The impact of migraines as a risk factor for cervicocerebral artery dissection was retrospectively investigated in patients who had a cervicocerebral artery dissection. We first evaluated the patients' medical records and history of migraine and then calculated the proportion of patients with migraine as well as the relevant vascular risk factors. The prevalence of migraine with respect to the location of the cervicocerebral artery dissection was also identified. Sixty-two patients (37 men, 25 women) had both a cerebral artery dissection and a record of migraine. Among them, 93.5% presented with an isolated headache, and 6.5% presented with a related stroke. Regarding the locations of the artery dissection, 56 (90.3%) were in the intracranial vertebral artery (VA), three (4.8%) were in the internal carotid artery, and one case each (1.6%) was in an anterior cerebral artery, basilar artery (BA), and both the VA and BA. Among the patients with VA dissection, 42 (73.7%) presented with migraines. Among the four patients with dissection of an artery of anterior circulation, only one (25%) had a migraine history. The frequency of migraines tended to be higher in the patients with VA dissection compared to those with a dissection of arteries of anterior circulation. These data suggest that (i) migraine is a potent risk factor for cerebral artery dissection, especially intracranial VA dissection, and (ii) the intracranial VA may be more susceptible to dissection compared to arteries of anterior circulation.

Dyslipidemia is a major risk factor for atherosclerosis, and high low-density lipoprotein (LDL) cholesterol is closely associated with the onset of atherosclerotic cardiovascular disease (ASCVD), including coronary artery disease. Numerous large-scale clinical trials have demonstrated that LDL cholesterol-lowering therapy, primarily involving statins, reduces not only coronary events, but also stroke, and has been established as a cornerstone of cardiovascular prevention. However, ischemic stroke is a group of diseases comprising different pathologies, such as atherothrombotic stroke, cardioembolic stroke, and small-vessel disease; the involvement of dyslipidemia and the efficacy of lipid-lowering therapy vary significantly depending on the subtype. Therefore, the evidence established for coronary artery disease cannot necessarily be applied directly to stroke management, and establishing lipid management strategies tailored to each subtype has become a critical challenge in stroke management. Furthermore, in recent years, in addition to LDL cholesterol-lowering therapy, treatments targeting hypertriglyceridemia, lipoprotein(a) [Lp(a)], and residual inflammatory risk have advanced, and the development of new therapeutic agents-such as PCSK9 inhibitors, selective PPARα modulators, and ATP citrate lyase inhibitors-is progressing, thus raising expectations for their application in stroke prevention. This article provides an overview of domestic and international guidelines for dyslipidemia and summarizes the association between dyslipidemia and ischemic stroke from the perspectives of pathophysiology, pathological findings, and imaging and blood biomarker. In addition, it outlines the latest evidence from large-scale clinical trials, new lipid-lowering therapies, acute-phase lipid management, and interventions targeting residual risk, and discusses the current status and future prospects of lipid management tailored to specific stroke subtypes.

Ischemic stroke is a leading cause of death and disability worldwide, and contributes substantially to the global burden of disease. Although reperfusion therapies such as intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) and mechanical thrombectomy have transformed acute management, the stringent eligibility criteria, narrow treatment windows, and limited accessibility restrict their use to <20% of patients. Many treated individuals have significant neurological deficits, and this underscores the urgent need for therapies that extend beyond revascularization. Two promising approaches have emerged: cell-based therapy and drug repurposing. Stem cell-based interventions, including mesenchymal stem cells, neural stem cells, and induced pluripotent stem cell-derived products, primarily act via paracrine mechanisms to modulate inflammation, attenuate oxidative stress, promote angiogenesis, and enhance neuroplasticity. Simultaneously, drug repurposing leverages the established safety and pharmacology of existing agents to accelerate clinical translation. Valproic acid, a histone deacetylase inhibitor, and perampanel, a selective AMPA receptor antagonist, target key mechanisms, such as excitotoxicity, oxidative injury, and epigenetic regulation. This review synthesizes the current evidence on both strategies and emphasizes mechanistic overlaps, clinical trial findings, translational barriers, and future directions. Unlike previous reviews that have addressed cell-based therapies or drug repurposing separately, we propose a unique phase-specific integrative framework that rationally combines these complementary strategies with reperfusion therapy and rehabilitation to achieve durable neuroprotection and meaningful recovery in ischemic stroke.

Ischemic stroke is one of the most prevalent neurological disorders, with primary injury typically localized to the neocortex. However, secondary damage often extends to anatomically distant regions, particularly the hippocampus. One of the early neuroendocrine responses to cerebral ischemia is activation of the hypothalamic-pituitary-adrenal (HPA) axis. Increased release of corticosterone (CORT) by the adrenal glands into the bloodstream leads to its accumulation in the hippocampus. We hypothesize that this process may contribute to the hippocampal damage and underlie delayed cognitive and affective impairments following stroke. To test this, we investigated the levels of neurotrophic factors reflecting the neuroprotective potential of the hippocampus using two established middle cerebral artery occlusion (MCAO) models that differ in their effects on CORT production: the Koizumi et al. (1986) model (MCAO1) and the Longa et al. (1989) model (MCAO2). Although both models produced comparable neurological deficits, mortality rates, and infarct volumes, they differed markedly in endocrine and hippocampal responses. Significant increases in circulating CORT and its accumulation in both ipsilateral and contralateral hippocampus were observed only in MCAO1. Moreover, correlations between the CORT levels (in the blood and hippocampus) and both rat body weight and neurological deficit were stronger in MCAO1 than in MCAO2. In both acute models, brain-derived neurotrophic factor (BDNF) levels were elevated in the ipsilateral hippocampus, whereas the content of glial cell line-derived neurotrophic factor (GDNF) remained unchanged. In contrast, ciliary neurotrophic factor (CNTF) increased in the ipsilateral hippocampus only in MCAO2. These findings suggest that differential activation of the HPA axis and consequent variations in corticosteroid signaling in the hippocampus selectively modulate the neurotrophic response during the acute phase following MCAO.

Background Intracerebral hemorrhage (ICH) is associated with high mortality and limited therapeutic options. The impact of statin therapy on outcomes following ICH remains controversial. Methods A retrospective cohort study was conducted using the TriNetX Global Collaborative Network. Adult patients (≥18 years) with nontraumatic ICH were identified and stratified based on statin use within three months prior to the index event. Propensity score matching (1:1) was performed to balance demographics, comorbidities, and medication use. The primary outcome was 30-day mortality. Secondary outcomes included ICU admission or mechanical ventilation, external ventricular drain (EVD) placement, seizures, and craniotomy or shunt procedures. Results After matching, 82,755 patients were included in each cohort. Pre-injury statin use was associated with significantly lower mortality (13.4% vs 19.7%; risk ratio (RR) 0.68, 95% CI 0.66-0.70, p<0.001). Statin use was also associated with lower rates of ICU admission or mechanical ventilation (10.9% vs 13.7%; RR 0.80, p<0.001) and EVD placement (4.0% vs 4.6%; RR 0.87, p<0.001). Rates of seizures were similar between groups. Statin users had slightly higher rates of craniotomy or shunt procedures (0.8% vs 0.6%; RR 1.33, p<0.001). Conclusion Pre-injury statin use was associated with reduced mortality and improved short-term outcomes following intracerebral hemorrhage. These findings demonstrate an association between pre-injury statin use and lower mortality and differences in short-term clinical outcomes following intracerebral hemorrhage. Given the retrospective observational design, causality cannot be established.