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Background: Atrial fibrillation (AF) can be known before the stroke (KAF) or be newly detected after stroke (AFDAS). It is unknown whether the outcome of stroke differs between KAF and AFDAS. We performed a propensity-matched analysis to investigate the outcome of patients with AFDAS and their counterparts with KAF. Methods: We analysed a consecutive series of patients enrolled into the EIDASAF study, a single centre, retrospective study of ischemic stroke patients with a diagnosis of AF before or after the event who had been admitted to the Hyperacute Stroke Unit of Imperial College Healthcare NHS Trust between 2010 and 2017. Results: Overall, our cohort included 959 patients with AF and acute ischemic stroke. After propensity score matching, 547 patients were matched (404 KAF group and 143 AFDAS group). The rates of in hospital death and of haemorrhagic transformation were significantly higher in KAF patients compared to AFDAS patients. Logistic regression analysis did not reveal a statistically significant influence of AF subtypes on the outcome of death. However, in logistic regression analysis KAF was associated with increased probability of haemorrhagic transformation (OR 9.64; CI 1.29–71.68, p = 0.022) after the index event. Conclusion: KAF is associated with an increased risk of haemorrhagic transformation but not of death when compared to AFDAS. [ABSTRACT FROM AUTHOR]

Heart failure (HF) is associated with poor outcome after stroke, but data from large prospective trials are sparse. We assessed the impact of HF on clinical endpoints in patients hospitalized with acute ischemic stroke or transient ischemic attack (TIA) enrolled in the prospective, multicenter Systematic Monitoring for Detection of Atrial Fibrillation in Patients with Acute Ischemic Stroke (MonDAFIS) trial. HF was defined as left ventricular ejection fraction (LVEF) < 55% or a history of HF on admission. The composite of recurrent stroke, major bleeding, myocardial infarction, and all-cause death, and its components during the subsequent 24 months were assessed. We used estimated hazard ratios in confounder-adjusted models. Overall, 410/2562 (16.0%) stroke patients fulfilled the HF criteria (i.e. 381 [14.9%] with LVEF < 55% and 29 [1.9%] based on medical history). Patients with HF had more often diabetes, coronary and peripheral arterial disease and presented with more severe strokes on admission. HF at baseline correlated with myocardial infarction (HR 2.21; 95% CI 1.02–4.79), and all-cause death (HR 1.67; 95% CI 1.12–2.50), but not with major bleed (HR 1.93; 95% CI 0.73–5.06) or recurrent stroke/TIA (HR 1.08; 95% CI 0.75–1.57). The data were adjusted for age, stroke severity, cardiovascular risk factors, and randomization. Patients with ischemic stroke or TIA and comorbid HF have a higher risk of myocardial infarction and death compared with non-HF patients whereas the risk of recurrent stroke or major hemorrhage was similar. Trial registration number Clinicaltrials.gov NCT02204267. [ABSTRACT FROM AUTHOR]

Background: Moyamoya disease (MMD) is a rare disorder causing ischemic and hemorrhagic juvenile stroke. It is associated with the founder susceptibility variant p.R4810K in the RNF213 gene in East Asia. Our aim was to enhance understanding of MMD in so far poorly characterized Southeast Asians and exploring differences with Caucasian Europeans. Methods: By retrospective analysis of medical records and systematic database search on PubMed for all published cases, we identified Southeast Asian patients with MMD. We extracted and pooled proportions using fixed-effects models. Our own cohort was tested for the East Asian RNF213 founder variant p.R4810K. One of our Southeast Asian patients underwent post-mortem histopathological examination. Results: The study cohort comprised 32 Southeast Asians. Mean age at onset in the entire cohort was 32.5 ± 20.3 years (n = 24), 43.4 ± 8.7 years in patients admitted to our center (n = 11), and 23.4 ± 22.4 years in patients from the international literature (n = 13). Female-to-male ratio was 1.6:1. MMD predominantly affected bilateral anterior intracranial vessels. Cerebral ischemia outnumbered transient ischemic attacks (TIAs) and intracranial hemorrhage. TIAs, arterial hypertension and obesity were significantly less frequent in Southeast Asian patients compared to Caucasian Europeans. p.R4810K was absent in all examined Southeast Asians despite of typical histopathological signs of MMD in one autopsy case. Conclusion: Clinical and histopathological manifestations of MMD in Southeast Asians are similar to those in Caucasian Europeans. The genotype of MMD in Southeast Asians differs from that of most East Asian patients. [ABSTRACT FROM AUTHOR]

Background: Moyamoya angiopathy (MMA) is a rare cause of stroke in Caucasians, but it is much more frequent in East Asia. Since 2021, diagnostic criteria not only comprise bilateral, but also unilateral MMA. Hitherto, progression of unilateral MMA has predominantly been described in East Asians. Our study aimed to analyze the occurrence and characteristics of progression of initially unilateral MMA in Caucasian Europeans. Methods: By retrospective analysis of medical records of 200 European Caucasians with MMA, admitted to our German center between 2010 and 2022, cases of unilateral MMA and its progression, i.e. progressive ipsi- or novel contralateral arterial stenosis, during follow-up were identified. Kruskal Wallis Test and Fisher's Exact Test were used to identify statistically significant differences between progressive and stable patients concerning demographic, clinical, laboratory, and radiographic features. Results: Our cohort comprised 63 patients with initially unilateral MMA. Fourteen (22.2%) had an ipsi- (n = 3, 21.4%) or contralateral (n = 11, 78.6%) progression. Mean age of patients with progressive MMA at symptom onset was 32 ± 14.1 years. The ratio of women to men in this subgroup was 2.5:1. Mean follow-up period was 5.4 ± 3.7 years, mean age at progression was 39.9 ± 12.7 years. Mean time interval between penultimate follow-up and progression was 4.8 ± 4.5 years. Patients with progression showed affection of the posterior cerebral artery (p = 0.009) and suffered from vertigo (p = 0.009) significantly more often. Conclusion: Unilateral MMA progresses in a substantial proportion in European Caucasians. Long-term follow-up is required due to potential late progression with consecutive symptoms and the need for bypass surgery. [ABSTRACT FROM AUTHOR]

Background: Fabry disease is an inherited metabolic disorder with various symptoms. Neurological manifestations are small fiber neuropathy, cerebral white matter lesions (WML), megadolicho basilar artery, and stroke. The relevance of the D313Y variant in the galactosidase alpha gene is controversially discussed. Objectives: We aimed at elucidating the implications of this differential diagnosis of multiple sclerosis (MS), focussing on the analysis of WML over time and correlations with other markers. Methods: We reviewed retrospectively the clinical, laboratory, and magnetic resonance imaging data of 21 carriers of the D313Y variant at a single German outpatient clinic for MS between 2004 and 2021. Results: In our cohort (15 females, 6 males), mean age at diagnosis was 44.1 ± 16.3 years, and mean follow-up duration was 3.1 ± 3.9 years. WML were rated on both, the Fazekas scale and the age-related white matter changes rating scale, and were of variable interindividual extent. Follow-up imaging showed virtually no progress. WML did not correlate with the severity of clinical findings or lysoGb3 levels. Symptomatic carriers of the variant are characterized by an almost complete lack of internal organ manifestations and laboratory findings, usually associated with Fabry disease. Conclusion: WML in carriers of the D313Y variant do not seem to be suitable for assessing or predicting the (para-) clinical status. Concerning MS patients, the variant and its clinical signs can be a differential diagnosis, but also a co-factor. Imaging and cerebrospinal fluid findings facilitate the distinction between both entities. [ABSTRACT FROM AUTHOR]

Background: Embolism as a cause of stroke is widely neglected in Moyamoya angiopathy (MMA), and recommendations for use of antiplatelet therapy (APT) vary. We examined the presence of microembolic signals (MES) during transcranial Doppler (TCD) monitoring and assessed the effects of APT on the occurrence of MES in MMA. Patients and methods: We retrospectively analysed patients with MMA treated at our centre between 2011 and 2021. TCD was performed at first presentation and at most visits, while number of visits varied between individual patients. TCD was performed for 30 min bilaterally. Patient demographics, vascular risk factors, and antiplatelet treatment were collected from each clinic visit and ischemic and haemorrhagic episodes were captured as recorded during follow-up visits. Results: 209 patients were included in the analysis (mean age 38.7 ± 15.3, 28% male). 21 patients with 27 MES-positive TCD examinations were identified (10%). Patient characteristics were similar in MES-positive and MES-negative groups. However, recent ischemic events were detected at a significantly higher rate in MES-positive patients (42.9% vs 4.8%, p < 0.001). After MES detection, change of antiplatelet drug regime was performed, leading to loss of MES in all cases. Dual APT was preferably used in the MES-positive group (p < 0.001) but no significant difference of haemorrhage during follow-up-visits was observed. Reduction of APT before bypass-surgery triggered MES in four patients. Conclusion: APT is required in patients with MMA. MES monitoring may help to identify risk patients in need of intensified APT. [ABSTRACT FROM AUTHOR]

In SS, this phenomenon is absent, but in contrast to DVBS a relevant portion of patients is - despite its non-vasculitic etiology - positive for antiphospholipid antibodies [[3]]. Dear Sirs, Divry van Bogaert syndrome (DVBS) and Sneddon's syndrome (SS) are rare non-inflammatory vasculopathies manifesting with recurrent stroke and livedo racemosa [[1]]. Novel heterozygous COL4A2 variant c.2572A > G, p.(I858V) mimicking Sneddon's and Divry van Bogaert Syndrome This case combines clinical features of COL4A2 mutations with others that are characteristic for DVBS and SS but have not been reported in COL4A2 mutations before. [Extracted from the article]

Even early at the beginning of the coronavirus disease 2019 (COVID‑19) pandemic, stroke was described as a manifestation or complication of infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Current meta-analyses reported a stroke rate of approximately 1.5%. Stroke in COVID‑19 positive patients occurs more frequently in severe courses of the infection and in older patients with cardiovascular comorbidities; however, young patients without cardiovascular risk factors are also not uncommonly affected. The mechanisms of stroke are predominantly embolic. The thrombi frequently occlude large intracranial vessels and in more than 20% affect multiple vascular territories, whereas infarctions due to small vessel disease are uncommon. The exact source of the embolism remains cryptogenic in more than 40% of patients. The mortality caused by the co-occurrence of a SARS-CoV‑2 infection and a stroke exceeds 15–30%. While acute stroke treatment was severely affected in some European regions, the rates of recanalization treatment in Germany largely remained stable during the first pandemic wave; however, 20–30% fewer patients with minor stroke and transient ischemic attacks (TIA) presented to hospitals during the first wave in spring 2020. The present narrative review summarizes the current evidence regarding the epidemiology and pathogenesis of stroke associated with COVID‑19 and describes the effect of the pandemic so far on the provision of acute stroke treatment. [ABSTRACT FROM AUTHOR]

Background: The lacking awareness of healthcare providers bears the risk of delayed or false diagnoses in rare diseases. No systematic data about misdiagnoses of Moyamoya angiopathy (MMA) are available. Objective: To evaluate the rate and pattern of missed diagnoses in MMA. Methods: Retrospective analysis of a consecutive case series from a single German referral center. Rates of missed or delayed diagnoses in Caucasian MMA patients were calculated based on discharge letters from other hospitals and systematic chart review. Results: Out of 192 Caucasian patients eventually diagnosed with MMA at our center, an initial misdiagnosis was identified in 119 patients (62%). The time between onset and diagnosis was 1 year in 24 patients, 2 years in 23 patients, 3 years in 10 patients, and > 3 years in 49 patients (mean 5.28, median 3, standard deviation 5.11, and range 4–26 years). The most common misdiagnoses were cerebral vasculitis (31%), etiologically ill-defined stroke diagnoses (30.2%), and MS (3.6%). Conclusions: This is the first systematic report which shows that patients with MMA are at high risk to be falsely diagnosed and treated. Depiction of typical vascular abnormalities in angiopathy is essential. Normal CSF cell counts, negative oligoclonal bands, and lack of infratentorial lesions as well as gadolinium-positive T1 lesions on MRI may be red flags differentiating this vasculopathy from vasculitis and MS. [ABSTRACT FROM AUTHOR]

Background: Intracerebral hemorrhage (ICH) is a life-threatening complication of non-vitamin K antagonist oral anticoagulants (NOAC). Little is known about the effect of intensity of anticoagulation on NOAC-ICH. We describe the current use of coagulation testing in the emergency setting and explore associations with baseline size and expansion of hematoma as determined in a previous study.Methods: Data from the prospective multicenter RASUNOA registry were analyzed. Patients with NOAC-ICH were enrolled between February 2012 and December 2014. Frequency of local test performance of specific (anti-factor Xa tests, diluted thrombin time) and non-specific tests (international normalized ratio (INR), activated partial thromboplastin time (aPTT), thrombin time) was analyzed. The association of anticoagulation intensity at admission with hematoma volume and hematoma expansion was explored.Results: In 61 NOAC-ICH patients enrolled at 21 centers, drug-specific coagulation testing was performed in 16 cases (26%), and only 29% of centers appeared to use drug-specific tests in NOAC-ICH at all. In some cases, INR and aPTT values were normal despite drug concentrations in the peak range. In patients with available drug-specific concentrations, 50% had drug levels in the peak range at admission. Higher intensity of anticoagulation was not associated with higher hematoma volume at admission or with subsequent hematoma expansion.Conclusion: Drug-specific tests are only infrequently used in NOAC-ICH. Normal results in non-specific coagulation do not reliably rule out peak range concentrations. Anticoagulation intensity at admission does not predict baseline hematoma volume or subsequent hematoma expansion. [ABSTRACT FROM AUTHOR]

Purpose of Review: We review the current evidence for medical and surgical treatments of spontaneous intracerebral hemorrhage (ICH). Recent Findings: Therapy with hemostatic agents (e.g. factor VIIa and tranexamic acid) if started early after bleeding onset may reduce hematoma expansion, but their clinical effectiveness has not been shown. Rapid anticoagulation reversal with prothrombin concentrates (PCC) plus vitamin K is the first choice in vitamin K antagonist-related ICH. In ICH related to dabigatran, anticoagulation can be rapidly reversed with idarucizumab. PCC are recommended for ICH related to FXa inhibitors, whereas specific reversal agents are not yet approved. While awaiting ongoing trials studying minimally invasive approaches or hemicraniectomy, the role of surgery in ICH remains to be defined. Therapies targeting downstream molecular cascades in order to prevent secondary neuronal damage are promising, but the complexity and multi-phased nature of ICH pathophysiology is challenging. Finally, in addition to blood pressure control, antithrombotic prevention after ICH has to consider the risk of recurrent bleeding as well as the risk of ischemic events. Summary: Treatment of acute ICH remains challenging, and many promising interventions for acute ICH await further evidence from trials. [ABSTRACT FROM AUTHOR]

Kidney disease is a risk factor for cerebral microangiopathy and spontaneous intracerebral hemorrhage (ICH). We aimed to determine the association of renal dysfunction (RD) with MRI correlates of different patterns of cerebral microangiopathies including cerebral microbleeds (CMB) and white matter lesions (WML) in patients with ICH. In a prospectively collected, single-center cohort of ICH patients, glomerular filtration rate (eGFR) was estimated using the Modification of Diet in Renal Disease equation. We classified the renal function in five categories: category 1 (eGFR ≥90 mL/min/1.73 m), category 2 (eGFR 60-89), category 3 (eGFR 30-59), category 4 (eGFR 15-29), and category 5 (eGFR <15) and dichotomized at an eGFR of 60. Number, location, and extent of CMB and WML were measured on MRI. ICH and CMB locations were classified as lobar or deep. 97 ICH patients with MRI (mean age 65.9 ± 13.9 years) were included. Intracerebral hemorrhage was lobar in 52.6 %. Median eGFR was 85.8 mL/min/1.73 m (IQR 34.3). Renal dysfunction was present in 12.4 % of the patients. At least one CMB was present in 57.7 % of patients, WML were even more frequent (97.7 %). Age and impaired renal function were factors independently associated with the presence of CMB. The presence of CMB was independently associated with the number and extent of WML. RD is a frequent comorbidity in patients with ICH. Associations of RD with hypertension and with CMB in deep location suggest a predominant impact of RD on deep rather than on lobar microangiopathy. [ABSTRACT FROM AUTHOR]

Background and purpose: Perihematomal edema exacerbates the mass effect of hematoma and contributes to early neurological deterioration after intracerebral hemorrhage (ICH). Oxygen therapy has protective effects on the blood-brain barrier (BBB). We aimed to examine the effects of oxygen therapy on edema formation and BBB permeability after ICH. Methods: ICH was induced in mice by injecting autologous blood (30 µL) or collagenase (0.03 U) intrastriatally. Development of posthemorrhagic edema formation and BBB disruption was characterized by wet-dry-weight assays and sodium- fluorescein fluorospectrometry 1d, 3d, and 7d after ICH induction. In subsequent experiments, mice received air, normobaric (NBO), or hyperbaric oxygen (HBO; 3ata) for 60 min starting either 30, 60, or 120 min after ICH induction. Expression of occludin, claudin-5, zonula occludens-1, matrix metalloproteinases (MMPs), and hypoxia-inducible factor-1α (HIF-1α) was measured by Western blot and zymography. Results: Posthemorrhagic edema formation (water content: blood-injection model 80.6 ± 0.3 %; collagenase injection model 83.3 ± 0.7 %) and BBB disruption (interhemispheric ratio of extravasated sodium fluorescein: blood-injection model 1.75 ± 0.07; collagenase injection model 3.02 ± 0.15) peaked 3d after ICH. NBO and HBO initiated within 30 min of ICH induction attenuated edema formation and BBB disruption (interhemispheric ratio of fluorescein; blood-injection air 1.75 ± 0.12, NBO 1.52 ± 0.08, HBO 1.49 ± 0.09; collagenase: air 3.04 ± 0.23, NBO 2.25 ± 0.21, HBO 2.17 ± 0.23) 3d after ICH, whereas delayed oxygen therapy had no effect. Early oxygen therapies prevented occludin degradation, MMP-9 activation, and reduced HIF-1α expression. Conclusion: Very early oxygen therapy can attenuate edema formation and BBB disruption after ICH, but the brief therapeutic time window suggests that the translational potential is limited. [ABSTRACT FROM AUTHOR]

Dementia and atrial fibrillation (AF) are common comorbidities in stroke patients. The potential role of AF in cognitive impairment prior to a first stroke has yet not been characterized. The aim of our study was to evaluate the prevalence of prestroke cognitive impairment in stroke patients, and to identify whether AF is associated with prestroke cognitive impairment. In this prospective, single-center, explorative, observational study, consecutive patients with first ever transient ischemic attack (TIA), ischemic (IS) or hemorrhagic stroke (ICH) were included. For each patient cardiovascular risk factors and the National Institutes of Health Stroke Scale were recorded. Cognitive status prior to the stroke/TIA was assessed using the informant questionnaire on cognitive decline in the elderly (IQCODE). AF was diagnosed according to a standardised procedure that included the documented medical history, ECG upon admission, 24-h Holter-ECG, continuos ECG monitoring, and was categorized into paroxysmal and persistent. Logistic regression analysis was used to evaluate association of AF and prestroke cognitive impairment. A total of 788 patients were enrolled in our study. Of these, 548 (69.5 %) had an IS, TIA was present in 168 (21.3 %) and ICH in 72 (9.1 %) patients. Mean IQCODE was 3.1 (SD 0.4). Prestroke cognitive impairment (IQCODE ≥3.44) was detected in 96 (12.5 %) patients. Of these, 33 patients (4.3 %) were demented before the actual stroke event. AF was independently associated with prestroke cognitive impairment. Patients with an acute stroke frequently show a history of cognitive impairment before the event. AF is independently associated with prestroke cognitive impairment. [ABSTRACT FROM AUTHOR]

Background: As intravenous thrombolysis frequently fails to recanalize occluded proximal intracerebral arteries, interventional recanalization therapy is increasingly being considered as treatment option in acute ischemic stroke patients. The optimal periprocedural patient management for these interventions is currently unknown. The aim of this study was to identify factors delaying door-to-treatment times, and to evaluate the effect of a fast-track intubation standard operating procedure (I-SOP) on door-to-angiography time. Methods: First, we retrospectively reviewed records of 48 acute stroke patients who were treated by interventional recanalization of intracranial occlusions between 2006 and 2009 at our institution. Time to angiography was defined as time from hospital admission to the beginning of the angiographic procedure. Second, an I-SOP for fast-track intubation was implemented and effects on door-to-angiography time were prospectively analyzed in 23 consecutive patients. Results: In the retrospective dataset ( n = 48), the mean door-to-angiography time was 2.2 ± 0.1 h (mean ± SEM). A clinically relevant time loss attributable to the intubation procedure was suggested by a 51 ± 21 min shorter door-to-angiography time for patients already intubated prior to admission ( P = 0.0189). Additional factors associated with a prolonged door-to-angiography time were: door-to-diagnosis time ( P < 0.001), onset-to-door time ( P = 0.0117), and male gender (mean difference +27 ± 15 min, P = 0.0822). In the prospective dataset ( n = 23), I-SOP implementation reduced mean door-to-angiography time by 25 ± 10 min ( P = 0.0164). Conclusions: In acute stroke patients, intubation prior to interventional recanalization therapy can delay treatment initiation. The implementation of an I-SOP accelerates interventional treatment initiation. [ABSTRACT FROM AUTHOR]

Background: Patients with extensive brain infarcts are at increased risk for stroke-associated respiratory tract infections (SARTI), which cause worse outcome. The benefit of general antibiotic prophylaxis is controversial. Early diagnosis of SARTI may improve patient selection for antimicrobial therapy. Procalcitonin (PCT) is widely recognized as serum marker for bacterial infections. Its diagnostic value with respect to SARTI has not been assessed systematically. Methods: Serum PCT levels were analyzed in ischemic stroke patients ( n = 50) at day 1 (d1) and day 4 (d4) after stroke onset. PCT test performance was assessed by receiver operator characteristics (ROC) curve analysis. Multivariable logistic regression analysis was applied to identify early predictors for SARTI. Results: Higher d4 serum PCT levels were associated with SARTI; ROC curve analysis revealed an area under the curve (AUC) of 0.79 (95%-confidence interval (CI) 0.61-0.96). A 0.25-ng/ml cutoff resulted in a test sensitivity and specificity of 42 and 96%, respectively. Positive (LR+) and negative (LR−) likelihood ratios were 10.8 and 0.6, respectively. In predicting SARTI, multivariable logistic regression analysis controlling for infarct volume ruled out an independent explanatory effect of serum PCT. Greater infarct volume (odds ratio (OR) 1.06, 95%-CI 1.02-1.1) prevailed as independent SARTI-predictor. Conclusions: In the absence of clinical signs, post-stroke screening for SARTI using serum PCT levels is not useful since test sensitivity is low. If the clinical suspicion for SARTI is strong, serum PCT-testing (>0.25 ng/ml) may improve diagnostic accuracy by improving specificity. [ABSTRACT FROM AUTHOR]

Background: Emergency reversal of the international normalized ratio (INR) in patients who develop nontraumatic subdural hemorrhage (SDH) due to oral anticoagulants (OAC) represents a primary treatment strategy but it is difficult to predict the amount of prothrombin complex concentrate (PCC) needed for reversal treatment. Moreover, repeated INR testings in central laboratories (CL) are time consuming. The usefulness of point-of-care INR coagulometers (POC) to test the success of INR reversal in OAC-SDH has not yet been investigated. Methods: Prospectively, INR reversal was performed by administering PCC to patients suffering from acute SDH-OAC using a predefined dosing schedule. Accuracy and time gained by using POC were assessed and compared with CL measurements. Results: A total of 10 patients were treated according to the protocol (male: 5). Bland-Altman analysis between POC and CL revealed a mean INR deviation of 0.013 for initial INR values and of 0.081 during reversal treatment. Using POC, the median initial net time gain (accounting for clinical examination and CT) for the start of PCC was 21 min. Median total time for POC-documented reversal was 27 min, as compared to 70 min for CL. The shortest interval between head CT and start of emergency SDH evacuation surgery was 37 min. By employing stepwise POC-guided reversal of the anticoagulatory effect of OAC, the calculated PCC dose could be reduced by 25% in the median. Conclusions: Using POC to measure INR values and patient-adapted PCC administration is a fast and economic method to reverse anticoagulation in patients with acute OAC-SDH. [ABSTRACT FROM AUTHOR]

Systemic and local inflammatory processes have a key, mainly detrimental role in the pathophysiology of ischemic stroke. Currently, little is known about endogenous counterregulatory immune mechanisms. We examined the role of the key immunomodulators CD4+CD25+ forkhead box P3 (Foxp3)+ regulatory T lymphocytes (Treg cells), after experimental brain ischemia. Depletion of Treg cells profoundly increased delayed brain damage and deteriorated functional outcome. Absence of Treg cells augmented postischemic activation of resident and invading inflammatory cells including microglia and T cells, the main sources of deleterious cerebral tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), respectively. Early antagonization of TNF-α and delayed neutralization of IFN-γ prevented infarct growth in Treg cell–depleted mice. Intracerebral interleukin-10 (IL-10) substitution abrogated the cytokine overexpression after Treg cell depletion and prevented secondary infarct growth, whereas transfer of IL-10–deficient Treg cells in an adoptive transfer model was ineffective. In conclusion, Treg cells are major cerebroprotective modulators of postischemic inflammatory brain damage targeting multiple inflammatory pathways. IL-10 signaling is essential for their immunomodulatory effect. [ABSTRACT FROM AUTHOR]

Introduction: Dysautonomia is a characteristic finding in Guillain-Barré syndrome (GBS). Sinus tachycardia, blood pressure instability, sustained hypertension or hypotension, cardiac arrhythmias, sweating abnormalities, gastrointestinal or urogenital symptoms, and neurogenic stunned myocardium have been previously described in patients with GBS. To our knowledge, increased intrapulmonary shunts in association with GBS have not yet been reported.Methods: We present a case of GBS with severe dysautonomia associated with clinical relevant intrapulmonary shunts. Autonomic functions were tested using baroreflex sensitivity and heart rate variability measures. Intrapulmonary shunts were calculated according to the Berggren formula.Results: Autonomic functions showed excessive sympathetic activation. Intrapulmonary shunts were increased up to six times compared to the norm. Other causes of increased intrapulmonary shunts, such as sepsis, pulmonal or cardiac complications, were excluded during hospitalization.Conclusion: Intrapulmonary shunts in GBS may relate to sympathetic overactivation and should be anticipated in GBS patients with unexplained respiratory deterioration. [ABSTRACT FROM AUTHOR]

Purpose of Review: A novel permanent carotid filter device for percutaneous implantation was developed for the purpose of stroke prevention. In this review, we cover rationale, existing preclinical and clinical data, and potential future directions for research using such a device. Recent Findings: The Vine™ filter was assessed for safety in sheep and in 2 observational human studies, the completed CAPTURE 1 (n = 25) and the ongoing CAPTURE 2 (planned n = 100). CAPTURE 1 has shown high procedural and long-term implant safety. A control group was not available for comparison. Summary: A mechanical filter for permanent stroke prevention can be implanted bilaterally in the common carotid artery safely and efficiently. A randomized trial is planned for 2021 (n = 3500, INTERCEPT) to demonstrate superiority of a filter + anticoagulation strategy over anticoagulation alone in patients at high risk for ischemic stroke. [ABSTRACT FROM AUTHOR]

A letter to the editor about a 46-year-old female patient with acute and regenerated brachial plexus pressure palsy is presented.

The article presents a study on the safety of intravenous thrombolysis in patients with acute ischaemic stroke who receives warfarin, conducted by Mazya and colleagues. It says that the findings confirmed the guidelines from American Heart Association (AHA), that thrombolysis in patients with an international normalized ratio (INR) 1.7 who are receiving vitamin K antagonists (VKA) is safe in patients who does not receive anticoagulants. It mentions the tissue plasminogen activator (tPA).

Recent clinical and experimental studies have highlighted a complex role for the immune system in the pathophysiological changes that occur after acute stroke. Sensors of the innate immune system such as Toll-like receptors, or effectors such as the lectin pathway of complement activation and innate immune cells, are activated by brain ischaemia and tissue damage, leading to amplification of the inflammatory cascade. Activation of the adaptive arm of the immune system, mediated by lymphocyte populations including T and B cells, regulatory T cells, and γδT cells, in response to stroke can lead to deleterious antigen-specific autoreactive responses but can also have cytoprotective effects. Increased incidence of infections is observed after acute stroke, and might result from activation of long-distance feedback loops between the CNS and peripheral immune organs, which are thought to play a part in stroke-induced immunodepression. Ongoing clinical trials are investigating whether the preventive use of antibiotics improves functional outcome after stroke. This Review discusses the multifaceted role of the immune system in the pathophysiology of acute stroke. [ABSTRACT FROM AUTHOR]