Objective:The treatment of carotid artery stenosis (CAS) for stroke prevention is a matter of debate due to conflicting data, missing recent data, and advances in medical treatment options but also in interventional techniques and surgery. Therefore, the establishment of an easily available marker for brain damage might be a key tool in this patient group to guide treatment. Methods:A retrospective cross-sectional study was conducted leveraging a vascular surgery biobank of 95 patients aged 60 to 80 years. Serum neurofilament light chain (sNfL) and serum glial fibrillary acid protein (sGFAP) were evaluated using highly sensitive electrochemiluminescence immunoassays and z-scores. Discriminatory performance was assessed to differentiate between 19 symptomatic and 76 asymptomatic patients with CAS and their correlation with the degree of stenosis according to ultrasound-based North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria. Results:SNfL levels were markedly elevated in symptomatic compared with asymptomatic patients (median 17.4 vs 3.8 pg/mL; P < .001). sNfL robustly discriminated between these patients (area under the curve = 0.83; 95% confidence interval, 0.72-0.94), as did the NfL z-score (area under the curve = 0.83; 95% confidence interval, 0.71-0.95). Interestingly, within the asymptomatic cohort, sNfL levels demonstrated a significant, positive correlation with the degree of stenosis (Spearman's ρ = 0.24; P = .036). Serum levels of SGFAP were also associated with symptomatic status, albeit with a P-value >.05 (0.1 vs 0.1 pg/mL; (P = .057). Conclusions:The study provides evidence of increased sNfL in symptomatic vs asymptomatic CAS and, of note, of ongoing neuronal or glial damage in some patients with clinically asymptomatic CAS, with a positive correlation between sNfL and the degree of CAS. sNfL is a promising and already accessible blood biomarker that may guide therapeutic decisions in this patient population. The role of sGFAP remains elusive and must be evaluated in larger studies. Clinical Relevance:The CREST-2 trial has recently highlighted the high efficacy of intensive medical management in asymptomatic carotid artery stenosis (CAS), making the selection of patients for revascularization increasingly complex. Our study addresses this challenge by evaluating serum neurofilament light chain (sNfL) and serum glial fibrillary acid protein (sGFAP) as an objective biomarker for neuronal injury. Using individualized z-scores, we demonstrate that sNfL effectively differentiates symptomatic status (area under the curve = 0.828) and significantly correlates with the degree of stenosis in asymptomatic cohorts. These results suggest that sNfL can detect subclinical "silent" damage, providing a valuable biological tool to pinpoint high-risk patients who may require intervention beyond medical therapy alone. This represents a significant step toward personalized stroke prevention and refined risk stratification in the highly debated field of CAS management.

Background:Timely reperfusion offers the greatest benefit in acute ischaemic stroke within the first hour after onset. However, geographic disparities in stroke care access persist across Germany. Despite the potential of telemedicine and mobile stroke units, nationwide data that quantify existing care gaps or systematically investigate the benefit of early imaging with subsequent thrombolysis in locally accessible, CT-equipped hospitals with telemedicine are lacking. This study modelled nationwide access and compared direct transfer to specialised hospitals with a hub-and-spoke strategy (nearest CT plus telemedicine) for early thrombolysis. Methods:We performed a cross-sectional geospatial analysis combining national facility registries and 2023 hospital quality reports (data collected February 1st-July 23rd, 2025). We mapped German CT-equipped hospitals (n = 1475), stroke-ready hospitals (≥100 annual cases of "complex neurological treatment of acute stroke", n = 463) and certified stroke units (n = 349). For these facilities we modelled driving-time access up to 60 min in 5-min intervals using a local installation of openrouteservice, overlaying these on population and settlement grids. Additional scenarios simulated variations in ambulance speed (default: standard openrouteservice vehicle speed) or additional in-hospital delays when using a hub-and-spoke scenario. We then compared hub-and-spoke versus direct transfer to specialised hospitals on a national, state- and county-level. Findings:Within 30 min, nearly all residents (82,484,915/83,420,000; 98.9%) could reach a CT-equipped hospital, 90.0% (75,051,793) a stroke-ready hospital, but only 85.0% (70,875,055) a certified stroke unit. Compared with direct transfer to a stroke unit, a hub-and-spoke pathway would let 36.4% of inhabitants start imaging ≥10 min sooner (assuming normal speed, other scenarios varying from 4.5% to 40.0%) and for 14.2% it could save ≥20 min (varying from 1.1% to 18.2% across scenarios). Estimated benefits of a hub-and-spoke model depended on assumed driving speed and declined with simulated CT delays. Rural regions had particularly pronounced access gaps to stroke care, as evidenced by lower levels of urbanisation in regions with a higher hub-and-spoke benefit potential. State-level analysis illustrated heterogeneity, with 48.6% of inhabitants potentially benefitting from a hub-and-spoke model in Saxony-Anhalt, but <5% in city-states (assuming normal driving speed and 10-min delay). Interpretation:Marked intra-national inequities in rapid accessibility to stroke care persist. Leveraging CT-equipped hospitals with telemedicine could enable timelier thrombolysis within a hub-and-spoke model. Open questions regarding implementation and economics should be investigated. Funding:University Hospital Düsseldorf, the B. Braun Foundation, and the Ministry of Economic Affairs, Innovation, Digitalization and Energy of the State of North Rhine-Westphalia (funding number 005-2008-0055).

Background Acute confusional migraine (ACM) is a rare migraine variant, primarily documented in paediatric populations. Its presentation in geriatric patients is extremely rare and can mimic acute ischemic stroke. Case We report on an 84-year-old male presenting with acute hemicrania followed by confusion and dysarthria. Despite initial systemic thrombolysis for suspected stroke, symptoms only resolved after sleep. Extensive diagnostics were unremarkable, leading to the diagnosis of ACM based on a 20-year history of stereotyped attacks. Conclusion This case represents the oldest reported patient with ACM to date. It highlights the importance of including ACM in the differential diagnosis of stroke mimics in the elderly to avoid unnecessary interventions.

Stroke is a common risk among patients with cancer, and the odds of a fatal stroke are estimated to be twice those of the general population. Due to the exclusion of cancer patients from major intravenous thrombolysis and thrombectomy trials, existing literature consists largely of small case series lacking sufficient statistical power. We aimed to evaluate the safety profile of acute stroke therapies in patients with active cancer, stratified by cancer localization, using a nationwide administrative dataset. This retrospective, large-scale cohort study utilized data from the German Federal Statistical Office (DESTATIS). We analyzed all inpatient cases of acute ischemic stroke receiving recanalization therapy (intravenous thrombolysis and endovascular thrombectomy) in Germany. The primary endpoints were in-hospital mortality and safety outcomes (intracranial bleeding, subarachnoid hemorrhage, and acute anemia). To control for baseline characteristics, adjusted odds ratios (aOR) were calculated using multivariable logistic regression. We analyzed 154,333 patients receiving intravenous thrombolysis (2482 with and 151,851 without cancer) and 39,534 receiving endovascular thrombectomy (1580 with and 37,954 without cancer). In the thrombolysis cohort, patients with cancer had significantly higher rates of in-hospital death (10.88

The evidence-based acute treatment of stroke patients in Germany is carried out according to standardized algorithms in more than 300 certified stroke units, and its quality is repeatedly assured by the German Stroke Society (DSG) and others. However, nationally structured and uniform stroke aftercare programs are missing, despite evidence that they contribute to the success of rehabilitation and improvement of everyday life. We used a 27-item online questionnaire, which was mailed to 4,195 outpatient physicians in the catchment area of the neurovascular network Neurovascular Network North Rhine plus (NEVANO+) located in the western part of Germany to assess actual structures of stroke aftercare, identify barriers, and possible solutions. Based on 152 completed anonymous answers to the questionnaire, a descriptive evaluation revealed that general practitioners and neurologists are seen to be responsible for stroke aftercare. Important improvement aspects, among others, were identified in intersectoral cooperation, the use of a post-stroke checklist, and connections to local self-help organizations. Stroke units could play a key role in stroke aftercare by providing these checklists, connecting self-help organizations, and offering education and coaching for supportive coordinating staff. Furthermore, existing neurovascular networks can be expanded to include rehabilitation clinics, geriatric clinics, and outpatient physicians to improve intersectoral communication, collaboration, and post-stroke care. Further studies should investigate whether intersectoral cooperation, checklists, and cooperation with self-help organizations within an extended neurovascular network have a positive impact on stroke aftercare and patients’ quality of life.

Cerebral small vessel disease (CSVD) often coexists with neurodegenerative pathologies, yet their role remains underexplored. This study aims to determine their prevalence, risk factors, and cognitive effects in patients with deep perforator arteriopathy (DPA) or cerebral amyloid angiopathy (CAA) using the biomarker-based ATN classification. In this cross-sectional study 186 patients (median age 75 years, 41

To investigate the feasibility of Retrieval-augmented Generation (RAG)-enhanced Large Language Models (LLMs) in answering questions about two German neurovascular guidelines. Four LLMs (GPT-4o-mini, Llama 3.1 405B Instruct Turbo, Mixtral 8 × 22B Instruct, and Claude 3.5 Sonnet) with RAG as well as GPT-4o-mini without RAG were evaluated for generating answers about two German neurovascular guidelines (“S3 Guideline for Diagnosis, Treatment, and Follow-up of Extracranial Carotid Stenosis” and “S2e Guideline for Acute Therapy of Ischemic Stroke”). The answers were classified as “correct”, “inaccurate”, or “incorrect” by two neurovascular experts in consensus. Additionally, retrieval performance of five retrieval strategies was analyzed on a synthetic dataset of 384 questions. Claude Sonnet 3.5 achieved the highest answer correctness (70.6

For the last 38 years, all neuroprotective agents for patients with ischemic stroke have failed in clinical trials. The innate immune system, particularly microglia, is a much-discussed target for neuroprotective agents. Promising results for neuroprotection by inhibition of integrins with drugs such as natalizumab in animal stroke models have not been translated into clinical practice. Our present study reveals the relevance of a β2 integrin, lymphocyte function-associated antigen-1 (LFA-1), as a potential key player in protecting neuronal cell death after oxygen-glucose deprivation in organotypic hippocampal cell cultures. In addition, we identified microglial cells as effector cells for LFA-1-mediated neuroprotection. The counterpart of LFA-1 on microglia is unclear, but we show strong expression of ICAM-5 in hippocampal neurons, suggesting a critical role for direct crosstalk between microglia and neurons for neuronal survival under oxygen-glucose deprivation. The enigma of neuroprotection after ischemic stroke remains to be solved, and our findings highlight the continuing importance and lack of understanding of integrin-mediated pathways after ischemic stroke and the need for further intensive research.

This study investigates the influence of carotid artery elongation on neurovascular intervention and outcome in acute stroke treatments proposing an easily assessable imaging marker for carotid elongation. 118 patients who underwent mechanical thrombectomy for middle cerebral artery occlusions were included. The carotid elongation ratio (CER), center-line artery length to scan’s Z-axis, was measured on the affected side in CT-angiographies. Full and partial correlations of CER with periprocedural times, complications and outcome were computed. Multivariate logistic regression, including comorbidities, for prediction of dichotomized mRS outcome after 3 months was performed. CER showed no significant correlation with recanalization success. Weak, outlier-driven correlation was found with recanalization time (p = 0.021, cor = 0.2). Weak correlations were found with improvement of NIHSS score at discharge and mRS score after 3 months (p = 0.023 and p = 0.031, each rho=-0.2). There was moderate correlation with NIHSS score at discharge (p = 0.001, rho = 0.3). Patients with favorable outcomes (mRS 0–2) exhibited lower CER (p = 0.012). Partial correlations of CER with favorable outcomes were observed after correcting for age, sex and cardiovascular risk factors (cor = 0.2, p = 0.048). Multivariate analysis (Nagelkerke’s R2 = 0.42) identified NIHSS score at admission, diabetes, hypertension and intervention time as significant factors for predicting outcome at 3 month, while CER showed the highest log Odd’s (2.97). Correlations between CER and clinical improvement suggest that carotid elongation might be a risk factor for poorer outcome without relevant effect on endovascular treatment and should not guide treatment decisions. Further studies should consider carotid elongation as an individual neurovascular risk factor, independent of hypertension. •The study investigates the influence of carotid elongation on endovascular stroke treatment and outcome. •There is correlation between carotid elongation and clinical improvement. However, no relevant effect on endovascular treatment was found. •Carotid elongation should not dictate acute stroke treatment. Rather it should be considered as an individual neurovascular risk factor.

To survive and thrive in our ever-changing environment, we need to be able to predict the consequences of our actions. We update these predictions by learning through trial and error, and associated prediction errors (PEs). Recent rodent data suggest that the cerebellum – a region typically associated with processing sensory PEs in supervised error-based learning – also processes PEs in reinforcement learning (RL-PEs; i.e., learning from action outcomes). A proxy of action outcome processing in regions traditionally associated with RL-PE coding, such as striatum and anterior cingulate cortex, can be measured in a component of the feedback-locked event-related potential (ERP), i.e., the feedback-related negativity (FRN). We tested the hypothesis that cerebellar output is necessary for this RL-PE coding in the FRN in a probabilistic feedback learning task. In that case, altered cerebellar output should result in changes in the FRN. Two complementary experiments were performed. First, patients with chronic cerebellar stroke were tested. Second, single-pulse cerebellar transcranial magnetic stimulation (TMS) was applied in healthy participants, thus implementing a virtual lesion approach. Different from controls and control (vertex) TMS, no significant RL-PE processing was observed in the FRN in patients with cerebellar stroke, and in participants receiving cerebellar TMS. Only minor deficits in behavioural flexibility were found, with learning success preserved, possibly due to compensation by other brain areas within the reinforcement learning network. Findings in both experiments show that frontal RL-PE processing depends on cerebellar output. Our results provide evidence for involvement of the cerebellum in processing of RL-PEs in humans, complementing and extending previous findings in rodents.

Aneurysmal subarachnoid hemorrhage (aSAH) is a highly fatal and morbid disease. Despite successful coiling or clipping of a ruptured aneurysm, the patients suffer post-aSAH complications, including early brain injury, cerebral vasospasm (CVS), delayed cerebral ischemia (DCI), and systemic infections that mainly determine the clinical outcomes. Diagnostic biomarkers to predict accurately post-aSAH complications are needed. In this prospective exploratory study, we investigated the predictive value of neutrophil extracellular traps (NETs) components for CVS after aSAH. In the study, 62 patients with aSAH, 17 patients with unruptured cerebral aneurysms, and 12 healthy controls were included. The serum levels of myeloperoxidase (MPO), elastase (ELA), and citrullinated histone H3 (cH3) on day 1 and day 4 of hospital admission were measured with ELISA. Data were scaled using the Yeo-Johnson transformation. Values in two groups were compared using a t-test and in multiple groups using ANOVA. Logistic regression was used to model the outcome probability, including CVS, as the function of ELISA values. Among the patients with aneurysms, those who suffered aSAH had significantly higher levels of MPO (113.9 ± 294.4 vs. 422.3 ± 319.0 ng/ml, p < 0.05), ELA (84.8 ± 221.0 vs. 199.2 ± 218.9 ng/ml, p < 0.05), and cH3 (0.0 ±0.0 vs. 2.8 ±1.5, ng/ml, p < 0.05) on day one after aSAH, suggesting the involvement of NETs components in pathophysiology of aSAH and the events following aSAH. Individually, MPO and ELA levels taken on day 1 after SAH did not differ between patients with CVS and patients without CVS. However, when taken together into a logistic model, they allowed for predicting CVS with high sensitivity (91%) and specificity (79%). MPO and ELA, along with other clinical parameters, can be used as early predictors of CVS in aSAH patients and can serve as guidance during treatment decisions in the management of aSAH.

Background: Co-occurrence of cerebral small vessel disease (CSVD) is common in aging and Alzheimer disease (AD) dementia, but, in symptomatic CSVD prevalence and role of AD and neurodegenerative co-pathologies have been less explored. Methods: In vivo determination of prevalence, predictors and relevance for cognition of AD and neurodegenerative co-pathologies in symptomatic CSVD, including deep perforator arteriopathy (DPA) and cerebral amyloid angiopathy (CAA), utilizing cerebrospinal fluid (CSF) biomarkers. Cross-sectional study from October 2010 to September 2021 of participants with magnetic resonance imaging (MRI) and CSF biomarkers (amyloid-beta 42/40 ratio, phosphorylated-tau, total-tau, neurofilament light). Biomarker levels were compared among groups; prevalence of ATN classification subtypes was estimated and related to clinical phenotype, CSVD MRI markers and global cognition. Results: The study comprised 229 individuals (median age 74 years; 47% females), 70 with AD dementia, 79 with probable CAA, 62 with DPA patients and 18 healthy controls. Participants were categorized based on the ATN classification: normal biomarkers (A-T-N-), AD pathology continuum (A+), and non-AD pathological changes, including primary age-related tauopathy (PART, A-T+N+) or isolated neurodegeneration (A-T-N+). Of 141 CSVD patients, 43 (30%) were A-T-N-, 39 (28%) A+, with lower prevalence in DPA than CAA (15% vs. 38%, p = .003), 18 (13%) A-T+N+, and 41 (29%) A-T-N+, with higher prevalence in DPA than CAA (42% vs. 19%, p = .002). A+ was associated with increasing age, female sex, lobar hemorrhages and low burden of deep white matter hyperintensities and lacunes. A-T-N+ was related to younger age, symptomatic stroke and lacunes. A-T+N+ had no specific predictors, except advanced age. Each pathological ATN profile was independently related to lower Mini Mental State Examination scores (A+: B = -2.7, p = .013; A-T+N+: B = -4.6, p = .002; A-T-N+: B = -2.3, p = .034), accounting for demographics, clinical phenotype and MRI CSVD severity. Conclusions: Using biomarkers, this study confirms in vivo that CSVD frequently co-occurs with AD or neurodegenerative pathologies, exerting independent effects on cognitive health. As disease-modifying therapies emerge, integrating interacting biomarkers will be crucial for the selection of patients with the greatest benefit.### Competing Interest StatementThe authors have declared no competing interest.### Funding StatementThis work was funded by the Deutsche Alzheimer Gesellschaft e.V. (DAlzG) and the Foerderstiftung Dierichs (www.foerderstiftung-dierichs.de) (MD‑DARS project) and by the German Research Foundation (GRK SynAge 2413). PA received a research scholarship by the Medical Faculty of the Otto-von-Guericke University Magdeburg.### Author DeclarationsI confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained.YesThe details of the IRB/oversight body that provided approval or exemption for the research described are given below:The local ethic committee (Ethikkommission, Otto-von-Guericke-Universitaet Magdeburg; No. 07/17, addendum 11/2021) approved this retrospective study.I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals.YesI understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance).YesI have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable.YesThe datasets analyzed during the current study are available from the corresponding author on reasonable request.

Abstract Background The reduction of processing times in the treatment of acute ischemic stroke is of outstanding importance. Our objective is to analyze the acute stroke care chain from onset to treatment in a city in Germany comprising three stroke units. Additionally, we discuss solutions for detected treatment delays. Methods We conducted an in-depth analysis of acute stroke care processing times across three local stroke centers in Düsseldorf among all emergency services transportations for suspected stroke. Isochrone mapping was performed to identify areas with prolonged transportation times. Results Among the 1,714 transportations, 943 patients had confirmed strokes. Prehospital care constituted 58% of total emergency care time until imaging. Patients with confirmed stroke had reduced in-hospital times while patients receiving treatment experienced faster in-hospital times. Isochrone mapping revealed disparities in transportation times within the city. Conclusions In conclusion, we identified confirmation of stroke symptoms as pre- and in-hospital and treatment eligibility as in-hospital process accelerators in stroke care. We propose the introduction of an in-ambulance video consulting model to accelerate contact to stroke-experts and accelerate processing times for patients eligible for treatment. Furthermore, we discuss the combination of in-ambulance video consulting with imaging and starting treatment outside traditional stroke centers, followed by transportation to a stroke center during thrombolysis, which might further accelerate treatment in specific cases.

Stroke is a major reason for persistent disability due to insufficient treatment strategies beyond reperfusion, leading to oligodendrocyte death and axon demyelination, persistent inflammation and astrogliosis in peri-infarct areas. After injury, oligodendroglial precursor cells (OPCs) have been shown to compensate for myelin loss and prevent axonal loss through the replacement of lost oligodendrocytes, an inefficient process leaving axons chronically demyelinated. Phenotypic screening approaches in demyelinating paradigms revealed substances that promote myelin repair. We established an ex vivo adult organotypic coronal slice culture (OCSC) system to study repair after stroke in a resource-efficient way. Post-photothrombotic OCSCs can be manipulated for 8 d by exposure to pharmacologically active substances testing remyelination activity. OCSCs were isolated from a NG2-CreERT2-td-Tomato knock-in transgenic mouse line to analyze oligodendroglial fate/differentiation and kinetics. Parbendazole boosted differentiation of NG2+ cells and stabilized oligodendroglial fate reflected by altered expression of associated markers PDGFR-α, CC1, BCAS1 and Sox10 and GFAP. In vitro scratch assay and chemical ischemia confirmed the observed effects upon parbendazole treatment. Adult OCSCs represent a fast, reproducible, and quantifiable model to study OPC differentiation competence after stroke. Pharmacological stimulation by means of parbendazole promoted OPC differentiation.

Purpose Occlusions of the internal carotid artery (ICA) may be caused by dissection, embolic or macroangiopathic pathogenesis, which partially influences the treatment; however, inferring the underlying etiology in computed tomography angiography can be challenging. In this study, we investigated whether computed tomography perfusion (CT-P) parameters could be used to distinguish between etiologies. Methods Patients who received CT‑P in acute ischemic stroke due to ICA occlusion between 2012 and 2019 were retrospectively analyzed. Group comparisons between etiologies regarding the ratios of CT‑P parameters between both hemispheres for relative cerebral blood volume (rCBV), relative cerebral blood flow (rCBF), time to maximum (Tmax), and mean transit time (MTT) were calculated by one-factorial analysis of variance (ANOVA) and compared by pairwise Bonferroni post hoc tests. An receiver operating characteristics (ROC) analysis was performed if differences in group comparisons were found. Multinomial logistic regression (MLR) including pretherapeutic parameters was calculated for etiologies. Results In this study 69 patients (age = 70 ± 14 years, dissection = 10, 14.5%, embolic = 19, 27.5% and macroangiopathic = 40, 58.0%) were included. Group differences in ANOVA were only found for MTT ratio ( p = 0.003, η 2 = 0.164). In the post hoc test, MTT ratio showed a differentiability between embolic and macroangiopathic occlusions ( p = 0.002). ROC analysis for differentiating embolic and macroangiopathic ICA occlusions based on MTT ratio showed an AUC of 0.77 ( p < 0.001, CI = 0.65–0.89) and a cut-off was yielded at a value of 1.15 for the MTT ratio (sensitivity 73%, specificity 68%). The MLR showed an overall good model performance. Conclusion It was possible to differentiate between patients with embolic and macroangiopathic ICA occlusions based on MTT ratios and to define a corresponding cut-off. Differentiation from patients with dissection versus the other etiologies was not possible by CT‑P parameters in our sample.

Neuromelioidosis is a rare CNS infection caused by Burkholderia pseudomallei and is characterized by high morbidity and mortality. Our report presents the diagnostic and therapeutic approach of the first case of neuromelioidosis confirmed in Europe. A 47-year-old man with a medical history of recurrent otitis with otorrhea and fever after tympanoplasty and radical cavity revision operation on the left ear was admitted with headache, decreased level of consciousness, dysarthria, left-sided hemiparesis, and urinary incontinence. After extensive investigations including MRI, microbiological, serological, and CSF analyses, and, ultimately, brain biopsy, a diagnosis of neuromelioidosis was established. Despite antibiotic treatment, the patient showed no clinical improvement and remained in a severely compromised neurological state under mandatory mechanical ventilation. Neuromelioidosis can pose a diagnostic challenge requiring an extensive diagnostic evaluation because of its uncommon clinical and radiological presentations.

Purpose: Endovascular treatment (ET) in occlusions of the M1- and proximal M2-segment of the middle cerebral artery (MCA) is an established procedure. In contrast, ET in distal M2-occlusions has not been sufficiently evaluated yet. The purpose of this study was to assess relevant parameters for clinical outcome, efficacy, and safety of patients undergoing ET in M1-, proximal M2-, and distal M2-occlusions. Methods: One hundred seventy-four patients undergoing ET in acute ischemic stroke with an occlusion of the M1- or M2-segment of the MCA were enrolled prospectively. Non-parametric analysis of variance in 3-month mRS, TICI scale, and complication rates were performed with Kruskal-Wallis test between M1- and proximal and distal M2-occlusions. Subsequent pairwise group comparisons were calculated using Mann-Whitney U-tests. Binary logistic regression models were calculated for each occlusion site. Results: There were no significant group differences in 3-month mRS, mTICI scale, or complication rates between M1- and M2-occlusions nor between proximal and distal M2-occlusions. Binary logistic regression in patients with M1-occlusions showed a substantial explanation of variance (NR2=0.35). NIHSS (p=0.009) and Maas Score as parameter for collateralization (p=0.01) appeared as significant contributing parameters. Binary logistic regression in M2-occlusions showed a high explanation of variance (NR2=0.50) of mRS but no significant factors. Conclusions: Clinical outcome and procedural safety of patients with M2-occlusions undergoing ET are comparable to those of patients with M1-occlusions. Clinical outcome of patients with M1-occlusions undergoing ET is primarily influenced by the initial neurological deficit and the collateralization of the occlusions. By contrast, clinical outcome in patients with M2-occlusions undergoing ET is more multifactorial.

Background Japanese encephalitis is an arthropod-borne zoonotic flavivirus infection endemic to tropical and subtropical Asia. A minority of infections leads to a symptomatic course, but affected patients often develop life-threatening encephalitis with severe sequelae. Literature review Myelitis with flaccid paralysis is a rare complication of Japanese Encephalitis, which-according to our literature search-was reported in 27 cases, some of which were published as case reports and others as case series. Overall, there is a broad clinical spectrum with typically asymmetric manifestation and partly severe motor sequelae and partly mild courses. Lower limb paralysis appears to be more frequent than upper limb paralysis. An encephalitic component is not apparent in all cases Case presentation We herein add the case of a 29 year-old female who developed encephalitis and myelitis with flaccid paralysis during a long-time stay in Indonesia. Diagnostic workup in Indonesia did not clearly reveal an underlying cause. Upon clinical stabilization, the patient was evacuated to her home country Germany, where further diagnostics confirmed Japanese encephalitis virus as the causative agent. The patient has partly recovered, but still suffers from residual paralysis of the upper limb. Conclusion Flaccid paralysis is a rare, and likely underdiagnosed complication of Japanese encephalitis, which, to the best of our knowledge, has never been diagnosed outside endemic areas before.