Background. Calcitonin gene-related peptide (CGRP) is regarded as an important molecule in trigeminovascular sensitization (TVS). CGRP-induced headaches (CGRP-IH) are evoked by intravascular administration of CGRP in nonmigraine and migraine subjects. CGRP might be associated with vasodilatation of the middle cerebral artery (MCA). It is unclear whether CGRP-induced hemodynamic changes relate to CGRP-IH in nonmigraine subjects. Methods. Twenty healthy subjects participated in our study. Polymodal recording of mean arterial velocity in MCA (vm MCA), end-tidal carbon dioxide partial pressure (Et-CO2), mean arterial pressure (MAP), and heart rate (HR) was employed using transcranial Doppler (TCD) sonography. During the experiment, we administered intravenous infusion of CGRP at a rate of 1.5 mcg/min. The vm MCA, Et-CO2, HR, and MAP were determined at time points
T
0
,
T
1
,
T
2
, and
T
3
. We calculated the responses at different time points and combined them into a single response vm MCAtot, Et-CO2tot, HRtot, and MAPtot. Results. We found significant differences along the time points in vm MCA (
p
=
<
0.001
), Et-CO2 (
p
=
0.003
), MAP (
p
<
0.001
), and HR (
p
<
0.001
). The relationship between vm MCAtot and Et-CO2tot was significant and positive (
p
=
0.005
). The
t
-test showed significant differences between CGRP-IH and non-CGRP-IH subjects in vm MCAtot (
p
=
0.021
) but not in Et-CO2tot (
p
=
0.838
), MAPtot (
p
=
0.839
), and HRtot (
p
=
0.198
). Only vm MCAtot showed a significant relationship with CGRP-IH (
p
=
0.028
). Conclusions. Our study provides evidence for vasodilatation of MCA in relation to CGRP-IH due to intravascular CGRP detected by multimodal TCD. In the context of TVS induced by CGRP, MCA vasodilatation seems to represent an epiphenomenon of the underlying TVS.
The Influence of Calcitonin Gene-Related Peptide on Cerebral Hemodynamics in Nonmigraine Subjects with Calcitonin Gene-Related Peptide-Induced Headaches
