Previous studies suggest a role of scalp perivascular structures in at least a substantial number of migraineurs. This study aimed to evaluate the presence of pressure-painful scalp arteries in patients with migraine. Pressure-painful points on scalp arteries were searched for in 100 consecutive patients affected with migraine, 84 females (F) and 16 males (M), 83 without aura (70 F) and 17 with aura (14 F), and in 30 healthy matched subjects. The examined arteries were, bilaterally, the superficial temporal and its frontal branch, the zygomatico-orbital, the occipital and the posterior auricular. We examined 75 patients interictally: 60 (80.0%) reported one or more (mean per subject 3.7 ± 1.9) pressure-painful arteries and 15 (20.0%) reported none. In the 30 controls, pressure-painful arteries were present in only nine (30.0%, mean per subject 1.3 ± 0.7), with highly significant differences (p < 0.001). During a migraine attack, of the 51 patients examined, 45 (88.2%, 38F) reported one or more (mean 3.8 ± 2.1) pressure-painful arteries and six (11.8%) reported none. Both when during an attack and interictally, the arteries most frequently involved were the occipital, the frontal branch, and the temporal. Scalp arteries are frequently painful to pressure in migraineurs, especially in females, both during headache and interictally. Painful arteries suggest hypersensitivity of periarterial nociceptive afferents, which is perhaps due to the local presence of endogenous algogenic products, as suggested by our previous studies.
Scalp arteries are frequently painful on pressure in children and adolescents with migraine, both in the absence of and during a migraine attack. Painful arteries suggest hypersensitivity of periarterial nociceptive afferents.
Because a prolonged compression of the major scalp arteries blocks migraine attacks in a substantial number of patients, we studied the effect of the use of a simple handmade device in blocking an incoming headache attack in children and adolescents. Thirty-seven consecutive ambulatory patients were instructed to apply, at the onset of each migraine attack, a handmade device firmly compressing both temporal arteries. Thirteen patients interrupted treatment because of intolerance of the local pain provoked by compression of the device. Of the remaining 24 patients, 17 reported benefit from using the device and 7 no effect. In these 17 patients, the percentage of attacks aborted or attenuated by early use of the device was 90.5% in the first month and 95.7% in the second month; the consumption of antipain drugs dropped from the mean 4.4 +/- 2.6 in the pre-device month to 1.3 +/- 1.6 in the first and 0.6 +/- 0.9 in the second month.
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