histamine/headache

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Histamine skin test in cluster headache: effects of dihydroergotamine with timed release.

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The histamine skin test, as modified by Giacovazzo, was carried out on 20 patients with cluster headache and on 20 control subjects, 10 of whom suffered from migraine and 10 who were healthy volunteers not presenting any form of headache. The test was carried out before and after 30 days treatment

Studies on nitroglycerin and histamine provoked cluster headache attacks.

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Attacks of cluster headache provoked by the administration of nitroglycerin (1 mg sublingually) or histamine (0.01 mg/kg subcutaneously) were studied. The constant latency time in individual patients during nitroglycerin and histamine provocation suggested that the same mechanism is involved in both

Therapy of cluster headache with histamine H1 and H2 receptor antagonists.

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Treatment with the histamine H2 receptor antagonist, cimetidine, alone and/or in combination with the histamine H1 receptor antagonist, chlorpyramine, in 13 patients showed that cimetidine alone was ineffective. 7 of 9 patients taking the combination of H1 and H2 receptor antagonists responded well

Cluster headache: trial of a combined histamine H1 and H2 antagonist treatment.

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Fifteen patients with symptomatic cluster headache participated in a double-blind crossover trial of a combined histamine H1 and H2 antagonist treatment. The trial lasted six weeks. There was no significant improvement on active treatment as regards mean number of headache attacks per week,

Urinary histamine excretion in migraine and cluster headache. Further observations.

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Urinary excretion of histamine, as well as histaminuria following intravenous L-histidine loading, were studied in patients with so-called vascular headache. It was found that urinary excretion of histamine was increased on one or more occasions in 7 of 22 patients with cluster headache. The

Cluster headache: histamine skin tests in the painful area.

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Histamine skin tests were performed in the painful area and on the opposite side in ten cluster headache patients. The studies were carried out with and without local anaesthesia. No differences between histamine skin response in the painful region compared with the contralateral side were revealed.

Basophil histamine release and leukotriene (LTB4-LTC4) production in cluster headache.

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Histamine release and leukotrienes (LTB4 and LTC4) production from circulating basophil have been studied in 13 patients with episodic cluster headache (CH) during the remission phase of symptoms, and in 9 normal subjects. Cell suspensions of basophils were stimulated with scalar dilutions of

Headache provocation by continuous intravenous infusion of histamine. Clinical results and receptor mechanisms.

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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. In the normal group no patients developed pulsating headache. In the migraine group 13

Serum beta-endorphin increase after intravenous histamine treatment of chronic daily headache.

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Histamine is able to induce spontaneous-like headache attacks in migraine and cluster headache subjects. Therefore, it has been considered as a possible agent in the pathogenesis of headache. Histamine desensitization is used for the treatment of cluster and other chronic headaches like migrains

Histamine metabolism in cluster headache and migraine. Catabolism of 14C histamine.

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Various parameters of histamine metabolism were studied in patients with migraine, cluster headache and chronic paroxysmal hemicrania. These included urinary excretion of radioactivity and of 14C histamine and its metabolites, exhaled 14CO2 and fecal radioactivity after oral as well as subcutaneous

Lithium carbonate therapy for cluster headache. Changes in number of platelets, and serotonin and histamine levels.

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Three groups of patients were studied: Group A consisted of 12 patients with cluster headache that was treated with lithium carbonate. Group B consisted of six patients with cluster headache that was managed with other drugs. Group C consisted of five patients with muscle contraction headache who

Nitric oxide synthase inhibition in the histamine headache model.

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Histamine has been widely used experimentally to induce headache in healthy subjects and migraine in migraineurs. There is evidence that the vascular effects of histamine are at least partially mediated by nitric oxide (NO). Hence we hypothesized that subjective symptoms and hemodynamic effects of

Histamine-free diet: treatment of choice for histamine-induced food intolerance and supporting treatment for chronic headaches.

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Histamine-induced food intolerance is not IgE-mediated. Skin-prick testing and specific IgE to food allergens are typically negative. Food rich in histamine or red wine may cause allergy-like symptoms such as sneezing, flush, skin itching, diarrhoea and even shortness of breath. The suspected reason

Nitroglycerin-induced headache is not dependent on histamine release: support for a direct nociceptive action of nitric oxide.

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The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric

The effect of nitric oxide synthase inhibition on histamine induced headache and arterial dilatation in migraineurs.

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We have previously proposed that histamine causes migraine via increased NO production. To test this hypothesis, we here examined if the NOS inhibitor, L-NG methylarginine hydrochloride (L-NMMA:546C88), could block or attenuate histamine induced migraine attacks and responses of the middle cerebral,

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