modification, identification, and elimination of foods that trigger attacks, magnesium supplementation, and low doses of propranolol 3-4 times/day in severe cases may prevent migraine in pregnant women.
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PMID:Migraine and pregnancy. 829 77

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.
J Pain Symptom Manage 1993 Feb
PMID:Sex hormones and headache. 849 7

In order to explore opioid, sympathetic and hormonal parameters, we evaluated plasma met-enkephalin (ME), catecholamines (CA), estradiol (E2) and progesterone (P) in different phases of the menstrual cycle and during menstrual crisis in women suffering from menstrual migraine (MM) and in controls. No differences in P and E2 were found between controls and patients. We observed an increase in plasma ME and a decrease in plasma free norepinephrine (NE) levels on day 22 in MM group and an increase in plasma ME, free NE and total epinephrine (E) during pain. Our data, although obtained in a small number of patients, show clear modifications in plasma ME and in the sympathoadrenal function, not only during pain but also in the mid luteal phase.
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PMID:Plasma met-enkephalin and catecholamine changes during the menstrual cycle and pain episode in menstrual migraine. 923 40


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