αCGRP-Induced Changes in Cerebral and Systemic Circulation; A TCD Study

Acta Neuro Scandinavica

et al. 2021

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Objectives 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. Results 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). Conclusions Cerebral hemodynamics differs between MO and MA, indicating a pronounced vasodilatation and TVS in MA, which could induce aura.

Section: Introductionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Calcitonin gene‐related peptide‐induced hemodynamic changes in migraine with and without aura

Zupan

Zaletel

Acta Neuro Scandinavica

et al. 2021

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“…In the third MRA study no differences in MCA diameter were detected before and after CGRP infusion (6). In our recent study in healthy subjects we found hemodynamic responses of MCA and PCA to CGRP infusion (7). By our knowledge, so far this was the only study of PCA reactivity to CGRP infusion.…”

Section: Introductionmentioning

confidence: 73%

The Responses to CGRP in The Teritory of the Posterior Cerebral Artery in Migraine

Zaletel²,

Žvan³

et al. 2021

Preprint

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Background Calcitonin gene-related peptide (CGRP) is important in trigeminovascular (TMV) sensitization with neurogenic inflammation which might be evolved in CGRP induced headache (CGRP-IH). Distribution of white matter lesions, migraine aura and functional neuroimaging indicate that posterior circulation is especially exposed to TMV sensitization. The transcranial doppler (TCD) is able to detect changes in posterior cerebral artery (PCA) during CGRP stimulation. Thus, we studied CGRP induced hemodynamic changes in PCA and CGRP-IH using TCD. Methods Twenty healthy subjects and 20 patients with migraine participated in our study. TCD was used to monitored mean arterial velocity in posterior cerebral artery (vm PCA). Simultaneously End tidal carbone dioxide (Et-CO2), mean arterial pressure (MAP) and heart rate (HR) were measured. During experiment we monitored the frequency of CGRP-IH. We determined the values of vmPCA, Et-CO2, MAP and HR and calculate response of vmPCA, Et-CO2, MAP and HR to CGRP. To test the differences and relationships statistical methods were applied using SSPS. Results We found significant decrease of vmPCA in migraine and control groups and found the vmPCA response to be significant lower in migraine (p = 0.018). Et-CO2 decreases in both groups and it is significantly lower in migraine (p > < 0.001). MAP is significantly higher in migraine(p = 0.001), while HR is not significantly higher in migraine (p = 0.570). CGRP-IH is significantly associated with vmPCA responses (p = 0.003) and migraine (p < 0.001). Conclusion We concluded that hemodynamic changes in PCA are significantly related to CGRP-IH. The TMV sensitization might be pronounced in posterior circulation explaining clinical and morphologic issues in migraine.

“…This study uses the method of Visočnik et al, and the method description partly reproduces their wording [ 8 ].…”

Section: Methodsmentioning

confidence: 99%

The Influence of Calcitonin Gene‐Related Peptide on Cerebral Hemodynamics in Nonmigraine Subjects with Calcitonin Gene‐Related Peptide‐Induced Headaches

Zupan

Zaletel

BioMed Research International

et al. 2021

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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.