Question: Is early neurological deterioration of ischemic origin (END i ) predictable in minor strokes with large vessel occlusion (LVO) treated with intravenous thrombolysis (IVT)?Findings: In a multicentric retrospective cohort of minor stroke patients (NIHSS≤5) with LVO intended for IVT alone (n=729), an easily applicable score based on occlusion site and thrombus length -two independent predictors of END i -showed good discriminative power for END i risk prediction, and was successfully validated in an independent cohort (n=347).Meaning: END i can be reliably predicted in IVT-treated minor strokes with LVO, which may help to select the best candidates for direct transfer for additional thrombectomy.

Background/Purpose: Perfusion computed tomography (CT) is capable of measuring the permeability surface product (PS). PS reflects the permeability of the blood-brain barrier, involved in the pathophysiology of hemorrhagic transformation (HT) of ischemic stroke. The aim of our study was to determine if an increased PS can predict HT. Methods: A total of 86 patients with ischemic stroke were included. They underwent multimodality CT, including the measurement of PS. We compared the clinical and radiological characteristics of patients who developed HT to those who did not, using univariate analysis. Multivariate regression analyses were then used to determine HT predictors. Results: HT was observed in 27 patients (31%). Infarct PS was significantly associated with HT (p = 0.047), as were atrial fibrillation (p = 0.03), admission National Institute of Health Stroke Scale score (p = 0.02), infarct volume (p = 0.0004), presence of large-vessel occlusion (p = 0.0005) and a poorer collateral status (p = 0.003). Using logistic regression modeling, an infarct PS >0.84 ml/100 g/min was an independent predictor of HT (OR 28, 95% CI 1.75-452.98; p = 0.02). Other independent predictors of HT were infarct volume and a history of atrial fibrillation. Conclusions: Our findings suggest thatinfarct PS can be a predictor of HT and may help clinicians to improve patient care around thrombolysis decisions in the acute phase of ischemic stroke.

Background and purposeBetter understanding the incidence, predictors and mechanisms of early neurological deterioration (END) following intravenous thrombolysis (IVT) for acute stroke with mild symptoms and isolated internal carotid artery occlusion (iICAo) may inform therapeutic decisions.MethodsFrom a multicenter retrospective database, we extracted all patients with both National Institutes of Health Stroke Scale (NIHSS) score <6 and iICAo (i.e. not involving the Willis circle) on admission imaging, intended for IVT alone. END was defined as ≥4 NIHSS points increase within 24 h. END and no‐END patients were compared for (i) pre‐treatment clinical and imaging variables and (ii) occurrence of intracranial occlusion, carotid recanalization and parenchymal hemorrhage on follow‐up imaging.ResultsSeventy‐four patients were included, amongst whom 22 (30%) patients experienced END. Amongst pre‐treatment variables, suprabulbar carotid occlusion was the only admission predictor of END following stepwise variable selection (odds ratio = 4.0, 95% confidence interval: 1.3–12.2; P = 0.015). On follow‐up imaging, there was no instance of parenchymal hemorrhage, but an intracranial occlusion was now present in 76% vs. 0% of END and no‐END patients, respectively (P < 0.001), and there was a trend toward higher carotid recanalization rate in END patients (29% vs. 9%, P = 0.07). As compared to no‐END, END was strongly associated with a poor 3‐month outcome.ConclusionsEarly neurological deterioration is a frequent and highly deleterious event after IVT for minor stroke with iICAo, and is of thromboembolic origin in three out of four patients. The strong association with iICAo site—largely a function of underlying stroke etiology—may point to a different response of the thrombus to IVT. These findings suggest END may be preventable in this setting.

ObjectiveCerebral venous thrombosis (CVT) is an uncommon form of stroke affecting mostly young individuals. Although genetic factors are thought to play a role in this cerebrovascular condition, its genetic etiology is not well understood.MethodsA genome‐wide association study was performed to identify genetic variants influencing susceptibility to CVT. A 2‐stage genome‐wide study was undertaken in 882 Europeans diagnosed with CVT and 1,205 ethnicity‐matched control subjects divided into discovery and independent replication datasets.ResultsIn the overall case–control cohort, we identified highly significant associations with 37 single nucleotide polymorphisms (SNPs) within the 9q34.2 region. The strongest association was with rs8176645 (combined p = 9.15 × 10−24; odds ratio [OR] = 2.01, 95% confidence interval [CI] = 1.76–2.31). The discovery set findings were validated across an independent European cohort. Genetic risk score for this 9q34.2 region increases CVT risk by a pooled estimate OR = 2.65 (95% CI = 2.21–3.20, p = 2.00 × 10−16). SNPs within this region were in strong linkage disequilibrium (LD) with coding regions of the ABO gene. The ABO blood group was determined using allele combination of SNPs rs8176746 and rs8176645. Blood groups A, B, or AB, were at 2.85 times (95% CI = 2.32–3.52, p = 2.00 × 10−16) increased risk of CVT compared with individuals with blood group O.InterpretationWe present the first chromosomal region to robustly associate with a genetic susceptibility to CVT. This region more than doubles the likelihood of CVT, a risk greater than any previously identified thrombophilia genetic risk marker. That the identified variant is in strong LD with the coding region of the ABO gene with differences in blood group prevalence provides important new insights into the pathophysiology of CVT. ANN NEUROL 2021;90:777–788

A total of 139 young stroke patients were consecutively examined and tested for antiphospholipid antibodies (APLA) to evaluate the role of these antibodies in cerebral ischaemia before the age of 45. APLA were found in 28.8% of patients. Two factors, hypertriglyceridaemia and alcohol abuse, were significantly more frequent in patients with a positive APLA test. The demographic characteristics, other risk factors, history of prior thrombotic events and distribution of aetiopathogenic types of cerebral ischaemia were not different in patients with or without APLA. Laboratory assays for APLA were highly positive for only two patients, who both had autoimmune diseases. These results suggest that with the exception of a clinical context of antiphospholipid syndrome or other autoimmune diseases, the usefulness of this diagnostic tool in the management of cerebral ischaemia remains limited.