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Vasodilation of the middle meningeal artery may occur at migraine onset on the pain side, according to a study published in Brain.
A total of 30 women aged 18 to 50 years experiencing migraine without aura (with unilateral pain in ≥70% of attacks) were enrolled for this study. Study participants were prescreened by using cilostazol to induce migraine, and those for whom it triggered a migraine were included. Patients also had to be migraine-free for ≥5 days before the beginning of the study.
For the study, migraines were induced using 200 mg oral cilostazol, and changes in the circumference of cranial arteries were measured using 3 T high-resolution magnetic resonance angiography. Scans were performed at baseline, migraine onset (4 hours after cilostazol induction; early attack scan), 1 hour after sumatriptan treatment (given to 12 of 30 participants; 6 mg subcutaneous injection; sumatriptan scan), and the next day (late-attack scan).
Headache intensity was assessed every hour with a verbal rating 0 to 10 scale. Patients were then allocated to receive a subcutaneous injection of 6 mg sumatriptan (n=11) or promethazine and metoclopramide. The circumference of the following arteries was measured: cerebral arteries (middle cerebral, cerebral, internal carotid [cavernous and cerebral parts], basilar [cerebral parts]) and extracerebral arteries (middle meningeal, superficial temporal, external carotid).
The middle meningeal artery was found to have greater increases in circumference on the pain vs nonpain side at migraine onset (early scan; 0.24±0.37 mm vs 0.06±0.38 mm, respectively; P =.002). Neither of the other arterial segments had migraine-associated changes in circumference (P >.05). A unilateral increase was measured in the circumference of the middle meningeal artery on the pain side during the early migraine attack compared with baseline (5.23±0.57 mm vs 5.00±0.50 mm, respectively; P =.005). Treatment with sumatriptan resulted in constriction of all extracerebral arteries (P <.05).
Limitations of the study include the small number of patients, the sole assessment of large brain arteries, and the short follow-up.
“We propose that this headache-specific dilation of [middle meningeal artery] precedes unilateral dilation of intracerebral arteries in the initiating cascade of migraine, suggesting a meningeal site of migraine headache,” the researchers concluded.
Reference
Khan S, Amin FM, Christensen CE, et al. Meningeal contribution to migraine pain: a magnetic resonance angiography study. Brain. 2019;142(1):93-102.
