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September 2004

LE Magazine September 2004

A correlation between migraine, histamine and immunoglobulin e.
Although migraine affects about 15% of population and many studies have been performed to find the mechanism and a successful management, the physiopathology of migraine is still largely unknown. The possibility of an immunoglobulin E (IgE)-mediated allergic mechanism and the role of histamine remain controversial. The aim of the present study was to evaluate serum total IgE and histamine levels in migraine patients and the influence of allergy on them. Seventy patients (18-58 years) with migraine without aura were divided into two groups according to their history of allergy (60% with and 40% without allergy). Serum samples were collected during fasting without allowing any premedication during the two periods of attack and remission. There was a control group containing 45 healthy volunteers. Serum total IgE and histamine levels were measured by enzyme-linked immunosorbent assay and fluorimetric methods, respectively. Mean and standard errors of serum histamine (ng/ml) and total IgE (IU/ml) levels were found in the control group to be 48.16 +/- 2.70 and 38.31 +/- 3.20, in the migraine with allergy group 159.11 +/- 4.60 and 303.30 +/- 42.50 and in the migraine without allergy group 105.01 +/- 8.50 and 79.07 +/- 2.70, respectively. Total IgE levels in migraine with allergy group were found to be significantly (P < 0.0001) above that in the control and another group, suggesting an influence of an IgE-mediated mechanism on migraine. Although the plasma histamine levels, which were significantly elevated (P < 0.0001) in patients with migraine, both during headache and symptom-free periods, when compared with the control group, indicate that there is an increased susceptibility to histamine in allergic conditions, this molecule has also an unrelated role in migraine. The relationship between allergy and migraine can be based, in part, on an IgE-mediated mechanism, and histamine release plays an important role. Thus, the avoidance of allergic conditions in migraine patients may be a simple, helpful way for prophylaxis or their treatment.

Scand J Immunol . 2003 Mar;57(3):286-90

One-year prevalence of migraine in Austria : a nation-wide survey.
This study presents the first nation-wide survey of migraine in Austria . A sample of 997 Austrian > or = 15 years old were interviewed personally (face-to-face) in a random sample in the whole country. Diagnosis of migraine was based on the International Headache Society (IHS) classification. Of the Austrian adult population 10.2% were identified to suffer from IHS migraine, 5.6% from migraine without aura, 2.3% from migraine with aura and 2.3% from borderline migraine. Another 8.5% have possible migraine. Other primary headaches were reported in 30.7%. Sex, age, working status and region were found to be the main demographic influencing factors. Further influences were stress, spinal column problems or weather changes. The most used acute medications were over-the-counter drugs, doctor attendance rate was very low. Working people with migraine dropped out of work 14 days per year, which adds up to 6.8 million working days per year. This remains a substantial economic factor. The findings indicate that migraine sufferers in Austria need to be more informed about their illness and what to do against it, especially encouraging doctor visits.

Cephalalgia . 2003 May;23(4):280-6

Pathophysiology, epidemiology, and impact of migraine.
Despite a decade of progress, migraine headache remains prevalent, disabling, underdiagnosed, and undertreated in the United States . Migraine affects approximately 12% of the population, and the economic burden in terms of annual cost of labor lost to migraine disability is between $5.6 and $17.2 billion. The threshold for migraine may be genetically determined, although recent genetic and neurophysiologic studies point to migraine as possibly a channelopathy. Cerebral cortical and brain stem changes occur in migraine. Head pain and associated symptoms of migraine can be explained by activation of the trigeminal vascular system. Evidence has also been accumulated that suggests the release of nitric oxide is an important trigger mechanism. Introduction of the triptans has dramatically advanced acute migraine pharmacotherapy, and preventive therapy has greatly improved; however, public health initiatives may be needed to further advance diagnosis and treatment of this common and disabling disorder.

Clin Cornerstone. 2001;4(3):1-17

The early use of ergotamine in migraine. Edward Woakes' report of 1868, its theoretical and practical background and its international reception.
Although ergot had been used in obstetrics for several centuries, it was proposed for the treatment of migraine only in the 19th century. The British ENT-surgeon Edward Woakes (1837-1912) recommended ergot as a vasoconstricting agent for migraine and other neurogenic conditions associated with vasodilatation in 1868. He subscribed to the theory of vasodilatation by sympathetic deficit, presented in the early 1850s by Brown-Sequard and Claude Bernard. Du Bois-Reymond proposed vasoconstriction by sympathetic overactivity as the cause of migraine in 1860; Brown-Sequard opposed this in favour of vasodilatation. Vasodilatation due to sympathetic deficit in migraine was again supported by Mollendorf, with clinical evidence, in 1867. Woakes' paper of 1868 introduced ergot as a vasoconstrictor for the same condition. Reception abroad was prompt. A German version appeared in 1869, and Eulenburg cited Woakes in his textbook of 1871. Eulenburg presented the use of ergot for migraine as a routine measure in the second edition of his textbook in 1878, and in a paper published in 1883. The method was internationally accepted, but it became really popular only after the isolation of pure ergotamine in 1918, resulting in the first reliable compounds with stable properties and predictable effects. Contrary to Woakes' theory, in the early 20th century ergot was used for migraine because of its well-documented adrenolytic properties, as migraine was by then again believed to be a sympathotonic and vasospastic condition.

Cephalalgia . 2002 Oct;22(8):686-91

Central 5-HT receptor hypersensitivity in migraine without aura.
Serotonin has long been implicated as a key neurotransmitter in migraine. There is a dearth of research specifically examining 5-HT1A receptor sensitivity in migraine despite the importance of this receptor in regulating central serotonergic tone. In this study we examined the hypothesis that migraine without aura is associated with hypersensitivity of central 5-HT1A receptors, using a 5-HT1A neuroendocrine challenge drug and comparing serum prolactin responses between a test group with migraine and a matched group of healthy controls. Twelve female subjects fulfilling International Headache Society (IHS) criteria for migraine without aura were evaluated. Following an overnight fast, subjects presented for testing at 9am . An intravenous canula was inserted and serum prolactin was assessed at baseline and every 30 min for 3 h following a single dose of 30 mg oral buspirone, a 5-HT1A-receptor agonist. Subjects were assessed during the first 5 days of the menstrual cycle. No subjects were taking psychotropic medication or migraine prophylactic treatment. Patients with current or previous psychiatric disorder, daily headache or analgesic overuse were excluded. 16 healthy female volunteers matched for age and menstrual status were also evaluated and served as controls. There was no difference in baseline prolactin between groups. There was a significant rise in prolactin following buspirone in both groups. Subjects with migraine had a significantly increased prolactin response to buspirone (delta max) compared to controls (P < 0.001). This study supports the hypothesis that migraine without aura is associated with a relative hypersensitivity of central 5-HT1A receptors. This is of relevance given the role of the 5-HT1A receptor in controlling raphe 5-HT tone and in the possible association between migraine and anxiety and depression.

Cephalalgia. 2003 Feb;23(1):29-34