It is known that perivascular application of CGRP induces cerebral vasodilatation. However, it is unclear whether intravenous alfa CGRP (αCGRP) induces changes in cerebral and systemic hemodynamics. ...Therefore, we studied the influence of an αCGRP intravenous infusion at a rate of 1.5 mcg/min in 20 min on mean arterial velocity in the middle cerebral artery (vm MCA) and in the posterior cerebral artery (vm PCA) in twenty healthy subjects using transcranial Doppler (TCD). We found out that αCGRP decreased vm MCA (
< 0.001), vm PCA (
< 0.001), mean arterial pressure (MAP) (
< 0.001) and end-tidal CO
(Et-CO
) (
= 0.030). The heart rate (HR) increased during αCGRP infusion (
< 0.001). In addition, we found a positive relationship between Et-CO
and vm MCA (
= 0.001) as well as vm PCA (
= 0.043). In our view, αCGRP induces changes in cerebral and systemic circulation in healthy volunteers. It might cause vasodilatation of MCA and PCA and a compensatory decrease of Et-CO
to αCGRP related hemodynamic changes.
Survivors of Hodgkin lymphoma are recognized to have an increased risk of stroke and carotid artery disease owing to neck irradiation (RT). However, it remains unclear whether the vascular ...modifications induced by the treatment of Hodgkin lymphoma during childhood persist over the long term.
Our matched study involved 79 survivors of Hodgkin lymphoma in childhood who received neck RT and 57 healthy controls. Parameters of arterial stiffness (AS), intima-media thickness (IMT), and flow-mediated dilation (FMD) of carotid arteries were assessed using ultrasound.
Our patient cohort demonstrated a significant increase in AS compared to controls (
< 0.05), though no such disparity was observed for FMD (
= 0.111). Neck RT intensified AS (B = 0.037,
= 0.000), while anthracyclines attenuated it (B = -0.803,
= 0.000). Multivariate analysis revealed a positive correlation between neck RT (
< 0.001) and AS. However, we found no significant association between neck RT and FMD (
= 0.277). We identified a substantial positive correlation between the dose of neck RT and AS.
Vascular changes in survivors of childhood Hodgkin lymphoma after neck RT seem to be long-term. Therefore, these patients may have an increased risk of stroke. We suggest refinement of international guidelines according to our results.
Sensitisation of the nervous system in a patient with migraine is supposed to be associated with calcitonin gene-related peptide (CGRP) activity. Therefore, the vascular response to human αCGRP ...(hαCGRP) could be a surrogate marker for the sensitization. We hypothesize that vascular response to hαCGRP is augmented in a patient with migraine.
Twenty healthy subjects and 20 patients with migraine participated in our study. TCD was used to monitor mean arterial velocity in the middle cerebral artery (vm MCA). Simultaneously, end-tidal CO
(Et-CO
), mean arterial pressure (MAP), and heart rate (HR) were measured. The reconstruction of the signals was made for basal conditions, during and after CGRP infusion which were compared using statistics.
In both groups, we found significant decrease between measurement points of vm MCA and Et-CO
during and after hαCGRP infusion. MAP did not show significant trends during the infusion, but it was significantly increased after the infusion in migraine patients only. Responses to hαCGRP, defined as differences between two measurement points, were significantly higher for vm MCA and Et-CO
in patients with migraine. A significant difference between groups was found in MAP response. Significant relationships were found between migraine and vm MCA, Et-CO
, and MAP.
In patients with migraine, vm MCA responses to hαCGRP are significantly higher and are associated with CGRP-induced headache which indicates that patients with migraine are more prone to sensitization.
Calcitonin gene-related peptide (CGRP) is important in trigeminovascular (TMV) sensitization with neurogenic inflammation which might be involved 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 the posterior cerebral artery (PCA) during CGRP stimulation. Thus, we studied CGRP-induced hemodynamic changes in PCA and frequency of CGRP-IH. Twenty healthy subjects and 20 patients with migraine participated in our study. TCD was used to monitor mean arterial velocity in posterior cerebral artery (vmPCA). Simultaneously, end-tidal carbon dioxide (Et-CO2), mean arterial pressure (MAP), and heart rate (HR) were measured. During the experiment, we monitored the frequency of CGRP-IH. We determined the values of vmPCA, Et-CO2, MAP, and HR and calculate the response of vmPCA, Et-CO2, MAP, and HR to CGRP. To test the differences and relationships, statistical methods were applied using SSPS. We found significant decrease in vmPCA in migraine and control groups and found the vmPCA response to be significantly 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). 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.
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.
Migraine aura can be associated with headache or it may occur without one, which suggests an independent mechanism for the aura and for migraine headache. The role of CGRP in migraine headache is ...well established, but the connection between CGRP and the aura is still lacking an explanation. Exogenous CGRP can induce CGRP headaches and migraine auras in patients with migraine. The results of our recent study suggest differences in the vascular response to CGRP stimulation between migraine without aura and migraine with aura. Therefore, we hypothesized that the magnitude of the posterior cerebral circulation response in migraine with aura is greater than in migraine without aura and that CGRP stimulation has different effects on the anterior and posterior circulation in migraine with aura and migraine without aura.
By using transcranial doppler, we studied the hemodynamic effects of CGRP intravenous infusion at a rate of 1.5 mcg/min in 20 min on the mean arterial velocity in the middle cerebral artery and in the posterior cerebral artery in twenty patients with migraine and in a control group of twenty healthy subjects. The same CGRP effects on cerebral hemodynamics were analyzed separately for the group of patients with migraine with aura and the group of patients with migraine without aura. Fifteen patients with migraine (75%) had migraine without aura and 5 patients (25%) had migraine with aura.
We found that migraine has a significant impact on the vasodilatory response of the anterior (B = 4,249, SE = 1.023, r = 0.363,
< 0.001) and posterior cerebral circulation (B = 3.634, SE = 1.461, r = 0.227,
= 0.014). Migraine with aura was significantly associated with changes in the anterior (B = 2.558, SE = 0.880, r = 0.275,
= 0.005) and posterior cerebral circulation (B = 7.565, SE = 2,368, r = 0.359,
= 0.002), while migraine without aura was only significantly associated with changes in the anterior circulation. In addition, we established a significant impact of migraine with aura on VR PCA (B = 5.901, SE = 2,546, r = 0.291,
= 0.024).
We conclude that TVR in the posterior cerebral circulation might be enhanced in MA and that aura might be a consequence of TVR enhancement.
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 T0, T1, T2, and T3. 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.
Changes in cerebral blood flow are one of the main features of migraine attack and have inspired the vascular theory of migraine. This traditional view has been reshaped with recent experimental ...data, which gave rise to the neural theory of migraine. In this review, we speculate that there might be an important link between the two theories, that is, the dysfunction of neurovascular coupling.
Migraine is associated with significant morbidity and a significantly negative impact on the quality of life. A better understanding of the economic impact of migraine is becoming increasingly ...important. This paper aims to shed light on absenteeism and presenteeism costs of migraine in Slovenia.
We use the administrative national-level database on sick leave due to migraine for 2016. The absenteeism cost estimate is based on the number of patients with migraine on physician-determined sick leave and average daily labour costs. We calculate productivity costs from a social perspective regardless of who incurs them. Data from the national registry on sick leave are coupled with data from a web-based self-reported survey to also include the cost of presenteeism. MIDAS and WPAI presenteeism items were used and several different scenarios were designed to assess presenteeism costs.
We estimated annual absenteeism costs per absentee due to migraine at the amount of EUR 531 in 2016 using the NIPH's administrative data on sick leave. Annual absenteeism costs per absentee due to migraine based on self-reported data amounted to EUR 626. The estimated annual presenteeism costs per patient range from EUR 344 - 900.
Estimating the economic burden of a disease is becoming increasingly important. This paper is an insight into the absenteeism and presenteeism costs of migraine in Slovenia.
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