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 and purpose: Dysphagia is associated with poor outcome, higher mortality, reduced quality of life, and social isolation. We investigate the relationship between swallowing impairment and symptoms of anxiety and depression after ischemic stroke.Methods: Consecutive patients with ischemic stroke participating in the prospective STROKE‐CARD Registry study from 2020 to 2022 were assessed for dysphagia on hospital admission (clinical swallowing assessment) and for persistence until discharge and 3‐month follow‐up (SINGER Independency Index). Anxiety and depression symptoms were recorded using Beck Depression Inventory (BDI) and Hospital Anxiety and Depression Scale (HADS) at 3‐month follow‐up.Results: Of 648 patients, 19.3% had dysphagia on admission, persisting in 14.8% at discharge and 6.8% at 3‐month follow‐up. With the presence or duration of dysphagia (no dysphagia, dysphagia at baseline, at discharge, at 3 months), score (mean ± SD) increased on the BDI (7.9 ± 6.7, 12.5 ± 8.7, 13.5 ± 9.0, 16.5 ± 10.2), HADS‐D (4.4 ± 3.7, 7.1 ± 4.2, 7.7 ± 4.4, 9.8 ± 4.3), and HADS‐A (4.4 ± 3.5, 5.4 ± 3.6, 6.0 ± 3.6, 7.0 ± 3.6). In linear regression analysis adjusting for age, sex, diabetes, dementia, and either functional disability or stroke severity, BDI and HADS‐D scores were significantly higher in patients with dysphagia across all points in time (admission, discharge, 3‐month follow‐up). An independent association with HADS‐A scores was only evident in patients with persisting dysphagia after 3 months. Patients with dysphagia were more likely to receive antidepressants, antipsychotics, or benzodiazepines at discharge and 3‐month follow‐up.Conclusions: Dysphagia after stroke is common and severely affects psychosocial functioning of individuals. Our results highlight swallowing impairment as an independent predictor for poststroke depressive and, to a lesser extent, anxiety symptoms.

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.

Introduction: Dysphagia is common after acute ischemic stroke and entails considerable morbidity and mortality. Here, we investigated the impact of intensified care on swallowing recovery after stroke. Patients and methods: In this secondary analysis of STROKE-CARD, a randomized intervention trial of intensified post-stroke care, dysphagia was assessed by speech therapists at admission for acute ischemic stroke, at hospital discharge, and after 12-months. Patients randomized to STROKE-CARD care additionally received a detailed dysphagia follow-up at 3-months, including a standardized dysphagia examination, instructions on further exercises and compensation mechanisms and, if necessary, referral for further speech therapy. Results: Dysphagia was present initially after stroke in 236 (16.6%; median age 82 (73–88), 44.1% female) of 1419 patients, with similar prevalence in both study groups at hospital admission (p = 0.239) and discharge (p = 0.870). At follow up, 14 (9.5%) of 147 in the intervention group and 18 (20.2%) of 89 in the control group suffered from persistent dysphagia (p = 0.020). There was better dysphagia recovery in the intervention group also under multivariable adjustment for age, sex, functional disability at 12-months, severe dysphagia at hospitalization, mode of feeding, cognitive impairment, thrombolysis, and stroke localization (odds ratio, 0.41, 95% confidence interval: 0.17 to 0.96). Discussion and conclusion: Intensified post-stroke care improved dysphagia recovery within 1 year after acute ischemic stroke, highlighting the potential of targeted interventions for enhancing stroke outcomes.

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.

Introduction: The progression of diabetes status in post-stroke patients remains under-investigated, particularly regarding new treatments for type II diabetes mellitus (DM II), like glucagon-like peptide 1 receptor agonists (GLP-1-RA) and sodium-glucose co-transporter-2 (SGLT-2) inhibitors, which have not been studied in the post-stroke setting. Patients and methods: Eight hundred eighty-four consecutive ischemic stroke patients recruited to our prospective STROKE-CARD Registry were assessed concerning their glycemic status at baseline (normoglycemia, prediabetes, DM II) and change over time within 1 year follow-up. Multivariate logistic regression was performed to identify factors associated with transitioning from normoglycemia to prediabetes or DM II. Additionally, we reviewed ongoing clinical trials for GLP-1-RA and SGLT-2 inhibitors in the context of acute ischemic stroke. Results: At baseline, 44.6% (n = 394) of individuals had normoglycemia, 33.9% (n = 300) were prediabetic, and 21.5% had DM II (n = 190). After 1 year, normoglycemia decreased by 12.1 percentage points (n = 107), whereas prediabetes and DM II increased by 10.2 percentage (n = 90) points and 1.9 percentage points (n = 17), respectively. Statin therapy was the only significant risk factor for progression. 23.4% (n = 207) of our cohort would have met eligibility criteria for a recent trial on semaglutide in obese non-diabetics with prior cardiovascular disease. However, only one ongoing trial aims at evaluating short-term cardiovascular risk reduction in stroke patients. Discussion: GPrediabetes and DM II are frequent in ischemic stroke patients. Even within an intensified post-stroke disease management setting, a considerable amount of stroke survivors convert to prediabetes or DM II within the first year. Our results demonstrate a notable proportion of patients qualifying inclusion in studies examining the efficacy of GLP-1-RA agonists and SGLT-2 inhibitors in secondary prevention. Conclusion: Given the high prevalence and progression of prediabetes and DM II in stroke survivors, there is a need for clinical trials evaluating the use of GLP-1-RA and SGLT-2 inhibitors in this population.