Abstract
Pathogenesis of migraine is believed to be neurogenic, with vascular changes having a role in the attack pathophysiology. Migraine patients have reported abnormalities in cerebral hemodynamics. Human monoclonal antibodies represent the new therapy of migraine, acting against the vasodilator effect of Calcitonin gene-related peptide. In this frame, the aim of the present study was to evaluate blood flow velocities in basal brain arteries and vasomotor reactivity of migraine patients using TCCD, before and after monoclonal antibody treatment with erenumab.
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