TY - JOUR
T1 - Involvement of calcitonin gene-related peptide in migraine: regional cerebral blood flow and blood flow velocity in migraine patients
AU - Lassen, L.H.
AU - Jacobsen, V.B.
AU - Haderslev, P.A.
AU - Sperling, B.
AU - Iversen, H.K.
AU - Olesen, J.
AU - Tfelt-Hansen, P.
N1 - Times Cited: 0ArticleEnglishTfelt-Hansen, PUniv Copenhagen, Glostrup Hosp, Dept Neurol, DK-2600 Glostrup, DenmarkCited References Count: 25361VNSPRINGER233 SPRING ST, NEW YORK, NY 10013 USANEW YORK
PY - 2008
Y1 - 2008
N2 - Calcitonin gene-related peptide (CGRP)-containing nerves are closely associated with cranial blood vessels. CGRP is the most potent vasodilator known in isolated cerebral blood vessels. CGRP can induce migraine attacks, and two selective CGRP receptor antagonists are effective in the treatment of migraine attacks. It is therefore important to investigate its mechanism of action in patients with migraine. We here investigate the effects of intravenous human alpha-CGRP (h alpha CGRP) on intracranial hemodynamics. In a double-blind, cross-over study, the effect of intravenous infusion of haCGRP (2 mu g/min) or placebo for 20 min was studied in 12 patients with migraine without aura outside attacks. Xenon-133 inhalation SPECT-determined regional cerebral blood flow (rCBF) and transcranial Doppler (TCD)-determined blood velocity (V-mean) in the middle cerebral artery (MCA), as well as the heart rate and blood pressure, were the outcome parameters. No change of rCBF was observed at the end of infusion [1.2% +/- 1.7 with h alpha CGRP, vs. -1.6% +/- 3.1 with placebo (mean +/- SD)] (P = 0.43). V-mean in MCA decreased to 13.5% +/- 3.6 with haCGRP versus 0.6% +/- 1.8 with placebo (P < 0.005). Since rCBF was unchanged, this indicates a dilation of the MCA. h alpha CGRP induced a decrease in MAP (12%) (P < 0.005) and an increase in heart rate (58%) (P < 0.0001). CGRP dilates cerebral arteries, but the effect is so small that it is unlikely to be the only mechanism of CGRP-induced migraine
Udgivelsesdato: 2008/6
AB - Calcitonin gene-related peptide (CGRP)-containing nerves are closely associated with cranial blood vessels. CGRP is the most potent vasodilator known in isolated cerebral blood vessels. CGRP can induce migraine attacks, and two selective CGRP receptor antagonists are effective in the treatment of migraine attacks. It is therefore important to investigate its mechanism of action in patients with migraine. We here investigate the effects of intravenous human alpha-CGRP (h alpha CGRP) on intracranial hemodynamics. In a double-blind, cross-over study, the effect of intravenous infusion of haCGRP (2 mu g/min) or placebo for 20 min was studied in 12 patients with migraine without aura outside attacks. Xenon-133 inhalation SPECT-determined regional cerebral blood flow (rCBF) and transcranial Doppler (TCD)-determined blood velocity (V-mean) in the middle cerebral artery (MCA), as well as the heart rate and blood pressure, were the outcome parameters. No change of rCBF was observed at the end of infusion [1.2% +/- 1.7 with h alpha CGRP, vs. -1.6% +/- 3.1 with placebo (mean +/- SD)] (P = 0.43). V-mean in MCA decreased to 13.5% +/- 3.6 with haCGRP versus 0.6% +/- 1.8 with placebo (P < 0.005). Since rCBF was unchanged, this indicates a dilation of the MCA. h alpha CGRP induced a decrease in MAP (12%) (P < 0.005) and an increase in heart rate (58%) (P < 0.0001). CGRP dilates cerebral arteries, but the effect is so small that it is unlikely to be the only mechanism of CGRP-induced migraine
Udgivelsesdato: 2008/6
M3 - Journal article
SN - 1129-2369
VL - 9
SP - 151
EP - 157
JO - Journal of Headache and Pain
JF - Journal of Headache and Pain
IS - 3
ER -