Spontaneous non-aneurysmal subarachnoid haemorrhage (NAPMSAH) (addressing point 1) is a relatively rare occurrence in clinical settings as it is rarely misdiagnosed and usually involves a significantly better prognosis than the classical aneurysmal pattern. We hereby focused on a comprehensive analysis of this distinct pathological entity with the purpose of analysing possible pathophysiological entities, outcomes and treatment options involving this diagnosis with a focus on demographical, epidemiological and clinical data. The clinical setting includes focal neurological signs related to the anatomical structures, while computer tomography followed by tomographic angiography are the most common diagnosis tools, with a typical hyperdense lesion involving the midbrain, fourth ventricle and subthalamic areas without an angiographic correspondent, such as an aneurysmal pathology. Further investigations can also be used to highlight this diagnosis, such as interventional angiography or magnetic resonance imaging. Given the rarity of this condition and its relatively better prognosis, treatment options usually remain conservative. In the present review, the main characteristics of NAPMSAH are discussed.

Background: Spontaneous intracerebral hemorrhage (ICH) has the highest case fatality of all stroke types, yet recent epidemiological and outcome data from Central and Eastern Europe remain limited. Methods: We retrospectively analyzed prospectively collected data for 601 consecutive adults with primary ICH admitted to Sibiu County Clinical Emergency Hospital, Romania (2017–2023). Demographics, Glasgow Coma Scale (GCS), CT-derived hematoma volume (ABC/2), anatomical site, intraventricular extension (IVH), treatment, comorbidities, and in-hospital death were reported with exact counts and percentages; no imputation was performed. Results: Mean age was 68.4 ± 12.9 years, and 59.7% were male. Mean hematoma volume was 30.4 mL, and 23.0% exceeded 30 mL. IVH occurred in 40.1% and doubled mortality (50.6% vs. 16.7%). Overall case fatality was 29.6% and climbed to 74.5% for brain-stem bleeds. Men, although younger than women (66.0 vs. 71.9 years), died more often (35.4% vs. 21.1%; risk ratio 1.67, 95% CI 1.26–2.21). Systemic hazards amplified death risk: Oral anticoagulation, 44.2%; chronic alcohol misuse, 51.4%; thrombocytopenia, 41.0%; chronic kidney disease, 42.3%. Conservative management (74.9%) yielded 27.8% mortality overall and ≤15 for small-to-mid lobar or capsulo-lenticular bleeds; lobar surgery matched this (13.4%) only in large clots. Thalamic evacuation was futile (82.3% mortality), and cerebellar decompression performed late still carried 54.5% mortality versus 16.6% medically. Multivariable analysis confirmed that low GCS, IVH, large hematoma volume, thrombocytopenia, and chronic alcohol use independently predicted in-hospital mortality. Limitations: This retrospective study lacked post-discharge functional outcome data (e.g., mRS at 90 days). Conclusions: This study presents the largest Romanian single-center ICH cohort, establishing national benchmarks and underscoring modifiable risk factors. Early ICH lethality aligns with Western data but is amplified by exposures such as alcohol misuse, anticoagulation, thrombocytopenia, and CKD. Priorities include preventive strategies, timely surgical access, wider adoption of minimally invasive techniques, and development of a prospective regional registry.

Cervical artery dissections (CAD) are a common cause of ischemic cerebrovascular events among the younger and middle-aged population. Altogether, CAD counts for up to 15% of all causes of stroke in patients aged 50 or younger. Among the known etiological causes, especially addressing the younger population with mechanical traumas and whiplash injuries are regarded as the main culprits. However, cases of spontaneous dissection are also widespread, with risk factors such as hypertension, migraine, and lifestyle factors increasing the risk of occurrence. Clinically, the symptoms associated with a cerebrovascular event caused by CADs are highly variable and can be classified as either compressive symptoms (such as Horner’s syndrome and cervical pain) or stroke syndromes attributable to cerebral ischemia. Therefore, establishing an early diagnosis might be particularly challenging as it requires particular attention and quick clinical reasoning when interviewing the patient. With these certain particularities, our main focus was to conduct a prospective study involving up to 54 patients who were diagnosed with CAD in our clinical facility between January 2015 and December 2022, with the focus of assessing certain individual parameters attributable to each patient and their influence and prognosis value for their short and long term evolution. An important emphasis was placed on parameters such as topographical localization, clinical presentation, severity of the questioned cerebrovascular event, outcomes, and causative factors. Statistical validity tools were applied when possible.

Background: MicroRNA-150 (miR-150) plays a critical role in immune regulation and has been implicated in autoimmune diseases like Multiple Sclerosis (MS). This review aims to evaluate miR-150’s potential as a biomarker for MS, necessitating this review to consolidate current evidence and highlight miR-150’s utility in improving diagnostic accuracy and monitoring disease progression. Methods: A comprehensive literature search was conducted in databases like PubMed, Scopus, Google Scholar, SciSpace, MDPI and Web of Science, adhering to PRISMA guidelines. Studies focusing on miR-150 implications in MS were included. Data extraction was conducted, while quality assessment was done using the NOS and AMSTAR 2 tools. With the extracted data a statistical analyses conducted. Results: 10 eligible articles were included in review. Findings show that miR-150 levels were consistently deregulated in MS patients compared to healthy controls, correlating with disease severity and clinical parameters such as (EDSS) scores and disease activity. Additionally, miR-150 is implicated in the inflammatory pathogenesis of MS, affecting immune cell regulation and inflammatory pathways. Conclusions: MiR-150 is a promising biomarker for MS, showing significant potential for improving diagnostic accuracy and monitoring disease progression. Its consistent deregulation in MS patients and correlation with clinical parameters underscore its clinical utility. Further research should validate miR-150’s salivary presence and its possible usage as a novel biomarker and therapeutic potential in the development of MS.

Background: Multiple sclerosis and periodontal disease are chronic inflammatory conditions that may share immune-mediated mechanisms, including cytokine activation, oral dysbiosis, oxidative stress, and systemic inflammatory burden. This systematic review aimed to synthesize recent evidence on common inflammatory pathways linking periodontal disease and multiple sclerosis. Methods: The review was conducted according to PRISMA 2020 guidelines. PubMed/MEDLINE, Cochrane Library, and Scopus were searched for English-language studies published between June 2020 and June 2026. Eligible studies addressed multiple sclerosis, periodontal disease, oral microbiome alterations, systemic inflammation, or neuroinflammatory outcomes. Study selection and data extraction were performed independently by three reviewers. Risk of bias was assessed using AMSTAR 2, the Newcastle–Ottawa Scale, and the Joanna Briggs Institute checklist, according to study design. Results: Seventeen studies were included in the qualitative synthesis. The main shared mechanisms were cytokine-mediated inflammation involving TNF-α, IL-1β, IL-6, and IL-17; NF-κB signaling; Th17/Treg imbalance; blood–brain barrier disruption; oxidative stress; matrix metalloproteinase activity; complement activation; and oral–gut–brain axis dysregulation. The evidence suggests that periodontal inflammation may contribute to systemic immune activation and may amplify neuroinflammatory processes in multiple sclerosis. Conclusions: Current evidence supports a biologically possible association between periodontal disease and multiple sclerosis through shared inflammatory and microbial pathways. However, causality remains unproven, and further longitudinal and interventional studies are needed.

Background: Parenchymal fluid-attenuated inversion recovery (FLAIR) hyperintensity within an acute diffusion-weighted imaging (DWI) lesion is a marker of ischemic tissue evolution, but whether it identifies patients at higher risk of hemorrhagic transformation after mechanical thrombectomy (MT) is uncertain. Methods: We conducted a structured narrative review of cohort studies relating pretreatment lesion FLAIR signal to hemorrhage after reperfusion therapy. Four PubMed searches (1051 unique records) were supplemented by reference-list screening. Studies were classified by treatment, FLAIR construct and hemorrhage endpoint, and synthesized by direction and precision of effect without pooling. Results: Eleven cohort studies (49–412 patients each; 1726 in total) and one meta-analysis were included; four were MT or MT-predominant cohorts. The point estimate favored more hemorrhage with FLAIR positivity in nine studies. Associations were consistent for any hemorrhage, which is dominated by hemorrhagic infarction (59% vs. 39% in an MT cohort; odds ratio 20.0 in an intravenous-thrombolysis cohort imaged within 3 h). For parenchymal hematoma and symptomatic hemorrhage, three studies reported significant associations, whereas the largest MT cohort (n = 412) found no significant difference in parenchymal hematoma type 2 (10.7% vs. 6.8%, p = 0.193), and four further cohorts reported null or near-null estimates. No study isolated early-onset M1-occlusion patients with near-complete reperfusion. Conclusions: The evidence is directionally consistent but imprecise and does not show that FLAIR positivity independently predicts clinically important hemorrhage after MT. FLAIR positivity alone should not be used to withhold MT. Adequately powered studies with standardized FLAIR reading and separately reported parenchymal hematoma and symptomatic hemorrhage are needed.