Background: Posterior circulation and anterior circulation strokes share many clinical, pathogenetic and radiological features, although some clinical signs are highly specific to posterior circulation strokes. Arterial stenosis and occlusions occur in significant numbers in both acute posterior circulation and anterior circulation strokes, making them good candidates for endovascular treatment. Among posterior circulation strokes, basilar artery occlusions stand out because of the diagnostic and acute treatment challenges. Methods: We reviewed the literature on clinical stroke syndromes and neuroimaging findings and systematically describe for each anatomical site of stroke the detailed clinical and radiological information (anatomical representation, diffusion weighted imaging and angiographic sequences). The principles of neuroimaging of posterior circulation strokes and the prognosis for each stroke localization are also discussed. Review summary: Stroke syndromes in the territories of the vertebral, basilar, cerebellar, and posterior cerebral arteries are presented. Features typical of posterior circulation strokes are highlighted, including patterns of basilar artery occlusions. Clinical severity and prognosis of posterior circulation strokes are highly variable, and given that they are more difficult to detect on CT-based neuroimaging, magnetic resonance imaging is the technique of choice in suspected posterior circulation strokes. Rapid identification of arterial occlusion patterns may provide prognostic information and support acute revascularization decisions. Conclusions: Posterior circulation stroke syndromes tightly reflect lesion localization and arterial occlusion patterns. Although many clinical and pathogenetic features are similar to anterior circulation strokes, notable differences exist in terms of clinical presentation, stroke mechanism, prognosis, and response to acute recanalization.

Objective To investigate the aetiology, subsequent preventive strategies and outcomes of stroke despite anticoagulation in patients with atrial fibrillation (AF). Methods We analysed consecutive patients with AF with an index imaging-proven ischaemic stroke despite vitamin K-antagonist (VKA) or direct oral anticoagulant (DOAC) treatment across 11 stroke centres. We classified stroke aetiology as: (i) competing stroke mechanism other than AF-related cardioembolism; (ii) insufficient anticoagulation (non-adherence or low anticoagulant activity measured with drug-specific assays); or, (iii) AF-related cardioembolism despite sufficient anticoagulation. We investigated subsequent preventive strategies with regard to the primary (composite of recurrent ischaemic stroke, intracranial haemorrhage, death) and secondary endpoint (recurrent ischaemic stroke) within 3 months after index stroke. Results Among 2946 patients (median age 81 years; 48% women; 43% VKA, 57% DOAC), stroke aetiology was competing mechanism in 713 patients (24%), insufficient anticoagulation in 934 (32%) and cardioembolism despite sufficient anticoagulation in 1299 (44%). We found high rates of the primary (27% of patients; completeness 91.6%) and secondary endpoint (4.6%; completeness 88.5%). Only DOAC (vs VKA) treatment after index stroke showed lower odds for both endpoints (primary: adjusted OR (aOR) (95% CI) 0.49 (0.32 to 0.73); secondary: 0.44 (0.24 to 0.80)), but not switching between different DOAC types. Adding antiplatelets showed higher odds for both endpoints (primary: aOR (95% CI) 1.99 (1.25 to 3.15); secondary: 2.66 (1.40 to 5.04)). Only few patients (1%) received left atrial appendage occlusion as additional preventive strategy. Conclusions Stroke despite anticoagulation comprises heterogeneous aetiologies and cardioembolism despite sufficient anticoagulation is most common. While DOAC were associated with better outcomes than VKA, adding antiplatelets was linked to worse outcomes in these high-risk patients. Our findings indicate that individualised and novel preventive strategies beyond the currently available anticoagulants are needed. Trial registration number ISRCTN48292829.

Background: In patients with atrial fibrillation who suffered an ischemic stroke while on treatment with nonvitamin K antagonist oral anticoagulants, rates and determinants of recurrent ischemic events and major bleedings remain uncertain. Methods: This prospective multicenter observational study aimed to estimate the rates of ischemic and bleeding events and their determinants in the follow-up of consecutive patients with atrial fibrillation who suffered an acute cerebrovascular ischemic event while on nonvitamin K antagonist oral anticoagulant treatment. Afterwards, we compared the estimated risks of ischemic and bleeding events between the patients in whom anticoagulant therapy was changed to those who continued the original treatment. Results: After a mean follow-up time of 15.0±10.9 months, 192 out of 1240 patients (15.5%) had 207 ischemic or bleeding events corresponding to an annual rate of 13.4%. Among the events, 111 were ischemic strokes, 15 systemic embolisms, 24 intracranial bleedings, and 57 major extracranial bleedings. Predictive factors of recurrent ischemic events (strokes and systemic embolisms) included CHA ₂ DS ₂ -VASc score after the index event (odds ratio [OR], 1.2 [95% CI, 1.0–1.3] for each point increase; P =0.05) and hypertension (OR, 2.3 [95% CI, 1.0–5.1]; P =0.04). Predictive factors of bleeding events (intracranial and major extracranial bleedings) included age (OR, 1.1 [95% CI, 1.0–1.2] for each year increase; P =0.002), history of major bleeding (OR, 6.9 [95% CI, 3.4–14.2]; P =0.0001) and the concomitant administration of an antiplatelet agent (OR, 2.8 [95% CI, 1.4–5.5]; P =0.003). Rates of ischemic and bleeding events were no different in patients who changed or not changed the original nonvitamin K antagonist oral anticoagulants treatment (OR, 1.2 [95% CI, 0.8–1.7]). Conclusions: Patients suffering a stroke despite being on nonvitamin K antagonist oral anticoagulant therapy are at high risk of recurrent ischemic stroke and bleeding. In these patients, further research is needed to improve secondary prevention by investigating the mechanisms of recurrent ischemic stroke and bleeding.

Background and objectives: The optimal methods for predicting early infarct growth rate (EIGR) in acute ischemic stroke with a large vessel occlusion (LVO) have not been established. We aimed to study the factors associated with EIGR, with a focus on the collateral circulation as assessed by the Hypoperfusion Intensity Ratio (HIR) on perfusion imaging, and determine whether the associations found are consistent across imaging modalities. Methods: Retrospective multicenter international study including anterior circulation LVO-related acute stroke patients with witnessed stroke onset and baseline perfusion imaging (MRI or CT) performed within 24hrs from symptom onset. To avoid selection bias, patients were selected from (1) the prospective registries of four comprehensive stroke centers with systematic use of perfusion imaging and including both thrombectomy-treated and untreated patients, and (2) one prospective thrombectomy study where perfusion imaging was acquired per protocol but treatment decisions were made blinded to the results. EIGR was defined as infarct volume on baseline imaging divided by onset-to-imaging time, and fast progressors as EIGR ≥10mL/hr. The HIR, defined as the proportion of Tmax>6s with Tmax>10s volume, was measured on perfusion imaging using RAPID software. The factors independently associated with fast progression were studied using multivariable logistic regression models, with separate analyses for CT- and MRI-assessed patients. Results: Overall, 1127 patients were included (CT, n=471; MRI, n=656). Median age was 74 years (IQR, 62-83), 52% were male, median NIHSS was 16 (IQR, 9-21), median HIR was 0.42 (IQR, 0.26-0.58) and 415 (37%) were fast progressors. The HIR was the primary factor associated with fast progression, with very similar results across imaging modalities: the proportion of fast progressors was 4% in the first HIR quartile (i.e. excellent collaterals), ∼15% in the second, ∼50% in the third, and ∼77% in the fourth (P<0.001 for each imaging modality). Fast progression was independently associated with poor 3-month functional outcome in both the CT and MRI cohorts (P<0.001 and P=0.030, respectively). Discussion: The HIR is the primary factor associated with fast infarct progression, regardless of imaging modality. These results have implication for neuroprotection trial design, as well as informing triage decisions at primary stroke centers.

BACKGROUND: The relative value of computed tomography (CT) and magnetic resonance imaging (MRI) in acute ischemic stroke (AIS) is debated. In May 2018, our center transitioned from using CT to MRI as first-line imaging for AIS. This retrospective study aims to assess the effects of this paradigm change on diagnosis and disability outcomes. METHODS: We compared all consecutive patients with confirmed diagnosis of AIS admitted to our center during the MRI-period (May 2018–August 2022) and an identical number of patients from the preceding CT-period (December 2012–April 2018). Univariable and multivariable analyses were performed to evaluate outcomes, including the number and delay of imaging exams, the rate of missed strokes, stroke mimics treated with thrombolysis, undetermined stroke mechanisms, length of hospitalization, and 3-month disability. RESULTS: The median age of the 2972 included patients was 76 years (interquartile range, 65–84), and 46% were female. In the MRI-period, 80% underwent MRI as first acute imaging. The proportion of patients requiring a second acute imaging modality for diagnostic ± revascularization reasons increased from 2.1% to 5% ( P _unadj <0.05), but it decreased in the subacute phase from 79.0% to 60.1% ( P _adj <0.05). In thrombolysis candidates, there was a 2-minute increase in door-to-imaging delay ( P _adj <0.05). The rates of initially missed AIS diagnosis was similar (3.8% versus 4.4%, P _adj =0.32) and thrombolysis in stroke mimics decreased by half (8.6% versus 4.3%; P _adj <0.05). Rates of unidentified stroke mechanism at hospital discharge were similar (22.8% versus 28.1%; P _adj =0.99). The length of hospitalization decreased from 9 (interquartile range, 6–14) to 7 (interquartile range, 4–12) days ( P _adj =0.62). Disability at 3 months was similar (common adjusted odds ratio for favorable Rankin shift, 0.98 [95% CI, 0.71–1.36]; P _adj =0.91), as well as mortality and symptomatic intracranial hemorrhage. CONCLUSIONS: A paradigm shift from CT to MRI as first-line imaging for AIS seems feasible in a comprehensive stroke center, with a minimally increased delay to imaging in thrombolysis candidates. MRI was associated with reduced thrombolysis rates of stroke mimics and subacute neuroimaging needs.

Objective Coronavirus disease (COVID-19) has been associated with a large variety of neurologic disorders. However, the mechanisms underlying these neurologic complications remain elusive. In this study, we aimed at determining whether neurologic symptoms were caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) direct infection or by either systemic or local proinflammatory mediators. Methods In this cross-sectional study, we checked for SARS-CoV-2 RNA by quantitative reverse transcription PCR, SARS-CoV-2–specific antibodies, and 49 cytokines/chemokines/growth factors (by Luminex) in the CSF +/− sera of a cohort of 22 COVID-19 patients with neurologic presentation and 55 neurologic control patients (inflammatory neurologic disorder [IND], noninflammatory neurologic disorder, and MS). Results We detected anti–SARS-CoV-2 immunoglobulin G in patients with severe COVID-19 with signs of intrathecal synthesis for some of them. Of the 4 categories of tested patients, the CSF of IND exhibited the highest level of cytokines, chemokines, and growth factors. By contrast, patients with COVID-19 did not present overall upregulation of inflammatory mediators in the CSF. However, patients with severe COVID-19 (intensive care unit patients) exhibited higher concentrations of CCL2, CXCL8, and vascular endothelium growth factor A (VEGF-A) in the CSF than patients with a milder form of COVID-19. In addition, we could show that intrathecal CXCL8 synthesis was linked to an elevated albumin ratio and correlated with the increase of peripheral inflammation (serum hepatocyte growth factor [HGF] and CXCL10). Conclusions Our results do not indicate active replication of SARS-CoV-2 in the CSF or signs of massive inflammation in the CSF compartment but highlight a specific impairment of the neurovascular unit linked to intrathecal production of CXCL8.