Exogenous calcitonin gene-related peptide (eCGRP) can induce CGRP-induced headaches (CGRP-IH) and aura in migraine with aura (MA). This implies a common pathophysiological mechanism of trigeminovascular sensitization (TVS) in migraine headaches and aura. The aim was to assess hemodynamic changes in cerebral circulation induced by eCGRP. We predicted that cerebral hemodynamic changes may differ between migraine without aura (MO) and MA.
Materials and methods
We included twenty participants with migraine, of whom 15 (75%) had MO, and 5 (25%) had MA. An intravenous infusion of eCGRP was administered. Polymodal recording of mean arterial velocity in MCA (vm MCA) and PCA (vm PCA), end-tidal carbon dioxide partial pressure (Et-CO2), mean arterial pressure (MAP), and heart rate (HR) was employed using transcranial Doppler sonography (TCD). The parameters were determined at different time points with single responses vm MCAtot, vm PCAtot, Et-CO2tot, MAPtot, and HRtot.
The CGRP-IH appeared in five participants with MA (100%) and in 11 participants with MO (73.3%) (p = .530). The difference of changes in vm MCAtot (p = .014) and vm PCAtot (p = .004) was significant, whereas in Et-CO2tot (p = .658), MAPtot (p = .392), and HRtot (p = .686), it appeared to be non-significant. We found significant associations between vm MCAtot and MA (p = .023; OR = 0.88; 95%C.I. 0.78–0.98), and vm PCAtot and MA (p = .018; OR = 0.85; 95%C.I. 0.74–0.97).
Cerebral hemodynamics differs between MO and MA, indicating a pronounced vasodilatation and TVS in MA, which could induce aura.