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In this neuropathological study, we investigated neuroinflammation surrounding recent and old cerebral microbleeds (CMBs) and cerebral microinfarcts (CMIs) in 18 cases of cerebral amyloid angiopathy (CAA). We used several serial stainings and immunolabellings to identify microvascular lesions, define their recent or old stage, and characterize neuroinflammatory response (scavenging activity and astrogliosis). We found that both CMBs and CMIs induce a neuroinflammatory response, which was more pronounced in old lesion than recent. Astrogliosis and scavenging activity were differentially prominent according to the ischemic/hemorrhagic nature of the lesion. Our findings provide insights into the pathophysiology of microvascular injuries in CAA.

Important advances from stroke research were reported in 2021, providing valuable insights for the field. In particular, the need to revisit the organisation of acute stroke care became evident. Although intravenous thrombolysis plus mechanical thrombectomy remains the best strategy for acute ischaemic stroke with large vessel occlusion, research from 2021 has stimulated fruitful discussions on how to organise the stroke care pathway. The conventional approach of awaiting the stroke patient's arrival at the hospital might soon be outdated given that flying doctors, mobile stroke units, or direct admission to the angiography suite are gaining attention.

Cerebral microbleeds (CMBs) are defined as hypointense foci visible on T2*-weighted and susceptible-weighted MRI sequences. CMBs are increasingly recognised with the widespread use of MRI in healthy individuals as well as in the context of cerebrovascular disease or dementia. They can also be encountered in major critical medical conditions such as in patients requiring extracorporeal mechanical oxygenation. The advent of MRI-guided postmortem neuropathological examinations confirmed that, in the context of cerebrovascular disease, the vast majority of CMBs correspond to recent or old microhaemorrhages. Detection of CMBs is highly influenced by MRI parameters, in particular field strength, postprocessing methods used to enhance T2* contrast and three dimensional sequences. Despite recent progress, harmonising imaging parameters across research studies remains necessary to improve cross-study comparisons. CMBs are helpful markers to identify the nature and the severity of the underlying chronic small vessel disease. In daily clinical practice, presence and numbers of CMBs often trigger uncertainty for clinicians especially when antithrombotic treatments and acute reperfusion therapies are discussed. In the present review, we discuss those clinical dilemmas and address the value of CMBs as diagnostic and prognostic markers for future vascular events.

Intracerebral haemorrhage (ICH) is a dramatic condition caused by the rupture of a cerebral vessel and the entry of blood into the brain parenchyma. ICH is a major contributor to stroke-related mortality and dependency: only half of patients survive for 1 year after ICH, and patients who survive have sequelae that affect their quality of life. The incidence of ICH has increased in the past few decades with shifts in the underlying vessel disease over time as vascular prevention has improved and use of antithrombotic agents has increased. The pathophysiology of ICH is complex and encompasses mechanical mass effect, haematoma expansion and secondary injury. Identifying the causes of ICH and predicting the vital and functional outcome of patients and their long-term vascular risk have improved in the past decade; however, no specific treatment is available for ICH. ICH remains a medical emergency, with prevention of haematoma expansion as the key therapeutic target. After discharge, secondary prevention and management of vascular risk factors in patients remains challenging and is based on an individual benefit–risk balance evaluation.This Primer by Cordonnier and colleagues describes the epidemiology, aetiology, pathophysiology, diagnosis and treatment of intracerebral haemorrhage.

Though headache is commonly observed after stroke and may affect survivors' quality of life, it has rarely been studied after spontaneous intracerebral haemorrhage (ICH). In a cohort of ICH survivors, we assessed the long-term prevalence and determinants of headache. We screened consecutive ICH survivors enrolled in the prospective, single-centre Prognosis of Intracerebral Haemorrhage study for headache 1, 3, and 6 years after ICH, according to the International Headache Society's criteria. Depressive and anxiety symptoms severity was measured at 1-year follow-up. Variables associated with the presence of headache 1 year after ICH were analyzed using univariate and multivariable models. Among the 146 patients included in this study, 31 (21%), 25 (19%), and 14 (20%) patients reported headache at 1-, 3-, and 6-year follow-up, respectively. In an age-adjusted model, patients with headache at ICH onset (adjusted odds ratio [aOR] 2.75; 95% CI 1.02-7.42) and previous history of headache (aOR 4.60; 95% CI 1.74-12.1) were associated with headache at 1-year follow-up. Patients with headache were more likely to report depressive and anxiety symptoms at 1-year follow-up (both p < 0.02). One in five ICH survivors suffered from headache and patients who reported headache at ICH onset were especially at risk.

Cerebral amyloid angiopathy (CAA) is an age-related small vessel disease, characterised pathologically by progressive deposition of amyloid β in the cerebrovascular wall. The Boston criteria are used worldwide for the in-vivo diagnosis of CAA but have not been updated since 2010, before the emergence of additional MRI markers. We report an international collaborative study aiming to update and externally validate the Boston diagnostic criteria across the full spectrum of clinical CAA presentations. In this multicentre, hospital-based, retrospective, MRI and neuropathology diagnostic accuracy study, we did a retrospective analysis of clinical, radiological, and histopathological data available to sites participating in the International CAA Association to formulate updated Boston criteria and establish their diagnostic accuracy across different populations and clinical presentations. Ten North American and European academic medical centres identified patients aged 50 years and older with potential CAA-related clinical presentations (ie, spontaneous intracerebral haemorrhage, cognitive impairment, or transient focal neurological episodes), available brain MRI, and histopathological assessment for CAA diagnosis. MRI scans were centrally rated at Massachusetts General Hospital (Boston, MA, USA) for haemorrhagic and non-haemorrhagic CAA markers, and brain tissue samples were rated by neuropathologists at the contributing sites. We derived the Boston criteria version 2.0 (v2.0) by selecting MRI features to optimise diagnostic specificity and sensitivity in a prespecified derivation cohort (Boston cases 1994–2012, n=159), then externally validated the criteria in a prespecified temporal validation cohort (Boston cases 2012–18, n=59) and a geographical validation cohort (non-Boston cases 2004–18; n=123), comparing accuracy of the new criteria to the currently used modified Boston criteria with histopathological assessment of CAA as the diagnostic standard. We also assessed performance of the v2.0 criteria in patients across all cohorts who had the diagnostic gold standard of brain autopsy. The study protocol was finalised on Jan 15, 2017, patient identification was completed on Dec 31, 2018, and imaging analyses were completed on Sept 30, 2019. Of 401 potentially eligible patients presenting to Massachusetts General Hospital, 218 were eligible to be included in the analysis; of 160 patient datasets from other centres, 123 were included. Using the derivation cohort, we derived provisional criteria for probable CAA requiring the presence of at least two strictly lobar haemorrhagic lesions (ie, intracerebral haemorrhages, cerebral microbleeds, or foci of cortical superficial siderosis) or at least one strictly lobar haemorrhagic lesion and at least one white matter characteristic (ie, severe visible perivascular spaces in centrum semiovale or white matter hyperintensities in a multispot pattern). The sensitivity and specificity of these criteria were 74·8% (95% CI 65·4–82·7) and 84·6% (71·9–93·1) in the derivation cohort, 92·5% (79·6–98·4) and 89·5% (66·9–98·7) in the temporal validation cohort, 80·2% (70·8–87·6) and 81·5% (61·9–93·7) in the geographical validation cohort, and 74·5% (65·4–82·4) and 95·0% (83·1–99·4) in all patients who had autopsy as the diagnostic standard. The area under the receiver operating characteristic curve (AUC) was 0·797 (0·732–0·861) in the derivation cohort, 0·910 (0·828–0·992) in the temporal validation cohort, 0·808 (0·724–0·893) in the geographical validation cohort, and 0·848 (0·794–0·901) in patients who had autopsy as the diagnostic standard. The v2.0 Boston criteria for probable CAA had superior accuracy to the current Boston criteria (sensitivity 64·5% [54·9–73·4]; specificity 95·0% [83·1–99·4]; AUC 0·798 [0·741–0854]; p=0·0005 for comparison of AUC) across all individuals who had autopsy as the diagnostic standard. The Boston criteria v2.0 incorporate emerging MRI markers of CAA to enhance sensitivity without compromising their specificity in our cohorts of patients aged 50 years and older presenting with spontaneous intracerebral haemorrhage, cognitive impairment, or transient focal neurological episodes. Future studies will be needed to determine generalisability of the v.2.0 criteria across the full range of patients and clinical presentations. US National Institutes of Health (R01 AG26484).

Background Cerebral small vessel disease (CSVD) is a common incidental MRI finding in patients with transient ischemic attack (TIA) and stroke and has been linked to cognitive decline. This study investigated the prevalence of CSVD imaging biomarkers in TIA patients and their association with cognitive performance over 3 years. Methods We included 246 TIA patients from the INSPiRE‐TMS study (ClinicalTrials.gov: NCT01586702). CSVD was assessed on baseline 3 T MRI using a composite score (0–4) including white matter hyperintensities (WMH), lacunes, cerebral microbleeds (CMBs), and enlarged perivascular spaces (PVS). Cognitive performance was evaluated using the Montreal Cognitive Assessment (MoCA) at baseline and annually for 3 years. Results At least one CSVD imaging biomarker was present in 58.5% of patients. Lacunes (36.6%) were the most common, followed by PVS (28.1%), WMH (19.5%), and CMBs (17.9%). Higher CSVD‐score was independently associated with greater cognitive decline over 3 years (β = −0.52, 95% CI −0.95– −0.08, p = 0.020), along with older age (β = −0.08, 95% CI −0.13 to −0.03, p = 0.001). CMB burden was the strongest predictive component of the CSVD‐score (β = 0.42, 95% CI −0.63 to −0.22, p < 0.001). CSVD‐score was particularly associated with decline in the memory domain (adjusted β of −0.18, 95% CI −0.32 to −0.04, p = 0.015). Conclusion CSVD imaging markers are present in over half of TIA patients and are independently associated with cognitive decline up to 3 years, with the strongest effect on memory. Whether the presence of CMBs is the strongest predictive imaging biomarker of cognitive decline in TIA patients requires confirmation in further studies. This study showed that CSVD imaging markers are present in over half of TIA patients and are independently associated with cognitive decline up to 3 years, with the strongest effect on memory. Also, CMBs seem to be the strongest predictive imaging biomarker of cognitive decline in TIA patients.

Introduction: Even with reperfusion therapies, the prognosis of patients with basilar artery occlusion (BAO) related stroke remains poor. We aimed to test the hypothesis that the presence of prodromal symptoms, an easily available anamnestic data, is a key determinant of poor functional outcome. Patients and methods: Data from patients with BAO treated in Lille, France, with mechanical thrombectomy (MT) between 2015 and 2021 were prospectively collected. The presence of prodromal symptoms was defined by previous transient neurological deficit or gradual progressive clinical worsening preceding a secondary sudden clinical worsening. We compared the characteristics of patients with and without prodromal symptoms. We built multivariate logistic regression models to study the association between the presence of prodromal symptoms and functional (mRS 0–3 and mortality), and procedural (successful recanalization and early reocclusion) outcomes. Results: Among the 180 patients, 63 (35%) had prodromal symptoms, most frequently a vertigo. Large artery atherosclerosis was the predominant cause of stroke (41.3%). The presence of prodromal symptoms was an independent predictor of worse 90-day functional outcome (mRS 0–3: 25.4% vs 47.0%, odds ratio (OR) 0.39; 95% confidence interval (CI) 0.16–0.86) and 90-day mortality (OR 2.17; 95% CI 1.02–4.65). Despite similar successful recanalization rate, the proportion of early basilar artery reocclusion was higher in patients with prodromal symptoms (23.8% vs 5.6%, p = 0.002). Discussion and conclusion: More than one third of BAO patients treated with MT had prodromal symptoms, especially patients with large-artery atherosclerosis. Clinicians should systematically screen for prodromal symptoms given the poor related functional outcome and increased risk of early basilar artery reocclusion. Graphical abstract

Abstract Introduction Predicting the occurrence of late seizures after intracerebral haemorrhage may help in making clinical decisions about treatment. Currently, the CAVE score is the best performing risk score. We aimed to design a different, pragmatic risk prediction score and compared it to the CAVE score. Patients and methods The South Limburg (Netherlands) intracerebral haemorrhage registry, consisting of patients with a primary intracerebral haemorrhage in 2004–2009, was used for the derivation cohort. We made a prediction model using Cox proportional hazard analyses; comparisons between models were made with the c-statistic. We validated our model externally in three independent cohorts. Results Our derivation cohort consisted of 781 patients, of whom 78 (10%) developed late seizures. We found the following independent predictors for late seizures: any neurosurgical procedure, age < 65 years, lobar haemorrhage, and early seizures (occurring within the first week). These formed our new prediction score (LEAN score), which had an optimism-corrected c-statistic of 0.80 (95%-confidence interval 0.78–0.86). The LEAN score predicts late seizure risk as 0.7%, 1.6%, 8.8%, 22.0%, 29.8%, 43.5%, 100% for the increasing score groups respectively. External validation showed comparable optimism-corrected c-statistics for both the LEAN score and the CAVE score. Conclusion The newly developed LEAN score consists of easily available clinical variables and performs equally to the CAVE score. Additionally, the high risk of late seizures in patients with the maximum LEAN score might make a diagnosis of epilepsy possible according to international guidelines despite these patients only had early seizures. Graphical Abstract Graphical abstract