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For both patients and clinicians, triptans—serotonin 5-HT1B/1D receptor agonists—were to migraine, nearly, what dopamine was to Parkinson disease.1 They provided specific therapy, offering a very substantial clinical improvement, and seemed to offer, in equal measure, insights into the pathophysiology of the disorder.2 However, migraine is complex and triptans are not dopamine, so as newer therapies emerge we must try to assess how they inform our understanding of migraine, even as we prepare to learn how to use them in clinical practice. In this issue, there is an important study by Asghar et al.3; important because it sheds some light on drug mechanisms, and perhaps the more important because it does so in humans, thereby illuminating the mechanisms in the target species.3
WHAT DID THE AUTHORS SHOW IN THE NEW WORK?
The authors carried out a randomized, placebo-controlled, double-blinded study of healthy subjects using magnetic resonance angiography to measure middle meningeal (MMA) and middle cerebral artery (MCA) diameter. These measurements were correlated to head pain scores and to the cumulative pain score (area under the curve). The authors administered …
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