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Introduction: 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. Methods: 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 CO2 (Et-CO2), 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. Results: In both groups, we found significant decrease between measurement points of vm MCA and Et-CO2 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-CO2 in patients with migraine. A significant difference between groups was found in MAP response. Significant relationships were found between migraine and vm MCA, Et-CO2, and MAP. Conclusion: 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.

Introduction: 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 aCGRP (haCGRP) could be a surrogate marker for the sensitization. We hypothesize that vascular response to hαCGRP is augmented in a patient with migraine. Methods: 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 CO2 (Et-CO2), 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. Results: In both groups, we found significant decrease between measurement points of vm MCA and Et-CO2 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-CO2 in patients with migraine. A significant difference between groups was found inMAP response. Significant relationships were found between migraine and vm MCA, Et-CO2, and MAP. Conclusion: 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. [ABSTRACT FROM AUTHOR]

It is known that perivascular application of CGRP induces cerebral vasodilatation. However, it is unclear whether intravenous alfa CGRP (aCGRP) induces changes in cerebral and systemic hemodynamics. Therefore, we studied the influence of an aCGRP intravenous infusion at a rate of 1.5 mcg/min in 20min 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 aCGRP decreased vm MCA (p < 0.001), vm PCA (p < 0.001), mean arterial pressure (MAP) (p < 0.001) and end-tidal CO2 (Et-CO2) (p = 0.030). The heart rate (HR) increased during αCGRP infusion (p < 0.001). In addition, we found a positive relationship between Et-CO2 and vm MCA (p = 0.001) as well as vm PCA (p = 0.043). In our view, aCGRP induces changes in cerebral and systemic circulation in healthy volunteers. It might cause vasodilatation of MCA and PCA and a compensatory decrease of Et-CO2 to aCGRP related hemodynamic changes. [ABSTRACT FROM AUTHOR]

Introduction: 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. Methods: 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. Results: We found that migraine has a significant impact on the vasodilatory response of the anterior (B = 4,249, SE = 1.023, r = 0.363, p < 0.001) and posterior cerebral circulation (B = 3.634, SE = 1.461, r = 0.227, p = 0.014). Migraine with aura was significantly associated with changes in the anterior (B = 2.558, SE = 0.880, r = 0.275, p = 0.005) and posterior cerebral circulation (B = 7.565, SE = 2,368, r = 0.359, p = 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, p = 0.024). Conclusion: We conclude that TVR in the posterior cerebral circulation might be enhanced in MA and that aura might be a consequence of TVR enhancement. [ABSTRACT FROM AUTHOR]

Background: Stroke expertise is critical for timely and appropriate intravenous thrombolysis (IVT) and affects IVT use. Introduction: In Slovenia, IVT is administered in general hospitals, which often lack on-site neurologic expertise. To overcome this obstacle, a national telestroke network, TeleKap, has been implemented. The aim of the study was to determine whether TeleKap is associated with enhanced IVT use. Materials and Methods: This investigation was a retrospective observational study comparing the number of acute ischemic stroke (AIS) patients and the use of IVT during the first 3 consecutive years. TeleKap, a decentralized hub-and-spoke telestroke model covering the entire nation, consists of one comprehensive stroke center and 12 spokes classified according to the availability of on-site neurologic expertise. Results: During the observation period, we treated a total of 1,316 patients with AIS, of which 508 (38.6%) received IVT. We found statistically significant positive trends in the number of IVT patients (142 in 2015, 158 in 2016, and 208 in 2017; B = 4.39, standard error (SE) = 1.59, p  = 0.01) and the number of AIS patients (326 in 2015, 424 in 2016, and 566 in 2017; B = 14.42, SE = 5.19, p  = 0.01) for all spokes. The trend in the IVT rate was numerically negative but did not reach statistical significance (43.5% in 2015, 37.3% in 2016, and 36.7% in 2017; p  = 0.30). Discussion: TeleKap enhanced IVT use regardless of on-site neurologic expertise. Conclusions: TeleKap proved to be efficient. It could serve as a model of telestroke care for other similar countries.

The effectiveness of homocysteine-lowering therapy on stroke prevention is still unclear. Although randomized controlled epidemiological trials have yielded mixed findings, a multicenter trial did not show any beneficial effect. Genetic studies are still lacking. Therefore, we report on a female patient with transient ischemic attacks and the thermolabile variant of methylenetetrahydrofolate reductase (TT genotype), who benefited from supplemental therapy for homocysteine lowering.