Fazekas Score Research Articles

A severity comparison of leukoaraiosis in ischemic and hemorrhagic stroke: a retrospective study

IntroductionLeukoaraiosis (LA) is a common neuroradiological finding in patients suffering from stroke. Cerebral small-vessel disease (SVD) is one of the primary causes of both ischemic stroke and hemorrhagic stroke (intracerebral hemorrhage, ICH) and the development of LA. Significant evidence that LA predicts the risk of functional dependency and mortality exists. However, studies examining the difference in LA severity between ischemic stroke and hemorrhagic stroke are lacking. We therefore aimed to compare the severity and abundance of LA in the two stroke subgroups.MethodsAll patients admitted to the Department of Neurology, Haukeland University Hospital, with an ischemic stroke and intracerebral hemorrhagic (ICH) stroke diagnosed between 2006 and 2020 were included in the study. We collected patient data on risk factors and clinical and radiological findings and outcomes from our local stroke registry. The presence and severity of LA were assessed using the Fazekas score based on CT imaging. We evaluated the outcome using the modified Rankin Score (mRS) 7 days post-stroke.ResultsA total of 5,084 patients were included in our analyses: 4437 (87%) with ischemic stroke and 647 (13%) with ICH. LA was present in 2476 (45%) patients. In our ordinal logistic regression model, adjusting for age, sex, known hypertension, known diabetes mellitus, and smoking, LA was more severe and more abundant in ICH patients compared to ischemic stroke patients (Fazekas score: 1, OR: 1.54; Fazekas score: 2, OR: 1.88; and Fazekas score: 3, OR 2.13; p < 0.001). Increasing severity of LA was associated with worse functional outcomes in both groups (ischemic stroke, OR: 1.49; p < 0.001 and ICH, OR: 1.36; p < 0.025).ConclusionIn this study, LA was more severe and abundant in patients with ICH.

Cerebral damage after malignant hypertensive crisis: cerebral MRI follow-up data

Abstract Background Malignant hypertension (MHT) crisis is characterized by acute and diffuse microvascular damages, and the brain is a primary target organ. While a recent MRI study has revealed extensive and frequent cerebral injuries during the acute phase of MHT crisis (1), there is a scarcity of follow-up data. Purpose This study aims to investigate the evolution of MRI markers of cerebral injury following the management of the acute phase of MHT. Methods In this retrospective analysis, we examined brain MRI data from patients admitted for acute MHT between 2008 and 2022 at our center. Eligible patients had at least one follow-up brain MRI available. A skilled operator conducted a comprehensive analysis of each brain MRI, searching for posterior reversible encephalopathy syndrome (PRES), acute stroke or cerebral hemorrhage and microangiopathy markers, blinded for clinical and demographical data. Results Among 149 patients enrolled, 104 had a brain MRI at inclusion, 47 individuals had at least one follow-up brain MRI and were included in the analysis. 72,3% were male, mean age was 48,2 ± 10.8 years and 45,7% presented blood pressure control at the time of the follow-up brain MRI. Median interval between initial and follow-up brain MRI was 228 (84 – 726) days. Five (10,6%) new recent strokes, 2 (4,3 %) cerebral hemorrhage and 0 PRES were recorded during follow-up. On the follow-up brain MRI, more patients presented chronic lacunar infarct and/or microbleeds, in higher numbers. On the contrary, overall Fazekas score was stable in 31 patients (66,0%), improved in 15 patients (31,9 %) and worsened in 1 patients (2,1%). Comparison of subgroups dichotomized according to blood pressure control or follow up duration showed no difference in brain MRI markers. Conclusion This study offers valuable insights into the risk of new cerebrovascular events and the evolution of brain MRI markers after managing the acute phase of MHT. Our findings emphasize the dynamic nature of cerebral microvascular burden and the potential for regression of white matter hyperintensities. A better understanding of these phenomena might contribute to improved diagnosis, tailored treatment, and proactive patient care in the context of MHT.

Non-classical monocyte levels correlate negatively with HIV-associated cerebral small vessel disease and cognitive performance

BackgroundDespite antiretroviral treatment (cART), aging people living with HIV (PWH) are more susceptible to neurocognitive impairment (NCI) probably due to synergistic/additive contribution of traditional cerebrovascular risk factors. Specifically, transmigration of inflammatory CD16+ monocytes through the altered blood brain barrier (BBB) may exacerbate cerebral small vessel disease (CSVD), a known cause of vascular cognitive impairment.MethodsPWH on cART (n=108) and age, sex, and Reynold’s cardiovascular risk score-matched uninfected individuals (PWoH, n=111) were enrolled. This is a longitudinal observational study but only cross-sectional data from entry visit are reported. Neuropsychological testing and brain magnetic resonance imaging (MRI) were performed. CSVD was diagnosed by Fazekas score ≥1. Flow cytometric analyses of fresh whole blood were conducted to evaluate circulating levels of monocyte subsets (classical, intermediate, and non-classical) and markers of monocyte activation (CCR2, CD40, PSGL-1, TNFR2 and tissue factor). ELISAs were used to measure sCD14, ICAM, and Osteoprotegerin. Two-way analysis of variance (ANOVA), and linear regression models were performed to study the effects of HIV status, CSVD status, and their interaction to outcome variables such as cognitive score. Two-sample t-tests and correlation analyses were performed between and within PWoH with CSVD and PWH with CSVD participants.ResultsPWH with CSVD (n=81) had significantly lower total cognitive scores, higher levels of NCMs and soluble CD14 and intracellular adhesion molecule 1 (ICAM-1) as compared to PWoH with CSVD group (n=68). sCD14 and ICAM1 were positively correlated with each other indicating that monocyte and endothelial activation are associated with each other. Cognition was negatively correlated with NCMs, especially in the PWH with CSVD group. Among other blood biomarkers measured, osteoprotegerin levels showed mild negative correlation with cognitive performance in individuals with CSVD irrespective of HIV status.ConclusionsElevated levels of NCMs may contribute to neuroinflammation, CSVD and subsequent cognitive impairment. This finding is of particular relevance in aging PWH as both HIV and aging are associated with increased levels of NCMs. NCMs may serve as a potential biomarker to address these comorbidities. Further longitudinal studies are needed to evaluate whether changes in NCM levels are associated with changes in CSVD burden and cognitive impairment.

Cerebral Small Vessel Disease and its relationship with all-cause mortality risk: results from the Amsterdam Ageing cohort

IntroductionCerebral Small-Vessel Disease (CSVD) is a complex condition affecting the brain's vascular network, linked to cognitive and physical decline, cerebrovascular disease, and death. This study assesses the relationship between CSVD (composite and individual features) and all-cause mortality in a large cohort of geriatric outpatients. MethodsData from 1305 geriatric outpatients (mean age 78 ± 7; 51% female) in the Amsterdam Ageing cohort were analysed. CSVD presence was based on brain imaging (MRI or CT), defined by a Fazekas score ≥ 2, presence of ≥ 1 lacunes, or (in MRI) ≥ 3 microbleeds. Mortality data (February 2016 - January 2024) was sourced from the Dutch Municipality Register. The relationship between CSVD and all-cause mortality was evaluated using a Cox proportional-hazards model, adjusting for key confounders. ResultsAt baseline, 835 (64%) of the 1305 patients had CSVD. During a median follow-up of 3.1 years (IQR 1.6 - 4.6 years), all-cause mortality was 40% (333 patients) in the CSVD group and 26% (121 patients) in the non-CSVD group, corresponding with incidence rates of 137 and 78 per 1000 patient-years, respectively. The age- and sex-adjusted hazard ratio for mortality in the CSVD group was 1.6 (95% CI: 1.3-2.0). This association remained significant after adjusting for cardiovascular disease and its risk factors, physical function (gait speed), and cognitive function (MMSE). ConclusionRadiographic CSVD presence is prevalent and its integration into daily care is important as it is independently linked to increased all-cause mortality in geriatric outpatients.

Quantitative Analysis of White Matter Hyperintensities as a Predictor of 1-Year Risk for Ischemic Stroke Recurrence.

This study evaluates the role of quantitative characteristics of white matter hyperintensities (WMHs) in predicting the 1-year recurrence risk of ischemic stroke. We conducted a retrospective analysis of 1061 patients with ischemic stroke from January 2018 to April 2021. WMHs were automatically segmented using a cluster-based method to quantify their volume and number of clusters (NoC). Additionally, two radiologists independently rated periventricular and deep WMHs using the Fazekas scale. The cohort was divided into a training set (70%) and a testing set (30%). We employed Cox proportional hazards models to develop predictors based on quantitative WMH characteristics, Fazekas scores, and clinical factors, and compared their performance using the concordance index (C-index). A total of 180 quantitative variables related to WMHs were extracted. A higher NoC in deep white matter and brainstem, advanced age (>90years old), specific stroke subtypes, and absence of discharge antiplatelets showed stronger associations with the risk of ischemic stroke recurrence within 1year. The nomogram incorporating quantitative WMHs data showed superior discrimination compared to those based on the Fazekas scale or clinical factors alone, with C-index values of 0.709 versus 0.647 and 0.648, respectively, in the testing set. Notably, a combined model including both WMHs and clinical factors achieved the highest predictive accuracy, with a C-index of 0.735 in the testing set. Quantitative assessment of WMHs provides a valuable neuro-imaging tool for enhancing the prediction of ischemic stroke recurrence risk.

Outcome of intravenous thrombolysis in acute ischemic stroke patients with small vessel disease

IntroductionLacunar stroke (LS) subtype accounts for a quarter of ischemic strokes. Intravenous thrombolysis (IVT) is known to improve overall stroke outcomes. Very few studies have focused on the outcome of IVT in lacunar strokes. Aim: To detect the outcome of IVT in LS patients compared to non-thrombolysed LS patients. MethodsFifty patients presenting with LS received the standard protocol of IVT (Group I). They were compared to fifty matched LS patients who presented beyond the time window and were selected as the control group (Group II). Clinical outcome was measured using NIHSS within 24 h, NIHSS at discharge, and MRS after 3 months. Risk factors that could have affected clinical outcomes were compared in the thrombolysis group. ResultsThe short-term clinical outcome of Group I showed statistically significant improvement of NIHSS after 24 hrs compared to Group II (mean NIHSS = 5.52±3.89 and 7.44±1.82 respectively), as well as on discharge (mean NIHSS = 3.88±3.50 and 5.78±2.97) respectively. For long-term outcomes, 94 % of GroupⅠ reached MRS 0, 1, and 2 (n = 47/50) versus 74 % (n = 36/50) in Group II. Longer door-to-needle time, severe WMCs (Fazekas score), and pneumonia were shown to be significant predictor factors for the worst outcome. ConclusionIVT has improved short- and long-term outcomes in LS patients. Longer door-to-needle time, severe WMCs, and pneumonia were shown to be significant predictor factors for the worst outcome.

Cerebrovascular Burden and Its Association with Ménière’s Disease: A Case-Control Study

Background: Ménière’s disease (MD) lacks a universally accepted pathogenesis model. Recent research has revisited the vascular hypothesis. This study aims to compare the cerebrovascular burden in patients with MD and age-matched controls, investigating the potential role of cerebrovascular dysfunction in MD. Methods: A total of 145 patients (70 MD, 75 controls) underwent magnetic resonance imaging (MRI) assessment for small-vessel disease (SVD) markers (including Fazekas and EPVS scores), cortical strokes, and baseline comorbidities. Statistical analyses were performed to compare the cerebrovascular burden between the groups, adjusting for potential confounders. Results: The MD group exhibited significantly higher mean SVD scores across various measures compared to controls (p < 0.05). This association persisted even after adjusting for age, sex, and comorbidities (ORs ranging from 1.746 to 2.495, p < 0.05). Neither the presence of cortical strokes nor comorbidities significantly differed between groups. Conclusions: This study is the first to compare cerebrovascular burden between MD patients and controls. The findings suggest that cerebrovascular dysfunction may contribute to MD incidence. Further research is needed to elucidate the relationship between cerebrovascular disease and MD, potentially leading to novel therapeutic avenues.

Baseline and Longitudinal MRI Markers Associated With 16-Year Mortality in Patients With Cerebral Small Vessel Disease.

Information on whether small vessel disease (SVD) reduces life expectancy is limited. Moreover, the excess mortality risk attributed specifically to SVD compared with controls from the general population has not been evaluated. This study aimed to investigate the baseline and progression of MRI markers of SVD associated with mortality in a 16-year follow-up cohort study and to determine the excess long-term mortality risk of patients with SVD. Participants with SVD from the Radboud University Nijmegen Diffusion Tensor and Magnetic Resonance Imaging Cohort (RUN DMC) study (with MRI assessments in 2006, 2011, 2015, and 2020) were followed until their death or December 1, 2021. Adjusted Cox regression analyses and linear mixed-effect regression models were used to investigate the association between MRI markers of SVD and mortality. The excess mortality risk of SVD was calculated by comparing mortality data of the RUN DMC study with the general population matched by sex, age, and calendar year. 200 of 503 (39.9%) participants died during a follow-up period of 15.9 years. Cause of death was available for 182 (91%) participants. Baseline white matter hyperintensity volume (HR 1.3 per 1-SD increase [95% CI 1.1-1.5], p = 0.010), presence of lacunes (1.5 [95% CI 1.1-2.0], p = 0.008), mean diffusivity (HR 1.1 per 1-SD increase [95% CI 1.1-1.2], p = 0.001), and total brain volume (HR 1.5 per 1-SD decrease [95% CI 1.3-1.9], p < 0.001) were associated with all-cause mortality after adjusting for age, sex, and vascular risk factors. Total brain volume decrease over time was associated with all-cause mortality after adjusting for age, sex, and vascular risk factors (HR 1.3 per 1-SD decrease [95% CI 1.1-1.7], p = 0.035), and gray matter volume decrease remained significant after additionally adjusting for its baseline volume (1.3 per 1-SD decrease [1.1-1.6], p = 0.019). Participants with a Fazekas score of 3, presence of lacunes, or lower microstructural integrity had an excess long-term mortality risk (21.8, 15.7, 10.1 per 1,000 person-years, respectively) compared with the general population. Excess long-term mortality risk only exists in patients with severe SVD (Fazekas score of 3, presence of lacunes, or lower microstructural integrity). This could help in assisting clinicians to predict the clinical outcomes of patients with SVD by severity.

Increased extracellular free water is related to white matter hyperintensity burden.

Extracellular free water (FW) has important roles in the occurrence and development of white matter hyperintensity (WMH). To explore the correlations between FW and WMH burden. A prospective analysis was conducted using magnetic resonance imaging (MRI) data from 126 individuals. WMH burden was determined based on WMH volumes and Fazekas scores from deep and periventricular white matter hyperintensity (DWMH and PWMH, respectively) in fluid-attenuated inversion recovery (FLAIR) images. FW values were taken from diffusion tensor imaging (DTI). Univariate analysis showed that FW values were correlated with WMH burden, including WMH volumes and DWMH and PWMH Fazekas scores (P < 0.05). After multivariate analysis, FW values were correlated with WMH volumes and DWMH and PWMH Fazekas scores when adjusted for age and hypertension (P < 0.05). Using MRI, increasing extracellular FW was related to WMH burden.

Evaluating cochlear implant outcomes in DFNA9 subjects: a comprehensive study on cerebral white matter lesions and vestibular abnormalities.

This study assessed whether the Fazekas score could account for the variability in cochlear implantation (CI) outcomes among individuals with DFNA9 and evaluated signal loss in the semicircular canals (SCCs) on magnetic resonance imaging (MRI) among individuals with DFNA9. This retrospective cross-sectional study included CI recipients with DFNA9. Pre-implantation MRI-scans were reviewed to determine the Fazekas score, localizing and grading cerebral white matter lesions (WML), and identify abnormalities in the SCCs. CI performance was assessed by evaluating phoneme scores one year post-implantation. The function of the SCCs was evaluated using rotatory chair testing with electronystagmography (ENG) and the video Head Impulse Test (vHIT). Forty-five subjects (49 ears) were enrolled. The phoneme scores significantly improved from 35% (IQR 11-50) pre-implantation to 84% (IQR 76-90) one year post-implantation. No correlation was observed between the Fazekas score and the one-year post-implantation phoneme score (rsp=0.003, p = 0.986). Signal loss in at least one SCCs was detected in 97.7% of subjects and 77.8% of ears. There was no correlation between vestibular test results and fluid signal loss in the SCCs on MRI. Most individuals with DFNA9 show improved speech recognition with CI. The observed variability in CI outcomes was not linked to the Fazekas score. Additionally, our study confirms a high prevalence of focal sclerosis in DFNA9. Recognizing the limitations of this study, further research is needed to explore the predictive role of the Fazekas score on CI outcomes and its relationship with vestibular function.

Analysis of predictors of hemorrhagic transformation after reperfusion therapy with recombinant tissue plasminogen activator in patients with acute ischemic stroke: a single-center experience

BackgroundHemorrhagic transformation (HT) is a serious complication of thrombolytic therapy for acute ischemic stroke, limiting its indications and affecting treatment plans and clinical prognosis. Identifying risk factors for HT could help improve the risk–benefit ratio of thrombolytic therapy. We aimed to analyze the predictors of HT after reperfusion therapy with recombinant tissue plasminogen activator (rTPA) in patients with acute ischemic stroke. This study included 115 patients who received rTPA. All patients underwent history taking, clinical examination, neurological examination including Glasgow Coma Scale and National Institutes of Health Stroke Scale scores (NIHSS), radiological investigation, and cardiac investigation. Patients were followed up strictly every 2 h for 1st 24 h then for two weeks clinically using the NIHSS and radiologically using CT or MRI to detect HT.ResultsPatients with HT represented 21.7% of all patients receiving rTPA, while symptomatic intracranial hemorrhage (sICH) represented 6.9%. Patients with HT had significantly higher blood pressure, respiratory rate, atrial fibrillation rate, NIHSS score, INR, prothrombin time, neutrophil-to-lymphocyte ratio (NLR), and lower platelet count, LDL level, higher Fazekas score, lower ASPECT score, and prolonged onset-to-needle time.ConclusionPredicting HT in acute ischemic stroke patients is crucial for optimizing management and potentially improving outcomes. In our study, six predictors were associated with HT: higher respiratory rate, higher atrial fibrillation rate, higher NLR, lower LDL level, higher Fazekas score, lower ASPECT score, and onset-to-needle time greater than 180 min.

Cerebrovascular Reactivity Assessed by Breath-Hold Functional MRI in Patients with Neurological Post-COVID-19 Syndrome-A Pilot Study.

Endothelial dysfunction represents a potential pathomechanism of neurological post-COVID-19 syndrome (PCS). A recent study demonstrated reduced cerebrovascular reactivity (CVR) in patients with PCS. The aim of this pilot study was to prospectively assess CVR in patients with PCS using breath-hold functional MRI (bh-fMRI). Fourteen patients with neurological PCS and leading symptoms of fatigue/memory issues/concentration disorder (PCSfmc), 11 patients with PCS and leading symptoms of myopathy/neuropathy (PCSmn), and 17 healthy controls underwent bh-fMRI. Signal change and time to peak (TTP) were assessed globally and in seven regions of interest and compared between the subgroups using one-way ANCOVA adjusting for age, time since infection, Fazekas score, and sex. No significant differences were observed. In PCS patients, the global CVR exhibited a slight, non-significant tendency to be lower compared to healthy controls (PCSfmc: 0.78 ± 0.11%, PCSmn: 0.84 ± 0.10% and 0.87 ± 0.07%). There was a non-significant trend towards lower global TTP values in the PCS subgroups than in the control group (PCSfmc: 26.41 ± 1.39 s, PCSmn: 26.32 ± 1.36 s versus 29.52 ± 0.93 s). Endothelial dysfunction does not seem to be the sole pathomechanism of neurological symptoms in PCS. Further studies in larger cohorts are required.

Brain MRI in patients with V30M hereditary transthyretin amyloidosis

Background Central nervous system dysfunction is common in longstanding hereditary transthyretin amyloidosis (ATTRv) caused by the V30M (p.V50M) mutation. Neuropathology studies show leptomeningeal amyloid deposition and cerebral amyloid angiopathy (CAA). Brain MRI is widely used in the assessment of Aβ associated CAA but there are no systematic studies with brain MRI in ATTRv amyloidosis. Methods we performed 3 T brain MRIs in 16 patients with longstanding (>14 years) ATTRV30M. We additionally retrospectively reviewed 48 brain MRIs from patients followed at our clinic. CNS symptoms and signs were systematically accessed, and MRIs were blindly reviewed for ischaemic and haemorrhagic lesions. Results in the prospective cohort, we found white matter hyperintensities in 8/16 patients (50%, Fazekas score> =1). There were no relevant microbleeds, large ischaemic or haemorrhagic lesions or superficial siderosis. In the retrospective cohort, microbleeds were found in 5/48 patients (10,4%), two of which with > =20 microbleeds. White matter hyperintensities were found in 20/48 cases (41.7%). White matter lesions, microbleeds and cortical atrophy were not associated with disease duration. Conclusions white matter hyperintensities are common in ATTRV30M, irrespective of disease duration. Haemorrhagic lesions are rare, even in patients with longstanding disease, suggesting the existence of other risk factors.

Cingulate sulcus sign: a descriptive analysis in a cerebral small vessel disease population.

The cingulate sulcus sign (CSS) has been observed in patients with idiopathic normal pressure hydrocephalus (iNPH), suggesting potential disruptions in cerebrospinal fluid circulation and compromised glymphatic system. Although there are similarities in the underlying mechanisms between cerebral small vessel disease (CSVD) and iNPH, the relationship between CSS and CSVD remains unclear. This study aimed to investigate the prevalence and potential mechanisms of CSS in patients with CSVD. Data from patients diagnosed with CSVD at Shengjing Hospital of China Medical University between January 2020 and October 2022 were retrospectively collected, including general information, global cognitive function [assessed by measuring Mini-Mental State Examination (MMSE)], and four CSVD magnetic resonance imaging (MRI) markers [(white matter hyperintensity (WMH), cerebral microbleeds (CMBs), lacunes, and enlarged perivascular spaces (EPVS)], CSS and the Evan's index (EI). A total of 308 patients were included, and CSS was detected in 80 patients (26%). Univariate analysis revealed that MMSE scores in the CSS group were significantly lower compared to the non-CSS group (p < 0.001). Multivariable analysis showed an independent correlation between CSS and the presence of lacunes (odds ratio [OR] 0.358, 95% confidence interval [CI] 0.193-0.663, p = 0.001), presence of lobar dominant CMBs (OR 2.683, 95%CI 1.385-5.195, p = 0.003), periventricular WMH Fazekas score (OR 1.693, 95% CI 1.133-2.529, p = 0.01), and EI (OR 1.276, 95% CI 1.146-1.420, p < 0.001). This preliminary study showed that CSS can be observed in some patients with CSVD. The presence of CSS may represent different mechanisms of CSVD pathogenesis and reflect differences in the degree of cerebrospinal fluid (CSF)/interstitial fluid (ISF) stasis.

The relationship between intracranial atherosclerosis and white matter hyperintensity in ischemic stroke patients: a retrospective cross-sectional study using high-resolution magnetic resonance vessel wall imaging.

Both intracranial atherosclerosis and white matter hyperintensity (WMH) are prevalent among the stroke population. However, the relationship between intracranial atherosclerosis and WMH has not been fully elucidated. Therefore, the aim of this study was to investigate the relationship between the characteristics of intracranial atherosclerotic plaques and the severity of WMH in patients with ischemic stroke using high-resolution magnetic resonance vessel wall imaging. Patients hospitalized with ischemic stroke and concurrent intracranial atherosclerosis at Beijing Tsinghua Changgung Hospital, a tertiary comprehensive stroke center, who underwent high-resolution magnetic resonance vessel wall imaging and conventional brain magnetic resonance imaging were continuously recruited from January 2018 to December 2018. Both intracranial plaque characteristics (plaque number, maximum wall thickness, luminal stenosis, T1 hyperintensity, and plaque length) and WMH severity (Fazekas score and volume) were evaluated. Spearman correlation or point-biserial correlation analysis was used to determine the association between clinical characteristics and WMH volume. The independent association between intracranial plaque characteristics and the severity as well as WMH score was analyzed using logistic regression. The associations of intracranial plaque characteristics with total white matter hyperintensity (TWMH) volume, periventricular white matter hyperintensity (PWMH) volume and deep white matter hyperintensity (DWMH) volume were determined using multilevel mixed-effects linear regression. A total of 159 subjects (mean age: 64.0±12.5 years; 103 males) were included into analysis. Spearman correlation analysis indicated that age was associated with TWMH volume (r=0.529, P<0.001), PWMH volume (r=0.523, P<0.001) and DWMH volume (r=0.515, P<0.001). Point-biserial correlation analysis indicated that smoking (r=-0.183, P=0.021) and hypertension (r=0.159, P=0.045) were associated with DWMH volume. After adjusting for confounding factors, logistic regression analysis showed plaque number was significantly associated with the presence of severe WMH [odds ratio (OR), 1.590; 95% CI, 1.241-2.035, P<0.001], PWMH score of 3 (OR, 1.726; 95% CI, 1.074-2.775, P=0.024), and DWMH score of 2 (OR, 1.561; 95% CI, 1.150-2.118, P=0.004). Intracranial artery luminal stenosis was associated with presence of severe WMH (OR, 1.032; 95% CI, 1.002-1.064, P=0.039) and PWMH score of 2 (OR, 1.057; 95% CI, 1.008-1.109, P=0.023). Multilevel mixed-effects linear regression analysis showed that plaque number was associated with DWMH volume (β=0.128; 95% CI, 0.016-0.240; P=0.026) after adjusted for age and sex. In ischemic stroke patients, intracranial atherosclerotic plaque characteristics as measured by plaque number and luminal stenosis were associated with WMH burden.

Age-associated gadolinium leakage into ocular structures in patients with acute traumatic brain injury

BackgroundGadolinium Leakage into Ocular Structures (GLOS) is common following acute cerebrovascular events. The objective of this study was to investigate the occurrence of GLOS in an acute traumatic brain injury (TBI) cohort without acute cerebrovascular injury and to explore associated factors. MethodsEnrolled acute TBI patients had a baseline MRI ≤48 h of injury (TP1) and follow-up MRI ≤72 h after baseline (TP2). Vitreous chamber enhancement and signal intensity ratios (SIRs) were calculated using pre- and post-contrast Fluid Attenuated Inversion Recovery (FLAIR). White matter hyperintensities (WMHs) were assessed using the Fazekas scale. ResultsOf the 128 TBI patients included, median age was 47 years, 70% male, and 66% presented with Glasgow Coma Scale of 15. No GLOS was detected at TP1 but was present in 23% of patients at TP2. GLOS+ patients were older (68 years [56–76] vs 39 years [27–53], p < 0.001), more likely to report falls as injury mechanism (62% vs 36%, p = 0.006), report history of hypertension (41% vs 19%, p = 0.025), and had a higher burden of WMHs (59% vs 14% with a total Fazekas ≥2, p < 0.001). Quantitative SIRs confirmed qualitative assessments: GLOS+ patients had higher SIRs at TP2 (0.43 vs 0.22, p < 0.001). Age (OR 3.28, 95%CI [1.88–5.71], p < 0.001) and prior TBI history (OR 4.99, 95%CI [1.46–17.06], p = 0.010) were independent predictors of GLOS. When age was removed, total Fazekas score (OR 2.53, 95%CI [1.60–4.00], p < 0.001) was an independent predictor of GLOS. ConclusionsGLOS is primarily associated with age and may serve as another imaging marker of chronic vascular disease.

Prevalence and Risk Factors of Cerebral Microbleeds among Egyptian Patients with Acute Ischemic Stroke.

Cerebral microbleeds (CMBs) are markers of underlying hemorrhage-prone cerebral small vessel disease detected on MRI. They are associated with a heightened risk of stroke and cognitive decline. The prevalence of CMBs among Egyptian patients with ischemic stroke is not well studied. Our aim was to detect the prevalence of CMBs and associated risk factors among Egyptian patients with ischemic stroke. A prospective, cross-sectional, single-center study of consecutive patients with ischemic stroke. Patients were recruited between January 2021 and January 2022 at the Assiut University Hospital in the south of Egypt. Patients with known bleeding diathesis were excluded. All participants underwent full neurological assessment, urgent laboratory investigations, and MRI with T2* sequence. The study included 404 patients, 191 (47.3%) of them were females. The mean age of the study population was 61 ± 1 years, and the mean NIHSS on admission was 12 ± 5. The prevalence of CMB was 26.5%, of whom 6.5% were young adults (age ≤45 years). CMBs were detected in 34.6% of patients with stroke caused by large artery atherosclerosis, 28.0% with small vessel disease stroke subtype, 25.2% with stroke of undetermined cause, and in 12.1% with cardioembolic stroke. History of AF, hypertension, dyslipidemia, Fazekas score &gt;2, dual antiplatelet use, combined antiplatelet with anticoagulant treatment, and thrombolytic therapy remained independently associated with CMBs following multivariable regression analyses. The high number of identified CMBs needs to inform subsequent therapeutic management of these patients. We are unable to determine whether the association between CMBs and antithrombotic use is a causal relationship or rather confounded by indication for these treatments in our observational study. To understand more about the underlying cause of this finding, more studies are needed.

Poststroke cognitive outcome is better accounted for by white matter abnormalities automated segmentation than visual analysis

Background and aimsThe association between white matter abnormalities (WMA) and cognitive decline previously reported in poststroke patients has been mainly documented using visual scales. However, automated segmentation of WMA provides a precise determination of the volume of WMA. Nonetheless, it is rarely used in the stroke population and its potential advantage over visual scales is still unsettled. The objective of this study was to examine whether automated segmentation of WMA provides a better account than the visual Fazekas and Wahlund scales of the decline in executive functions and processing speed in stroke patients. MethodsThe analyses were conducted on the 358 patients of the GRECogVASC cohort with an MRI performed at six months poststroke in the Amiens center. WMA were visually analyzed using the Fazekas (subcortical abnormalities) and Wahlund scales. Segmentation was performed using LST (3.0.3). Following preliminary studies to determine the optimal segmentation threshold, we examined the relationship between cognitive status and WMA volume computed at each threshold using receiver operating characteristic (ROC) curves. Finally, we assessed the ability of both Fazekas and Wahlund visual scores and WMA volume to account for cognitive scores by using a bivariate Pearson correlation analysis, comparing correlation coefficients with the Fisher transformation and repeating correlation analysis after adjustment for the lesion volume. ResultsIncreasing the threshold led to an underestimation of WMA (P=0.0001) (significant for a threshold ≥0.2) and an improvement in correct rejection of signal changes in the stroke cavity (P=0.02) (significant for a threshold ≤0.5), susceptibility artifacts (P=0.002) (significant for a threshold ≤0.6), and corticospinal degeneration (P=0.03) (significant for a threshold ≤0.5). WMA volume decreased with increasing threshold (P=0.0001). Areas under the curve (AUC) did not differ according to the threshold (processing speed: P=0.85, executive cognitive functions: P=0.7). Correlation coefficients between cognitive scores and WMA were higher for WMA volume than the Fazekas (processing speed: Z=−3.442, P=0.001; executive functions: Z=−2.751, P=0.006) and Wahlund scores (processing speed: Z=−3.615, P=0.0001; executive functions: Z=−2.769, P=0.006). Adjustment for lesion volume did not alter the correlations with WMA volume (processing speed: r=−0.327 [95%CI: −0.416; −0.223], P=0.0001; executive functions: r=−0.262 [95%CI: −0.363; −0.150], P=0.0001). ConclusionThis study shows that WMA volume assessed by automated segmentation provides a better account of cognitive disorders than visual analysis. This should favor its wider use to refine imaging determinants of poststroke cognitive disorders.

Endothelial Dysfunction and Pre-Existing Cognitive Disorders in Stroke Patients.

The origin of pre-existing cognitive impairment in stroke patients remains controversial, with a vascular or a degenerative hypothesis. To determine whether endothelial dysfunction is associated with pre-existing cognitive problems, lesion load and biological anomalies in stroke patients. Patients originated from the prospective STROKDEM study. The baseline cognitive state, assessed using the IQ-CODE, and risk factors for stroke were recorded at inclusion. Patients with an IQ-CODE score >64 were excluded. Endothelial function was determined 72 h after stroke symptom onset by non-invasive digital measurement of endothelium-dependent flow-mediated dilation and calculation of the reactive hyperemia index (RHI). RHI ≤ 1.67 indicated endothelial dysfunction. Different biomarkers of endothelial dysfunction were analysed in blood or plasma. All patients underwent MRI 72 h after stroke symptom onset. A total of 86 patients were included (52 males; mean age 63.5 ± 11.5 years). Patients with abnormal RHI have hypertension or antihypertensive treatment more often. The baseline IQ-CODE was abnormal in 33 (38.4%) patients, indicating a pre-existing cognitive problem. Baseline IQ-CODE > 48 was observed in 15 patients (28.3%) with normal RHI and in 18 patients (54.6%) with abnormal RHI (p = 0.016). The RHI median was significantly lower in patients with abnormal IQ-CODE. Abnormal RHI was associated with a significantly higher median FAZEKAS score (2.5 vs. 2; p = 0.008), a significantly higher frequency of periventricular lesions (p = 0.015), more white matter lesions (p = 0.007) and a significantly higher cerebral atrophy score (p < 0.001) on MRI. Vascular biomarkers significantly associated with abnormal RHI were MCP-1 (p = 0.009), MIP_1a (p = 0.042), and homocysteinemia (p < 0.05). A vascular mechanism may be responsible for cognitive problems pre-existing stroke. The measurement of endothelial dysfunction after stroke could become an important element of follow-up, providing an indication of the functional and cognitive prognosis of stroke patients.

Comparison of qualitative and fully automated quantitative tools for classifying severity of white matter hyperintensity

ObjectiveIn this study, we aimed to compare the Fazekas scoring system and quantitative white matter hyperintensity volume in the classification of white matter hyperintensity severity using a fully automated analysis software to investigate the reliability of quantitative evaluation. Materials and MethodsPatients with suspected cognitive impairment who underwent medical examinations at our institution between January 2010 and May 2021 were retrospectively examined. White matter hyperintensity volumes were analyzed using fully automated analysis software and Fazekas scoring (scores 0–3). Using one-way analysis of variance, white matter hyperintensity volume differences across Fazekas scores were assessed. We employed post-hoc pairwise comparisons to compare the differences in the mean white matter hyperintensity volume between each Fazekas score. Spearman's rank correlation test was used to investigate the association between Fazekas score and white matter hyperintensity volume. ResultsAmong the 839 patients included in this study, Fazekas scores 0, 1, 2, and 3 were assigned to 68, 198, 217, and 356 patients, respectively. White matter hyperintensity volumes significantly differed according to Fazekas score (F=623.5, p<0.001). Post-hoc pairwise comparisons revealed significant differences in mean white matter hyperintensity volume between all Fazekas scores (p<0.05). We observed a significantly positive correlation between the Fazekas scores and white matter hyperintensity volume (R=0.823, p<0.01). ConclusionsQuantitative white matter hyperintensity volume and the Fazekas scores are highly correlated and may be used as indicators of white matter hyperintensity severity. In addition, quantitative analysis may be more effective in classifying advanced white matter hyperintensity lesions than the Fazekas classification.