Disease relevance of Migraine without Aura

• To investigate whether the novel, potent and highly selective 5-hydroxytryptamine3 (5-HT3) receptor antagonist ICS 205-930 can prevent migraine attacks, we conducted simultaneously two randomized, double-blind, placebo-controlled, multicentre, international trials, involving a total of 204 patients, suffering from classic or common migraine [1].
• Serotonin levels were increased to a moderate degree in classic migraine, but not in common migraine [2].
• Methionine-enkephalin in migraine and tension headache. Differences between classic migraine, common migraine and tension headache, and changes during attacks [3].

High impact information on Migraine without Aura

• The platelet content of 5-hydroxyindoleacetic acid was equally reduced in both classic and common migraine [2].
• Beta-thromboglobulin plasma levels in common migraine [4].
• Histamine, 0.16, 0.33 and 0.66 microgram/kg/min, was infused intravenously to 13 normal non-headache-prone volunteers, 10 patients with chronic muscle contraction headache and 25 patients with common migraine [5].
• Abnormal MCP performance was measured in 15 of 19 migraine-with-aura subjects, and 11 of 17 migraine-without-aura subjects [6].
• Results from this study exclude the HTR2A gene, which has been localized to chromosome 13q14-q21, for involvement with common migraine [7].

Chemical compound and disease context of Migraine without Aura

• A placebo-controlled, double-blind, cross-over trial of flunarizine in common migraine [8].
• In a multicentre study including 96 patients calculation of 95% confidence limits demonstrated that timolol and propranolol are equally effective in common migraine prophylaxis [9].
• Metoprolol and pizotifen in the prophylactic treatment of classical and common migraine. A double-blind investigation [10].
• The efficacy of nimodipine in the prophylaxis of migraine was assessed in a double-blind, placebo-controlled, cross-over study carried out on 33 patients, 20 of whom suffered from classic and 13 from common migraine [11].
• Platelet NE was selectively increased in common migraine [12].

Biological context of Migraine without Aura

• Platelet function in vitro and in vivo (ADP-induced platelet aggregation, circulating platelet aggregates, beta-thromboglobulin plasma levels) has been studied in children with common migraine, in headache-free intervals [13].

Anatomical context of Migraine without Aura

• In order to evaluate the role of the sympathetic autonomic nervous system (SANS) in common migraine we measured platelet catecholamine levels in a group of patients and in control subjects after 1 and 30 min of supine rest [14].

Gene context of Migraine without Aura

• However, testing of the known ATP1A2 gene mutations (for FHM) in common migraine probands of pedigrees showing excess allele sharing was negative [15].
• Thyroid-stimulating hormone and prolactin responses to thyrotropin-releasing hormone in common migraine [16].
• METHODS: Given this role of ion channels in migraine, we assessed the potassium channel KCNN3 as a candidate gene for common migraine [17].
• Ten women with common migraine underwent TRH stimulation test (200 micrograms i.v.) before and after a 30-day FLU therapy (10 mg per os) [18].
• These findings may indicate the possible role of somatostatin in the pathogenesis of common migraine, and support earlier observations that beta-endorphin is involved in the development in this disorder [19].

Analytical, diagnostic and therapeutic context of Migraine without Aura

• Aspirin 650 mg and metoclopramide 10 mg in an effervescent preparation (Migravess) were compared with effervescent aspirin 650 mg (Alka-Seltzer) and placebo for common migraine attacks with a double-blind cross-over design [20].
• Metoprolol and propranolol in the prophylactic treatment of classical and common migraine. A double-blind study [21].
• We, therefore, studied the EEG topographic frequency analysis in 19 symptom-free, otherwise healthy, unmedicated patients with common migraine and in 19 age- and sex-matched controls before nitroglycerin, at the time of maximum pain, and 30 minutes after sumatriptan [22].
• Ten female patients with episodic common migraine (age 20-35 years, age of disease onset 16.2 +/- 5.1 years, illness duration 13.6 +/- 10.7 years) were treated by 16 twice-weekly electromyographic biofeedback and relaxation training sessions with breathing exercises [23].

References