Calcitonin gene-related peptide (CGRP)-targeted therapies, including monoclonal antibodies (mAbs) and gepants, represent a major advancement in migraine prevention, offering greater efficacy and improved tolerability compared with traditional treatments. These agents selectively inhibit the CGRP pathway, a key mediator in migraine pathophysiology, and are increasingly used even as first-line options in selected patients. While clinical trials and real-world data suggest a favorable cardiovascular (CV) safety profile, particularly in patients without major risk factors, evidence remains limited for those with established vascular disease or recent vascular events. Concerns persist regarding long-term effects and the safety of CGRP blockade in high-risk populations. This narrative review focuses on the CV and cerebrovascular safety of CGRP-targeted migraine treatments-an area of growing clinical relevance. We compare these newer agents with traditional migraine preventives and highlight the paucity of data in patients with previous stroke, subarachnoid hemorrhage, myocardial infarction, or significant CV comorbidities. In addition, we discuss the emerging topic of dual CGRP pathway blockade (mAbs plus gepants), which has not previously been reviewed in the context of vascular risk. Based on currently available scientific evidence, we offer structured clinical considerations to guide the use of CGRP-targeted therapies in patients with vascular risk or cerebrovascular disease. Our aim is to support informed decision making in a population that has often been excluded from clinical trials but is becoming increasingly important in clinical practice.

Background: Post‐stroke dysphagia is known to have a pronounced effect on mortality and quality of life of stroke patients. Here, we investigate whether this extends to post‐stroke fatigue, a major contributor to morbidity after ischemic stroke.Methods: Patients with acute ischemic stroke (recruited consecutively in the STROKE‐CARD Registry from 2020 to 2023 at the study center Innsbruck, Austria) were examined for dysphagia via clinical swallowing examination at hospital admission. Post‐stroke fatigue was assessed using the Fatigue Severity Scale (FSS) at study specific in person follow‐up visits within the first year after ischemic stroke.Results: Among 882 ischemic stroke patients (mean age 72.4 ± 13.5 years, 36.8% females), dysphagia was present in 22.0% at hospital admission and persisted in 16.2% until hospital discharge. Post‐stroke fatigue affected 52.2% of the total cohort during follow‐up and was significantly more prevalent among those with dysphagia (68.4% vs. 49.0%, p < 0.001). The prevalence of fatigue increased with the severity of dysphagia, with the highest proportion (86.7%) in those with severe dysphagia. After multivariable adjustment for other factors associated with post‐stroke fatigue, including age, sex, pre‐stroke disability, cognitive impairment, stroke severity, inability to walk at discharge, and need for antidepressants at discharge, dysphagia remained independently associated with post‐stroke fatigue during the first year after stroke (odds ratio [OR]: 2.03, 95% confidence interval [CI]: 1.22–3.38).Conclusions: Dysphagia is common after ischemic stroke and increases the risk of post‐stroke fatigue. Patient‐tailored measures are warranted to reduce fatigue after stroke and therefore enhance quality of life.

Migraine and stroke are neurological disorders with significant global prevalence and impact. Recent advances in migraine therapy have focused on the calcitonin gene-related peptide (CGRP) pathway. This review examines the shared pathomechanisms between migraine and stroke, with emphasis on the role of CGRP. We analyze the current literature on CGRP’s functions in cerebrovascular regulation, edema formation, neuroinflammation, and neuroprotection. CGRP acts as a potent vasodilator and plays a crucial role in trigeminovascular activation during migraine attacks. In stroke, CGRP has demonstrated neuroprotective effects by improving collateral circulation and reducing ischemia-reperfusion injury. Concerns have been raised about the potential impact of CGRP inhibitors on stroke risk and outcomes. Studies in animals suggest that CGRP receptor antagonists may worsen cerebral ischemia by impairing collateral flow. We discuss the implications of these findings for the use of CGRP-targeting therapies in migraine patients, especially those at increased risk of stroke. Additionally, we explore the complex interplay between CGRP, endothelial function, and platelet activity in both conditions. This review highlights the need for further research to elucidate the long-term cerebrovascular safety of CGRP pathway inhibitors and to identify potential subgroups of migraine patients who may be at higher risk of adverse cerebrovascular events with these novel therapies.

Background: Anti-CGRP (receptor) antibodies are approved for the preventive treatment of migraines and are increasingly used due to their favorable safety profile and potent efficacy. However, as CGRP is one of the most potent vasodilators, concerns have been raised regarding the possible impact of these drugs on arterial blood pressure. Methods: We present a retrospective cohort study at a tertiary headache center including a total of 259 patients with episodic and chronic migraine who received anti-CGRP antibody treatment for migraine prevention. Blood pressure was measured in a hospital using a standardized setting at baseline and at least at two follow-up visits. Significant increase in blood pressure was defined as an increase in systolic blood pressure ≥ 20 mmHg and/or an increase in diastolic blood pressure ≥ 10 mmHg from the baseline value. Results: Mean age of our population was 39.9 years (±12.1), and 217 (83.8%) were female. Blood pressure measurements between T0 and T2, incorporating all CGRP-antibody groups, showed a significant reduction in systolic (−3.3 mmHg; p = 0.001) and diastolic blood pressure (−2.3 mmHg; p = 0.021), respectively. The repeated-measures generalized linear model analysis revealed no significant variations between the CGRP antibodies relative to blood pressure. The most robust factor predicting systolic hypertensive measurements in the course of anti-CGRP antibody treatment was pre-existing hypertension at baseline (sum of mean squares 7.4; p = 0.019). Conclusions: Our data indicate that treatment with anti-CGRP (receptor) antibodies does not significantly increase blood pressure. However, it seems to be important to monitor patients with pre-existing arterial hypertension.

Migraine and stroke are neurological disorders with significant global prevalence and impact. Recent advances in migraine therapy have focused on calcitonin gene-related peptide (CGRP) pathway. This review examines the shared pathomechanisms between migraine and stroke, with emphasis on the role of CGRP. We analyze current literature on CGRP's functions in cerebrovascular regulation, edema formation, neuroinflammation, and neuroprotection. CGRP acts as a potent vasodilator and plays a crucial role in trigeminovascular activation during migraine attacks. In stroke, CGRP has demonstrated neuroprotective effects by improving collateral circulation and reducing ischemia-reperfusion injury. Concerns have been raised about the potential impact of CGRP inhibsitors on stroke risk and outcomes. Studies in animals suggest that CGRP receptor antagonists may worsen cerebral ischemia by impairing collateral flow. We discuss the implications of these findings for the use of CGRP-targeting therapies in migraine patients, especially those at increased risk of stroke. Additionally, we explore the complex interplay between CGRP, endothelial function, and platelet activity in both conditions. This review highlights the need for further research to elucidate the long-term cerebrovascular safety of CGRP pathway inhibitors and to identify potential subgroups of migraine patients who may be at higher risk of adverse cerebrovascular events with these novel therapies.

BACKGROUND: Poststroke dysphagia is associated with poor functional recovery and psychological consequences, including depression and fatigue, which may impede successful rehabilitation. Here, we investigate whether antidepressants may improve dysphagia recovery after acute ischemic stroke. METHODS: In this prospective cohort study, patients with acute ischemic stroke (aged ≥18 years; consecutively enrolled in the STROKE-CARD trial (Post-Stroke Disease Management) 2014 to 2019 and registry 2020 to 2023 in Innsbruck, Austria) were examined for poststroke dysphagia (by standardized clinical and instrumental examinations) and antidepressant intake at hospital admission, discharge, and inpatient 3-month follow-up. The outcome was full oral diet resumption 3 months poststroke. Associations were analyzed using multivariable logistic regression and are presented as adjusted odds ratios, adjusting for age, sex, stroke severity, dysphagia severity, depression severity, stroke localization, thrombolysis, cognitive impairment, functional disability before stroke and at hospital discharge, and study type. RESULTS: Poststroke dysphagia affected 380 (18.6%) of the total cohort of 2046 patients at hospital admission (mean age, 72.7±14.1 years; 37.8% women) and persisted in 290 (14.7%) and 95 (4.6%) patients until hospital discharge and 3-month follow-up, respectively. Among the 290 patients with persistent dysphagia at discharge included in the outcome analysis, antidepressant intake increased from 4.8% before stroke to 27.6% at hospital discharge and 49.0% at 3 months ( P <0.001). A total of 195 (67.2%) of 290 patients with persistent dysphagia regained full oral diet by 3 months, with significantly higher recovery rates in those who were discharged on antidepressants (78.8% versus 62.9%; P =0.010). Antidepressant intake at hospital discharge was independently associated with improved dysphagia recovery at 3 months (adjusted odds ratio, 2.98 [95% CI, 1.51–5.87]; P =0.002). CONCLUSIONS: Antidepressant intake was associated with better dysphagia recovery after acute ischemic stroke. As these findings are observational, randomized trials are required to clarify whether antidepressants can support dysphagia rehabilitation.