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Sumatriptan, a novel selective 5-hydroxytryptamine1d (5-HT1d) receptor agonist, which is highly effective in the acute treatment of migraine attacks, blocks dural neurogenic plasma extravasation and constricts cranial blood vessels in animal experiments. We measured intra- and extracranial blood flow velocities (BFV) with a transcranial Doppler device in 67 patients during a spontaneous migraine attack, before and after treatment with 3 mg or 6 mg subcutaneous sumatriptan or placebo. Sumatriptan, but not placebo, significantly increased BFV (cm/sec) in the internal carotid and middle cerebral arteries on both sides, without detectably changing the BFV in the common and external carotid arteries. The rise in BFV increased with the dose of sumatriptan, parallel to an increase in proportion of patients improved. There were no significant changes in heart rate, blood pressure, or respiratory frequency after treatment with sumatriptan. The increase in BFV probably reflects vasoconstriction of the large basal intracranial arteries, which may be a mechanism for the antimigraine action of sumatriptan.

In this study, blood flow velocity in the basilar artery and both vertebral and middle cerebral arteries was measured with a transcranial Doppler device in 23 migraineurs during and outside a migraine attack. The aim of the study was to compare blood flow velocities during and outside an attack and to examine vascular reactivity to voluntary hyperventilation during both conditions. No differences in blood flow velocity were found. Although blood pressure was increased and end-expiratory CO2 decreased during the attack, this exerted no influence on blood flow velocity. Neither was a difference in vascular reactivity to voluntary hyperventilation detected between the two conditions. These findings support the notion of functional integrity of the examined large arteries during migraine attacks without aura.