Background.—It has been known that in a migraine attack intracranial and extracranial arteries on the headache side dilate and when the migraine attack has subsided, the intracranial arteries show segmental narrowing. We hypothesized that patients with migraine had an underlying systemic vasomotion abnormality and there might be an increased nitrate-mediated vasodilatory response in the brachial artery of migraineurs. Accordingly we aimed to measure endothelium dependent and independent functions of brachial artery in migraineurs and healthy subjects.
Materials and Methods.—Twenty-four patients who fulfilled the diagnostic criteria of migraine were enrolled in the study. Twenty-six age- and sex-matched healthy control subjects comprised the control group. Flow-mediated dilatation and nitrate-mediated dilatation were measured in all patients and control subjects by means of brachial artery ultrasonography.
Results.—Flow-mediated dilatation of patients with migraine was significantly lower than that of control subjects (7.6 ± 3.7% vs 10.4 ± 3.5%, respectively, P= .008). However, nitrate-mediated dilatation in migraineurs was significantly higher than that of nonmigraineurs (25% vs 14%, respectively, P< .001).
Conclusion.—We have shown that migraineurs have decreased endothelium dependent function whereas increased nitrate-mediated response in their brachial artery. It can be suggested that the mechanism underlying migraine may be a diffuse vascular vasomotion abnormalities and migraine may be a local manifestation of systemic vascular abnormality rather than a primary cerebral phenomenon.