Search Results (1,506)

Objective: In moyamoya disease (MMD), the internal carotid and proximal cerebral arteries narrow, potentially leading to stroke or hemorrhage from fragile collaterals. Disease activity and progression may be detected by contrast-enhanced (CE) high-resolution (HR) vessel wall imaging (CE-VWI) on T1-weighted MRI. However, this imaging approach needs standardization for the evaluation of signal intensity and longitudinal reproducibility. Methods: MMD patients with at least two separate CE-VWI examinations on the same and on different scanners were included. Signal intensity of the vessel wall, pituitary stalk, and temporal lobe white matter were measured and normalized using manually selected regions of interest. Intraindividual longitudinal reproducibility of MRI was analyzed and the clinical course was correlated with vessel wall enhancement data. Results: Eighty-seven patients were analyzed. Primary analysis included 60 patients with two or more CE-VWI measurements (n = 129) with median 14.8 months between examinations (range: 2–36 months) on the same scanner. Intraindividual variation in pituitary stalk enhancement (positive control) and temporal lobe white matter enhancement (negative control) showed median signal variability of 20.5% and 17.5%, respectively. The pituitary-to-temporal lobe signal intensity ratio remained stable over time (p = 0.843) with 9.4% median variability. Correlation analysis revealed a significant positive association between pituitary and temporal lobe signal changes (ρ = 0.717, p < 0.001). A total of 75% of patients showed vessel wall contrast enhancement with fluctuating signal intensity over approximately 15.9 months, likely depicting disease activity. Conclusions: CE-VWI is important for screening disease activity in moyamoya patients. Our findings demonstrate longitudinal intraindividual reproducibility when normalized to pituitary stalk, enabling quantified evaluation of disease progression through longitudinal vessel wall contrast-enhancement changes. Full article

Ischemic stroke is now widely recognized as a disease with a strong inflammatory profile. Cerebral vascular damage is both preceded and followed by a chain of molecular events involving immune cells and inflammatory markers, irrespective of the etiology of the ischemic injury. Over time, an increasingly comprehensive understanding of these markers has led to a better insight into the mechanisms behind the vascular event and recovery following ischemic stroke. However, to date, there are still no available circulating or tissue biomarkers for early diagnosis or prognostic stratification, making ischemic stroke diagnosis contingent on clinical and instrumental investigations. However, neurological and internal medicine research is progressing in identifying markers that could potentially take on this role. This manuscript, therefore, aims to review the most recent and innovative results of medical advances, summarising the current state of the art and future perspectives. If ischaemic stroke is an inflammatory disease, it is also true that it is not just a singular condition, but a group of entities with their own neuroinflammatory features. Thus, given that, in ischemic cerebral vascular damage, “time is brain,” tracking increasingly accurate markers in the diagnosis of ischemic stroke is a valuable tool that will potentially enable earlier recognition of this disease and, hopefully, make it less disabling and more widely treated. Full article

Spontaneous intracerebral hemorrhage (ICH) is a devastating form of stroke, disproportionately affecting older adults and is associated with high rates of mortality, functional dependence, and long-term cognitive decline. Aging profoundly alters the structure and function of the cerebral vasculature, predisposing the brain to both covert hemorrhage and the development of cerebral microbleeds (CMBs), small, often subclinical lesions that share common pathophysiological mechanisms with ICH. These mechanisms include endothelial dysfunction, impaired cerebral autoregulation, blood–brain barrier breakdown, vascular senescence, and chronic inflammation. Systemic factors such as age-related insulin-like growth factor 1 (IGF-1) deficiency further exacerbate microvascular vulnerability. CMBs and ICH represent distinct yet interconnected manifestations along a continuum of hemorrhagic small vessel disease, with growing recognition of their contribution to vascular cognitive impairment and dementia (VCID). Despite their increasing burden, older adults remain underrepresented in clinical trials, and few therapeutic approaches specifically target aging-related mechanisms. This review synthesizes current knowledge on the cellular, molecular, and systemic drivers of ICH and CMBs in aging, highlights diagnostic and therapeutic challenges, and outlines opportunities for age-sensitive prevention and individualized care strategies. Full article

Background: Stroke is a major cerebrovascular disease characterized by disrupted cerebral blood flow, leading to neuronal damage and significant physical, cognitive, and emotional sequelae. While advancements in acute stroke management have improved survival rates, long-term complications such as cognitive impairment and depression continue to hinder recovery. This study addresses these dimensions within the context of ischemic stroke. Aim: The aim of this study was to analyze the cognitive status, functionality, and depressive symptoms in patients with ischemic stroke, exploring interrelations between cognitive, functional, and emotional outcomes to prioritize clinical interventions. Design: This was an analytical, observational, cohort, and prospective study. Methods: The study included 81 subjects diagnosed with ischemic stroke admitted to the Neurology Department of Lucus Augusti University Hospital. Data were collected at three time points—admission, discharge, and follow-up—using validated instruments such as the National Institutes of Health Stroke Scale, Mini-Mental State Examination, Barthel Index, and Beck Depression Inventory. Statistical analyses included Spearman’s correlation, Kruskal–Wallis, and Mann–Whitney tests. Results: Patients with greater cognitive impairment at admission showed poorer functional recovery and higher depressive symptoms during follow-up. Depressive symptoms remained minimal in most cases, but correlations with cognitive and functional deficits were significant. NIHSS scores at admission strongly predicted both functional and emotional recovery, reinforcing its value in early prognosis and therapeutic planning. Conclusions: This study highlights the importance of integrating cognitive, functional, and emotional dimensions into stroke care protocols to optimize patient recovery and improve long-term outcomes. Full article

Cerebral ischemia/reperfusion (I/R) injury remains a significant contributor to adult neurological morbidity, primarily due to exacerbated neuroinflammation and cell apoptosis. These processes amplify brain damage through the release of various pro-inflammatory cytokines and pro-apoptotic mediators. Although long non-coding RNAs (lncRNAs) are increasingly recognized for their involvement in regulating diverse biological pathways, their precise role in cerebral I/R injury has not been fully elucidated. In the current study, transcriptomic profiling was conducted using a rat model of focal cerebral I/R, leading to the identification of lncRNA-1810026B05Rik—also referred to as CHASERR—as a novel lncRNA responsive to ischemic conditions. The elevated expression of this lncRNA was observed in mouse brain tissues subjected to middle cerebral artery occlusion followed by reperfusion (MCAO/R), as well as in primary cortical neurons derived from rats exposed to oxygen-glucose deprivation and subsequent reoxygenation (OGD/R). The results suggested that lncRNA-1810026B05RiK mediates the activation of the nuclear factor-kappaB (NF-κB) signaling pathway by physically binding to NF-kappa-B inhibitor alpha (IκBα) and promoting its phosphorylation, thus leading to neuroinflammation and neuronal apoptosis during cerebral ischemia/reperfusion. In addition, lncRNA-1810026B05Rik knockdown acts as an NF-κB inhibitor in the OGD/R and MCAO/R pathological processes, suggesting that lncRNA-1810026B05Rik downregulation exerts a protective effect on cerebral I/R injury. In summary, the lncRNA-1810026B05Rik has been identified as a critical regulator of neuronal apoptosis and inflammation through the activation of the NF-κB signaling cascade. This discovery uncovers a previously unrecognized role of 1810026B05Rik in the molecular mechanisms underlying ischemic stroke, offering valuable insights into disease pathology. Moreover, its involvement highlights its potential as a novel therapeutic target, paving the way for innovative treatment strategies for stroke patients. Full article

Malignant cerebral infarction (MCI) is rare but often fatal. Early identification helps guide monitoring and decompressive surgery. This study evaluated whether serum biomarkers add predictive value beyond clinical and imaging data in severe stroke patients with anterior circulation large vessel occlusion (LVO). In this prospective study, 73 acute severe LVO stroke patients underwent whole-brain CT perfusion (CTP) with rCBV-based core measurement at admission and follow-up MRI at 24 ± 12 h for infarct and edema volume assessment. Serum biomarkers (s100b, NSE, VEGF, ICAM1) were sampled a median of 20.5 h after baseline imaging. Logistic regression models predicted MCI using baseline variables (NIHSS, ASPECTS, rCBV < 30%), adding treatment data (rtPA, mTICI, NIHSS posttreatment), and adding serum biomarkers. Performance was assessed by AUC, accuracy, F1, and cross-validated R². MCI occurred in 18/73 (24%) patients. Baseline models showed an AUC of 0.72; adding treatment improved the AUC to 0.88. Biomarkers slightly increased the AUC (0.90) but did not improve F1. Higher s100b was associated with more severe injury but did not enhance the prediction of MCI. Models with baseline imaging and treatment best explained infarct (R² ≈ 0.27) and edema (R² ≈ 0.58). In conclusion, admission severity, CTP, and early treatment response are the main predictors of MCI and aid early risk stratification of patients. Despite their pathophysiologic relevance, serum biomarkers do not add substantial predictive value. Full article

Background and Clinical Significance: Moyamoya disease (MMD) is a progressive intracranial vasculopathy characterized by stenosis or occlusion of the terminal internal carotid arteries and the development of fragile collateral networks. It predisposes patients to ischemic and hemorrhagic strokes. Although both direct and indirect revascularization procedures are recommended to restore cerebral blood flow, recurrent cerebrovascular events may still occur, and delayed hemorrhage following revascularization is particularly uncommon. Case Description: We report the case of a 42-year-old woman who presented with seizure, syncope, and aphasia. Cranial computed tomography (CT) revealed a large left temporal–insular intraparenchymal hematoma with a midline shift. Computed tomography angiography (CTA) demonstrated bilateral internal carotid artery narrowing and collateral vessel proliferation, without aneurysm. Her history indicated a hemorrhagic stroke 15 years earlier, at which time MMD was diagnosed by magnetic resonance angiography (MRA) and managed with multiple burr hole surgeries. She remained free of cerebrovascular events until the current presentation. The patient underwent emergent hematoma evacuation, followed by intensive care management. Postoperatively, she demonstrated neurological improvement, though with residual motor aphasia and right-sided weakness, and was discharged for rehabilitation. Conclusions: This case underscores the rare occurrence of delayed intracerebral hemorrhage 15 years after indirect revascularization in MMD. Although revascularization surgery remains the standard therapeutic approach, this report highlights the importance of sustained long-term surveillance, strict risk factor management, and careful postoperative follow-up. The key point is that late hemorrhagic complications, though uncommon, must be considered in the long-term care of MMD patients following revascularization. Full article

Background/Objectives: The relationship between thrombus imaging features and the natural evolution of stroke remains poorly defined. We aimed to investigate the associations between thrombus characteristics on CT and perfusion parameters, as well as subsequent infarct progression, in untreated patients experiencing an anterior circulation acute ischemic stroke (AIS). Methods: This retrospective analysis enrolled 81 untreated patients with AIS who underwent baseline non-contrast CT (NCCT), CT angiography (CTA), CT perfusion (CTP), and a follow-up NCCT. We evaluated the thrombus length, location, and clot burden score (CBS). CTP parameters included the ischemic core, hypoperfused tissue, and penumbra volumes. Infarct growth was the difference between the final infarct volume on a follow-up NCCT and the initial core volume on CTP. Univariate and multivariate regression models were performed. Results: Higher CBS values and shorter thrombi are associated with a reduced ischemic core (coefficients B of −3.9 and 0.88, p < 0.01), diminished hypoperfused tissue (coefficients B of −12.2 and 2.87, p < 0.001), and smaller penumbra volume (coefficients B of −7.9 and 1.99, p < 0.001). More distal occlusions were associated with smaller perfusion deficits. Importantly, a higher CBS and more distal thrombus location were significantly associated with a smaller final infarct volume and infarct growth volume. Conclusions: In untreated AIS patients, a lower thrombus burden (higher CBS, shorter length, distal location) is associated with more favorable baseline perfusion parameters and predicts a slower, less severe natural evolution of AIS. These findings underscore the prognostic value of baseline thrombus characteristics in determining the intrinsic course of a stroke. Full article

Background/Objectives: The rapid progression of stroke often results in irreversible brain damage and poor outcomes when treatment is delayed. Prophylactic administration of FAD012 (3,5-dimethyl-4-hydroxycinnamic acid), a synthetic derivative of ferulic acid (FA), has demonstrated cerebroprotective effects in ischemic models through antioxidant and endothelial protective mechanisms. This study investigated the effects of FAD012 on cerebral infarction and blood–brain barrier (BBB) integrity using a photothrombotic stroke model in rats. Methods: Male Sprague Dawley rats received a single intraperitoneal injection of FAD012 or FA (100 or 300 mg/kg) 60 min prior to stroke induction. Under isoflurane anesthesia, the middle cerebral artery was exposed, and stroke was induced by intravenous administration of Rose Bengal followed by green laser irradiation. Cerebral blood flow (CBF) was monitored by laser Doppler flowmetry. BBB disruption was evaluated by Evans Blue extravasation and immunohistochemistry for tight junction (TJ) proteins. Results: Control rats exhibited extensive infarction, BBB disruption, and reduced expression of claudin-5, occludin, and ZO-1, along with fragmented collagen IV. In contrast, FAD012 (300 mg/kg) significantly attenuated CBF reduction, reduced infarct size, preserved BBB integrity, and maintained TJ protein expression, with greater efficacy than an equivalent dose of FA. FAD012 also preserved the expression and phosphorylation of endothelial nitric oxide synthase (eNOS), a key marker of vascular integrity. The CBF-preserving effect of FAD012 was completely abolished by N^G-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Conclusions: These findings suggest that FAD012 protects endothelial function, thereby contributing to the maintenance of CBF and BBB integrity, supporting its potential as a prophylactic therapeutic agent for ischemic stroke. Full article

Reperfusion therapy uses thrombolysis and clot removal to restore blood flow in the brain after stroke; however, three months after reperfusion therapy, roughly 46% of stroke patients become independent again. MiRNAs (micro RNA) regulate cerebral ischemia/reperfusion injury, and their transfer between cells via exosomes may differentially affect recipient cells. We examined serum exosomal miRNA levels, stroke treatments, and functional outcomes in stroke patients, and we explored the potential role of estimated differentially expressed miRNA (DEmiRNA) target genes in the brain’s reaction to reperfusion after ischemia. The patients in the study received aspirin or reperfusion therapy with either intravenous thrombolysis (rt-PA), mechanical thrombectomy (MT), or a combination of both (rt-PA/MT). Serum samples were collected from stroke patients on days 1 and 10 post-stroke. Serum exosomes’ miRNA was analyzed using qRT-PCR. We identified DEmiRNAs, estimated their targets, and performed enrichment analysis. Functional outcomes were assessed using the modified Rankin Scale (mRS) on days 10 and 90 post-stroke. Among studied treatments, only rt-PA/MT lowered DEmiRNA by day 10 vs. other groups. Specifically, patients with unfavorable mRS score exhibited decreased levels of miR-17, miR-20, miR-186 and miR-222 after combined stroke therapy. Functional analysis identified target genes and pathways associated with cytoskeleton remodeling, cell death, autophagy, inflammation, and dementia. In conclusion, unfavorable stroke outcomes following poor rt-PA/MT response could result from lower miRNA expression levels, thus activating cell death and neurodegenerative processes in brain. Full article

Background and Objective: Cerebral cavernous malformation (CCM) is a vascular disorder causing seizures, neurological deficits, and hemorrhagic stroke. It can be sporadic or inherited via CCM1, CCM2, or CCM3 gene mutations. Inflammation is broadly recognized as a promoter of cerebral vascular malformations. This study explores inflammatory mechanisms and differences behind CCM-related hemorrhage and epilepsy. Material and Methods: The study group comprised 28 patients, ten patients with CCM-related epilepsy, and 18 patients who clinically presented with a cerebral hemorrhage at diagnosis. All patients underwent microsurgical resection of the CCMs. Formaldehyde-fixed, paraffin-embedded tissue samples were immunohistochemically stained using a monoclonal antibody against Cyclooxygenase 2 (COX-2) (Dako, Santa Clara, CA; Clone: CX-294) and NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) (ABCAM, Cambridge, MA, USA; ab214185). MRI and clinical data were correlated with immunohistochemical findings, and the analysis was conducted utilizing the Trainable Weka Segmentation algorithm. Results: Median CCM volume was 1.68 cm³ (IQR: 0.85–3.07 cm³). There were significantly more NLRP3-positive cells (32.56% to 91.98%; mean: 65.82%, median: 68.34%; SD: ±17.70%), compared to COX-2-positive cells (1.82% to 79.69%; mean: 45.87%, median: 49.06%; SD: ±22.56%). No correlation was shown between the volume of CCMs and a hemorrhage event (p = 0.13, 95% CI: 0.99–1.02). Symptomatic brain hemorrhage showed a significantly increased inflammatory enzyme upregulation from both COX-2 (p < 0.001) and NLRP3 (p = 0.009) versus patients with symptomatic CCM-related epilepsy at first diagnosis. Conclusions: Inflammatory processes in CCMs seem to be driven by broad and multiple pathways because both COX-2 and NLRP3-driven inflammatory pathways are consistently activated. As a novelty, this study showed that patients with symptomatic hemorrhage showed upregulated inflammatory enzyme activity compared to patients with CCM-related epilepsy. No direct links between NLRP3, COX-2 expression, and radiological, pathological, or preexisting patient conditions were found. Full article

Introduction. Cervical artery dissection (CAD) is a rare condition, being one of the leading causes of stroke in patients under the age of 45, with a reported prevalence of up to 20%. The management of CAD remains controversial due to its rarity and the lack of large-scale randomized controlled trials. The aim of this study was to report the long-term outcomes of CAD in a real-world setting. Methods. This retrospective, observational, single-center study included patients diagnosed with CAD between 2010 and 2019 (approval number: 153/2015/U/Oss/AOUBo). Clinical presentation, risk factors, and medical therapies were prospectively analyzed. Management strategies included both medical and interventional approaches. Follow-up consisted of annual clinical visits and carotid duplex ultrasound (DUS), with telephone interviews every six months. The primary endpoint was defined by the overall long-term stroke/death rate and in relation to the type of medical treatment, localization of the dissection and clinical manifestations. Results. A total of 62 patients were included, predominantly male (65%) with a mean age of 58 (±2) years. Thirteen dissections (21%) were trauma-related. CAD locations included the common carotid artery in 6 cases (10%), extracranial internal carotid artery in 29 (46%), intracranial internal carotid artery in 9 (14%), and vertebral artery in 16 (25%). One patient (2%) had dissections in both the extracranial internal carotid and vertebral arteries, and another (2%) in both the vertebral and basilar arteries. Bilateral dissections were observed in 5 patients (8%). Ischemic manifestations occurred in 43 patients (68%): 10 transient ischemic attacks (16%), 17 minor strokes (27%), and 16 major strokes (25%), with ischemic lesions on cerebral CT in 31 cases (72%). Fifty-eight (93%) patients were treated medically (anticoagulants and/or antiplatelets), while 4 patients (7%) underwent surgical or endovascular intervention. The mean follow-up was 81 ± 35 months. During this period, 2 patients (4%) experienced stroke and 15 (24%) died. The estimated 10-year survival rate was 71%, and the 10-year stroke/death-free survival rate was 70%. Among medically treated patients, the 10-year stroke/death-free survival was 86% for those on anticoagulation and 67% for those on antiplatelet therapy (p = 0.1). Patients presenting with ischemic symptoms had a lower estimated 10-year stroke/death-free survival rate compared to those with non-ischemic presentations (61% vs. 69%, p = 0.7). Patients with dissection of the common carotid artery had a significantly lower estimated 10-year stroke/death-free survival rate (25%), compared to dissections in other cervical arteries (p = 0.001). Conclusions. In this real-world, single-center experience, cervical artery dissection was associated with a favorable long-term prognosis in most cases, especially among patients managed conservatively with medical therapy. Stroke and mortality rates were relatively low during extended follow-up. Although no statistically significant difference was observed between anticoagulation and antiplatelet therapy, the trend favored anticoagulation for stroke/death-free survival. Patients with CCA dissections had significantly worse 10-year stroke/death-free survival compared to those with dissections in other cervical arteries. Full article

Background/Objectives: Global warming and concomitant extreme weather events have markedly increased the incidence of heat stroke. Heat stroke (HS) poses a substantial threat to cerebral health by triggering neuroinflammation and accelerating neurodegenerative processes. The activation of the Nod-like receptor protein 3 (NLRP3) inflammasome for interleukin-1β (IL-1β) secretion has been implicated as a critical mechanism underlying HS-related fatalities. However, the potential role of specific dietary factors to counteract heat stroke-induced neurotoxicity remains largely underexplored. We previously reported that eicosapentaenoic acid (EPA) and urolithin A (UroA), a gut metabolite of ellagic acid, effectively suppress NLRP3 inflammasome activation against metabolic or pathogenic insults. This study aimed to assess the impact of eicosapentaenoic acid (EPA), urolithin A (UroA), and their combination on mitigating heatstroke-mediated NLRP3 inflammasome activation in microglial cells. Methods: In vitro heatstroke conditions were replicated by subjecting murine BV2 microglial cells to a high temperature (41 °C) under hypoxic conditions. To achieve nutrient loading, BV2 cells were preincubated with either EPA (50 µM) or UroA (10 µM). NLRP3 inflammasome activation was evaluated by proinflammatory gene expression, caspase-1 cleavage in cells, and IL-1β secretion to the medium. The caspase-1 activation was determined using a luciferase-based inflammasome and protease activity reporter (iGLuc) assay. Results: Exposure to high temperatures under hypoxia successfully mimicked HS conditions and promoted NLRP3 inflammasome activation in BV2 cells. Both EPA and UroA substantially attenuated the heat stroke-induced priming of proinflammatory genes. More importantly, EPA and UroA demonstrated a synergistic effect in mitigating HS-induced active caspase-1 production, leading to a dramatic decrease in IL-1β secretion. This synergistic effect between EPA and UroA was further confirmed by the iGLuc reporter assay. Conclusions: Dietary enrichment with EPA and UroA precursors may constitute an efficacious strategy for mitigating heat stroke-mediated neuroinflammation and neurodegenerative diseases. Full article

Transcatheter Aortic Valve Implantation (TAVI) has revolutionized the treatment of severe aortic stenosis in high-risk and inoperable patients. Despite significant advancements in patient selection, techniques, and the evolution of TAVI devices, stroke persists as a consistent adverse event over time, presenting a devastating complication of TAVI procedures and exerting a significant negative prognostic impact. Both acute and subsequent strokes following TAVI continue to pose significant challenges, with substantial implications for patient morbidity and mortality. This paper reviews the incidence, mechanisms, risk factors, and preventive strategies for stroke in TAVI, highlighting recent advancements, particularly in current protective devices, and ongoing challenges in minimizing this adverse outcome. Full article

Objectives: We aimed to determine the frequency and factors related to oropharyngeal dysphagia in adults in a health center in Colombia evaluated by videofluroscopy of swallowing. Methods: We reviewed the records of 144 patients evaluated through videofluroscopy of swallowing. In order to analyze the results, descriptive, bivariate statistical analysis, and multivariate regression were used. Results: This investigation revealed that 23.6% of adults had oropharyngeal dysphagia. Older adults had a higher percentage of occurrence, and the factors associated with this symptom were having a history of cerebral stroke and being medicated with anticholinergic drugs. Conclusions: These findings strongly suggest that older adults with other comorbidities have a high percentage of presenting oropharyngeal dysphagia. Further research is needed to characterize the entity in other populations. Full article