Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Headache 1991 May
PMID:Magnesium prophylaxis of menstrual migraine: effects on intracellular magnesium. 186 Jul 87

A 27-year-old woman with no family or personal history of migraine presented with headache associated with unilateral paresthesias and blurred vision. This was her first, and so far only, attack of migraine with aura and led to the diagnosis of her pregnancy and to this review. Migraine can begin for the first time with pregnancy, particularly in the first trimester. Cases of migraine with aura are the most commonly reported. Preexisting migraine usually improves with pregnancy, particularly if it was associated with menstrual migraine. Headache occurs frequently in the post-partum period, particularly in known migraineurs. Migraineurs have no increased risk of complications during pregnancy and their children have no increased incidence of birth defects.
Headache 1991 Jun
PMID:Review article: migraine and pregnancy. 188 76

The aim of the present study was to investigate the effects of biofeedback training in the treatment of menstrual and nonmenstrual migraine. Accordingly, 39 female patients suffering from both migraine associated, and migraine not associated, with menstrual periods were drawn from a pool of research volunteers enrolled in a biofeedback treatment program for migraine headaches. All patients were required to complete 5 weeks of daily self-monitoring of headache and menstruation activity immediately before and after treatment, and again at 6-month follow-up. Within-subjects comparisons of the effects of biofeedback on menstrual and nonmenstrual migraine, and between-subjects comparisons of the effects of biofeedback on patients suffering predominantly from either menstrual or nonmenstrual migraine showed that biofeedback is just as effective in reducing menstrual migraine as it is in reducing nonmenstrual migraine. Questions as to whether or not these conclusions can apply to patients who experience migraine headaches only during, or shortly before or after, menstruation, are raised.
Headache 1991 Feb
PMID:The differential effects of biofeedback in the treatment of menstrual and nonmenstrual migraine. 177 69

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.
Cephalalgia 1990 Feb
PMID:Opioid control of the hypothalamus-pituitary-adrenal axis cyclically fails in menstrual migraine. 231 51

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.
Headache 1989 Apr
PMID:Relevance of prostaglandins in true menstrual migraine. 271 74

Sympathetic reactivity in patients suffering from menstrual migraine has been evaluated by means of blood pressure, heart rate and catecholamine monitoring during the tilt-table test performed either in the follicular or in the luteal phase of menstrual cycle. A sympathoadrenal activation mainly described by increased plasma epinephrine levels, has been documented in menstrual migraine not only during the luteal period but also in the early phases of migraine attacks. On the other hand, the interval phases seem to be characterized by a sympathetic chronic hypofunction. Variations in catecholaminergic reactivity are discussed as factors conditioning headache pathophysiology and attack epiphenomena.
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PMID:Disordered sympathetic reactivity in menstrual migraine. A cardiopressor and biochemical evaluation. 273 99

The treatment of patients suffering with menstrual migraine is sometimes a difficult and frustrating problem for the physician. As many menstrual migraine headaches are refractory to abortive therapy, prophylactic therapy is often needed. Ergonovine maleate, an ergot derivative with vasoconstrictive properties, has been used with some success in migraine headache patients. Forty patients who were treated with intermittent prophylactic ergonovine were studied over six months. The patients ranged in age from 22 to 40 years, and all suffered with menstrual migraine headaches which were refractory to abortive therapy. Each patient took ergonovine maleate 0.2 mg three to four times daily during menses and recorded headache occurrence and severity. After three months, 24 patients (60%) reported significantly less severe attacks, six patients (15%) reported less frequent headaches and 14 patients (35%) reported no improvement. After six months there was a decrease in effectiveness with 20 patients (50%) reporting significantly less severe headaches and two patients (5%) reporting less frequent headaches. This limited study suggests that ergonovine maleate may be of value in the treatment of difficult menstrual migraine patients.
Headache 1989 Jun
PMID:Menstrual migraine and intermittent ergonovine therapy. 275 44

Out of the knowledge of various headache syndromes the physician has to develop a clear diagnostical and therapeutical concept. This is especially true for migraine. Relevant pathophysiological hypotheses are presented e.g. the neurogenic-vascular model of migraine. Metoclopramide and domperidone in combination with mono-analgesics, ergotamine and nonsteroidal-antiinflammatory drugs are favoured in the treatment of the acute migraine attack. 2 to 4 mg ergotamine for the attack, respectively 16 to 20 mg per month should not be exceeded. Mixed compounds, containing ergots, analgesics, codeine, caffeine, tranquilizers and barbiturates should be avoided as these drugs may induce rebound-headache. A prophylaxis of migraine is indicated if a migraineur suffers from at least 2 attacks per month or if a migraine attack lasts longer than 4 days. In the first place, beta-blockers and flunarizine, in some cases verapamil or naproxen, should be used; the effect of dihydroergotamine is questionable. Because of its severe side effects, methysergide should only be given if all other prophylactic drugs fail. Naproxen is standard medication in the short time prophylaxis of menstrual migraine.
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PMID:[Drug therapy of migraine]. 290 93

The authors reviewed the connection between sex hormones and migraine crisis. Besides other exogenous factors, the fall in estradiol blood levels during the late luteal and premenstrual phase seems a causal factor in the origin of menstrual-related headaches. The behavior of migraine crisis during the various events of the female reproductive period support this view. The role of prolactin, follicle stimulating hormone, testosterone, and luteinizing hormone were also discussed. At the same time, menstrual migraine represents a model that fits perfectly with a neuroendocrine hypothesis which is based on a faulty chronobiological response of the so-called antinociceptive system.
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PMID:Menstrual migraine, old and new. 293 89

Migraine has been considered a manifestation of sympathetic dysfunction. Serum dopamine beta-hydroxylase (D beta H) has been shown to be an index of peripheral sympathetic activity by some workers and there are two reports of elevated activity of the enzyme during the migraine headache as well as in the headache-free interval. We studied the enzyme in seven women complaining of regular attacks of menstrual migraine and eleven controls during the mid-follicular (days 10 +/- 2) and premenstrual (days 28 +/- 2) phases of the menstrual cycle. Although levels were on average 26% and 10% higher respectively than in control subjects, the difference failed to reach statistical significance because of the large normal range for enzyme activity. However, the premenstrual results were significantly lower (p less than 0.001) than the mid-follicular measurements in the migraine group, little difference being found in controls. This finding, and the effects of successful therapy with anovulatory doses of oestradiol implants in not only significantly lowering serum D beta H but also significantly reducing the difference in enzymic activity between the early and late phases of the menstrual cycle, suggest that if this enzyme is an index of sympathetic activity, it is excessive fluctuations of the sympathetic nervous system that may be relevant in menstrual migraine.
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PMID:Serum dopamine beta-hydroxylase activity in menstrual migraine. 403 48


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