In this study, changes in plasma levels of calcitonin gene-related peptide (CGRP) and substance P (SP) during a spontaneous-like cluster headache attack provoked by nitroglycerin were evaluated. Peptide variations after spontaneous or sumatriptan-induced remission were also assessed. Blood was collected from the external jugular vein homolateral to the pain side of 30 male cluster headache patients; 18 men were in an active and 12 in a remission one. Plasma levels of CGRP and SP were determined using sensitive radioimmunoassays for each peptide. CGRP-like immunoreactivity (CGRP-LI) was found to be augmented in patients in an active period and became elevated further at the peak of the provoked attack. A complete reversal occurred both after spontaneous and sumatriptan-induced remission. On the contrary, nitroglycerin neither provoked a cluster headache attack nor altered CGRP-LI in the patients in a remission period. The augmented levels of CGRP-LI measured before and after nitroglycerin administration, when the provoked attack reached the maximum intensity, suggest an activation of the trigeminovascular system during the active period of cluster headache. Moreover, the clinical and biochemical actions showed by sumatriptan stress the involvement of serotonin in cluster headache mechanisms.

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Indomethacin, a new nonsteroid anti-inflammatory agent causes headache, a marked decrease in cerebrospinal fluid pressure, and an increase in retinal arterial pressure, while it produces little and inconstant change in the pressure of the carotid and brachial arteries. Despite the headache, indomethacin was investigated in sub;ects with vascular headache because of its vasoconstrictor action. Clinical improvement similar 01' slightly inferior to that with ergotamine was observed.

SYNOPSIS Migraine frequently induces hypotension, which has a large postural component. Since pain and other symptoms of the migraine syndrome have been suggested to be central in nature, an involvement of the dopaminergic pathways within the central nervous system that mediate hypotensive responses, might be postulated in migraine patients. In the study, a test dose (2.5 mg) of bromocriptine, a brain dopamine agonist, induced an intense hypotensive reaction in migraineurs, but not in controls. During bromocriptine‐induced hypotension, serum dopamine β‐hydroxylase activity did not change. The fall of blood pressure, due to bromocriptine, in migraine patients could be considered as an indirect expression of brain dopamine receptor supersensitivity caused by a deficiency of dopamine and or endogenous morphine‐like substances. This mechanism is compatible with the hypothesis which considers migraine as a clinical condition of chronic natural opioid abstinence.

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