Search Results (688)

Exposure to blast waves without kinetic, penetrating, thermal, or toxic components causes a distinct form of traumatic brain injury, termed primary blast-induced TBI (pbTBI). Clinical manifestations of pbTBI span a wide spectrum, ranging from life-threatening intracranial hemorrhage, hyperemia, and delayed cerebral edema to mild and transient neurological symptoms without detectable structural abnormalities on routine imaging. At the mild end of the spectrum, symptoms after a single exposure may resolve quickly, yet repeated exposures—even at very low levels, termed “subconcussive”—can develop into post-concussive syndrome (PCS) or persistent post-concussive symptoms (PPCS) in a subset of individuals. Despite extensive studies, the molecular pathobiology linking primary blast exposure to delayed and sometimes chronic neurobehavioral deficits remains incompletely understood. A mechanistic framework connecting blast-wave physics to biomechanics to biological vulnerability may therefore help define exposure hazards, interpret clinical symptomatology, and guide diagnostic and therapeutic development. This review summarizes the physics of primary blast waves, the resulting biomechanical responses, and candidate biological substrates, emphasizing structures and interfaces with distinct acoustic impedances across anatomical, tissue, cellular, and molecular scales. We synthesize evidence supporting the hypothesis that the cerebral vasculature and endothelial cells represent critically vulnerable substrates of primary blast-wave injury, in part because the vascular tree constitutes the brain’s largest and most widely distributed interface between compartments with different acoustic impedances. Across experimental and human studies, endothelial stress, vascular injury, and downstream neuroinflammation emerge as convergent molecular responses to primary blast exposure. Temporal dynamics are central to understanding pbTBI because many blast-induced processes unfold in sequential phases. These observations support conceptualizing pbTBI as a condition characterized by prominent cerebrovascular injury of varying severity with secondary consequences for neuronal signaling, network function, and behavior. Within this framework, cerebrovascular and neurovascular unit (NVU) dysfunction provides a parsimonious bridge between primary blast-wave exposure and chronic symptom trajectories, where vascular pathology may offer more accessible therapeutic targets than neuronal injury. Key knowledge gaps include identifying which physical component(s) of the blast are most injurious, establishing biologically meaningful dose–response relationships at molecular and physiological levels, and defining windows of vulnerability during recovery that are relevant to repeated exposures. Addressing these gaps is essential for refining safety protocols, improving diagnostic specificity through mechanism-informed biomarkers, and developing evidence-based molecular and vascular therapeutic targets for pbTBI-associated conditions. Progress will require integrating waveform-aware dosimetry with longitudinal physiological and molecular monitoring across both preclinical and human cohorts. Such integration offers a practical path toward translating blast physics into actionable medical guidance for prevention, triage, and recovery management. Full article

Background: Asymptomatic intracranial atherosclerotic arterial stenosis (ICAS) is an underrecognized entity for which vascular risk-factor optimization is the primary management strategy, with no current indication for routine antiplatelet therapy or endovascular intervention for primary stroke prevention. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) reduce major adverse cardiovascular events, including stroke, in high-risk cardiometabolic populations, but their association with outcomes in asymptomatic ICAS is yet to be evaluated. The present study aims to evaluate the association between GLP-1RA use and cerebrovascular outcomes in adults with asymptomatic ICAS. Materials and Methods: We used the TriNetX US Collaborative Network (71 healthcare organizations) to identify adults (≥18 years) with ICAS between 1 January 2016 and 31 December 2025, and excluded patients with prior cerebral infarction, intracranial hemorrhage, or cerebrovascular ischemic syndromes. Exposure was defined as initiation of any GLP-1 receptor agonist (lixisenatide, semaglutide, liraglutide, tirzepatide, dulaglutide) during the 6 months before or on the date of index ICAS diagnosis. Outcomes were assessed at 1 year, and included ischemic stroke, all-cause mortality, and a composite of ischemic stroke or mortality. Propensity-score matching (1:1) was performed, including demographics, vascular risk factors, comorbidities, antithrombotics, lipid/diabetes therapies, and cardiometabolic laboratory/physiologic measures. Results: Before matching, 1746 GLP-1RA users and 71,792 non-users met inclusion criteria; after matching, 1728 patients remained in each cohort. GLP-1RA use was associated with lower 1-year risk of ischemic stroke (4.40% vs. 6.10%; hazard ratio [HR] 0.70, 95% CI 0.52–0.95; p = 0.044), lower all-cause mortality (3.40% vs. 9.40%; HR 0.35, 95% CI 0.26–0.47; p < 0.001), and lower composite outcome risk (7.50% vs. 15.00%; HR 0.48, 95% CI 0.39–0.59; p < 0.001). Notably, these associations were observed despite matching for HbA1c, LDL cholesterol, BMI, and systolic blood pressure, suggesting potential effects beyond measured cardiometabolic risk profiles. Conclusions: In this large, propensity-matched cohort of adults with a-ICAS, GLP-1RA use was associated with lower ischemic stroke, all-cause mortality, and composite outcome at 1 year. These findings are hypothesis-generating and require further prospective studies to confirm this observation. Full article

Introduction: Hyponatremia is common after nontraumatic intracerebral hemorrhage (ICH) and has been associated with worse outcomes, although prior studies have been limited by smaller sample sizes and heterogeneous exposure definitions. This study evaluated the association between severity-stratified hyponatremia and mortality, survival, and complication rates following nontraumatic ICH. Methods: A retrospective cohort study was performed using the TriNetX database. Patients with nontraumatic ICH were stratified by serum sodium measurements obtained within 7 days of diagnosis. Two separate propensity score-matched analyses were conducted: moderate hyponatremia versus normonatremia (17,547 patients per cohort) and severe hyponatremia versus normonatremia (5010 patients per cohort). The primary outcome was 30-day mortality. Secondary outcomes included seizures, cerebral edema, hydrocephalus, external ventricular drain placement, tracheostomy, percutaneous endoscopic gastrostomy (PEG) placement, pulmonary embolism, deep vein thrombosis, ischemic stroke, and myocardial infarction. Statistical significance was set at p < 0.05. Results: Moderate hyponatremia was associated with increased 30-day mortality (17.5% vs. 13.3%; HR 1.324, 95% CI 1.255–1.398; p < 0.001), while severe hyponatremia demonstrated a greater increase in mortality (18.7% vs. 12.9%; HR 1.473, 95% CI 1.332–1.628; p < 0.001). Both cohorts had higher rates of seizures, cerebral edema, hydrocephalus, tracheostomy, PEG placement, deep vein thrombosis, and myocardial infarction compared with matched normonatremic controls. External ventricular drain placement was also more frequent in both cohorts. Pulmonary embolism increased in moderate hyponatremia but was not significantly different in severe hyponatremia. Ischemic stroke occurred less frequently in both cohorts. Conclusions: Moderate and severe hyponatremia were associated with increased mortality and complications in patients with nontraumatic ICH, with stronger associations observed in severe hyponatremia. These findings support serum sodium as a clinically relevant marker for risk stratification and monitoring during acute ICH care. However, causality cannot be established, and whether correction of hyponatremia improves outcomes requires prospective studies. Full article

Background: Cerebral arteriovenous malformations (AVMs) are high-flow shunts in which abnormal arteriovenous connections expose draining veins to venous hypertension, arterialization, and altered oxygenation. While digital subtraction angiography (DSA) remains the reference standard for dynamic angioarchitecture, it does not directly characterize venous oxygenation or microhemorrhagic tissue changes. Objective: To synthesize current evidence on susceptibility-based MRI-susceptibility-weighted imaging (SWI) and quantitative susceptibility mapping (QSM) for characterization, risk-related features, and treatment monitoring in cerebral AVMs. Methods: Narrative review of the foundational and contemporary literature on AVM pathophysiology, SWI and QSM technical principles, and clinical applications including venous drainage depiction, microhemorrhage detection, oxygenation-related biomarkers, and post-treatment surveillance. Results: SWI provides high-resolution, non-contrast depiction of venous drainage and perinidal hemorrhagic/calcific components, improving visualization of draining veins and microhemorrhages compared with conventional MRI and complementing TOF-MRA. Arterialized draining veins may show altered SWI signal consistent with elevated venous oxygen saturation, though interpretation is indirect and influenced by flow and orientation. QSM extends susceptibility imaging by quantifying tissue susceptibility and enabling indirect estimation of venous oxygenation (SvO₂), offering a potential physiological biomarker of shunt severity and treatment response after radiosurgery or embolization. Key limitations include lack of dynamic flow timing, flow-related artifacts, orientation dependence, confounding from hemorrhage/calcification, and limited standardization and prospective validation. Conclusions: Susceptibility-based MRI does not replace DSA but meaningfully enriches multimodal AVM assessment by adding structural and physiological information-particularly venous mapping, microhemorrhage detection, and oxygenation-sensitive biomarkers. Standardized acquisition/reconstruction and prospective studies are needed to validate susceptibility-derived metrics for risk stratification and longitudinal monitoring. Full article

Background and Objectives: Ischemia-modified albumin (IMA) has previously been identified as a biomarker for early ischemia, rapidly formed by acidosis and free radical modification of the N-terminus of human serum albumin. This study aimed to compare albumin and IMA levels in blood and cerebrospinal fluid (CSF) from 30 patients with spontaneous subarachnoid hemorrhage (SAH) and 15 patients with normal pressure hydrocephalus (NPH) at a single center between 2021 and 2022. Materials and methods: This prospective study included 30 patients diagnosed with subarachnoid hemorrhage (SAH), confirmed radiologically, who were admitted to the Health Sciences University İzmir Bozyaka Training and Research Hospital and constituted the study group. The control group consisted of 15 patients diagnosed with normal pressure hydrocephalus (NPH) without a history or radiological evidence of subarachnoid hemorrhage or any other intracranial hemorrhagic pathology. In the control group, no pathological findings suggestive of hemorrhage or inflammation were detected in serum or cerebrospinal fluid (CSF) analyses. Blood and CSF samples were collected simultaneously from all participants, and albumin and ischemia-modified albumin (IMA) levels were measured. Serum and CSF albumin and IMA levels were compared between the study and control groups. Results: Of the 30 patients included in the study, 19 (63.3%) were male and 11 (36.7%) were female. The albumin level was lower in the patient group compared to the NPH group (3.8 g/dL [1.8–4.7] vs. 4.3 g/dL [3.2–5.0], respectively, p = 0.008). The serum IMA level was higher in the patient group compared to the NPH group (0.36 ABSU [0.30–0.65] vs. 0.25 ABSU [0.05–0.32], respectively, p = 0.010). The serum IMA level was higher in the vasospasm group compared to the group without vasospasm. Conclusions: In patients with SAH, a condition associated with high morbidity and mortality, modified albumin levels were found to be significantly higher in both CSF and blood compared to the NPH group. IMA may be a potential biomarker associated with SAH and vasospasm; however, further large-scale studies with multivariable analysis and external validation are required to confirm its diagnostic and prognostic utility. Full article

Background: Subarachnoid hemorrhage (SAH) is associated with high morbidity and mortality despite advances in neurocritical care. Vitamin D plays a role in immune modulation, endothelial function, and neuroprotection; however, its impact on outcomes following SAH remains poorly defined. We evaluated the association between low vitamin D status and clinical outcomes in patients with nontraumatic SAH. Methods: We conducted a retrospective propensity score-matched cohort study using the TriNetX Research Network database. Adult patients with nontraumatic SAH and at least one recorded serum 25-hydroxyvitamin D level obtained within 3 months on or before diagnosis were included. The low vitamin D cohort was defined as 0–20 ng/mL, and the comparator cohort as 20–40 ng/mL. Cohorts were matched 1:1 using propensity scores adjusted for demographic and clinical covariates, including chronic kidney disease, liver disease, osteoporosis, and intestinal malabsorption. The primary outcome was 30-day all-cause mortality. Secondary outcomes included seizures, hydrocephalus, cerebral edema, and external ventricular drain placement. Results: After matching, 2314 patients were included in each cohort. Thirty-day mortality occurred in 9.3% of patients in the low vitamin D cohort and 7.6% of patients in the comparator cohort (hazard ratio [HR] 1.229; 95% CI, 1.006–1.503; p = 0.043). Seizures were more frequent in the low vitamin D cohort (8.6% vs. 6.9%; odds ratio [OR] 1.274; 95% CI, 1.026–1.581; p = 0.028). Hydrocephalus was also more common among patients with low vitamin D (5.1% vs. 3.9%; OR 1.328; 95% CI, 1.003–1.758; p = 0.047). No significant differences were observed in cerebral edema or external ventricular drain placement. Conclusions: Low vitamin D status was associated with increased short-term mortality, seizure incidence, and hydrocephalus following nontraumatic SAH. These findings suggest that vitamin D status may represent a potential prognostic biomarker warranting prospective investigation. Full article

Background: The introduction of flow diverters (FDs) has greatly enhanced the treatment of cerebral aneurysms. This study compares two FDs, the Pipeline Embolization Device (PED) and the Derivo Embolization Device (DED), in terms of technical, angiographic and clinical aspects. Methods: A total of 103 patients with unruptured aneurysms were treated with the PED (n = 56) and DED (n = 47) between 2012 and 2019. Aneurysm occlusion, procedural complications, occurrence of In-stent stenosis and clinical outcome were evaluated retrospectively. Results: Implantation of the flow diverters was technically successful in all patients. There were no significant differences between baseline characteristics and aneurysm morphology. Angiographic follow-up was available with a median short-term follow-up of 3 months and a median long-term follow-up time of 16 months. Adequate aneurysm occlusion at long-term follow-up was substantially but not significantly greater with the DED (95.8%, 45/47) compared to the PED (87.5%, 49/56) (p = 0.084). In-stent stenoses were significantly less frequent with the DED (29.8%; 14/47) than with the PED (53.6%, 30/57) at short-term follow-up (p = 0.017), although moderate and asymptomatic overall. Thromboembolic or hemorrhagic events occurred in 10.7% (6/56) of cases with the PED and 8.5% (4/47) with the DED (p = 0.752). Morbidity rates were similar between devices (PED 3.6% (2/56), DED 2.1% (1/47), p = 1.0). There was no procedural mortality. Conclusions: Clinical outcomes and complications were comparable between the PED and DED while aneurysm occlusion was considerably greater at long-term follow-up and in-stent stenosis significantly less frequent at short-term follow-up with the DED. The surface-modified design of the DED may contribute to reduced thrombogenicity and early advantages in preventing in-stent stenosis. Further comparative studies are necessary to investigate these findings, particularly comparing surface-modified flow diverters with newer-generation devices featuring true coatings. Full article

Background: The Circle of Willis (CoW) is a key collateral pathway that enables communication between the anterior and posterior cerebral circulations. However, anatomical variations in the A1 segment of the anterior cerebral artery, such as hypoplasia or aplasia, can alter hemodynamics and may compromise this collateral function. While incomplete CoW configurations have been linked to aneurysm formation and altered patterns of hemorrhage, their role in the distribution of cerebral infarctions remains controversial. We aimed to explore the association between A1 segment hypoplasia/aplasia and infarct laterality across different etiological subtypes. Methods: We retrospectively analyzed patients with unilateral anterior circulation infarction admitted between April 2017 and March 2023. The CoW was assessed by magnetic resonance angiography (MRA). A1 segment hypoplasia was defined as a segment diameter <1 mm, and A1 aplasia was defined as non-visualization on MRA. The side with hypoplasia or aplasia was defined as the minor side, and the contralateral side as dominant. We assessed whether infarction occurred on the minor or dominant side. Results: Among 198 patients with unilateral anterior circulation infarction classified as lacunar, cardioembolic stroke (CES), or embolic stroke of undetermined source (ESUS), 30% had A1 hypoplasia or aplasia, with similar prevalence across subtypes. Infarcts occurred on the A1 dominant side in 53% of lacunar, 55% of ESUS, and 75% of CES cases. Although this difference did not reach statistical significance (p = 0.43), it should be interpreted with caution given the limited sample size. Conclusions: The rates of A1 hypoplasia and aplasia were similar across stroke types. No statistically significant association was identified. The findings remain inconclusive given the limited sample size. These results should be considered exploratory and hypothesis-generating. Full article

Background: Nimodipine is routinely used in aneurysmal subarachnoid hemorrhage (aSAH), but the optimal route of administration remains uncertain. Intravenous and enteral delivery differ in pharmacokinetics, yet the clinical relevance of these differences is unclear. This scoping review aimed to map evidence on the pharmacokinetics (PK) and pharmacodynamics (PD) of intravenous and enteral nimodipine and their relationship with clinical outcomes. Methods: A scoping review was conducted following PRISMA-ScR guidelines. PubMed, Scopus, and Web of Science were searched from 1982 to March 2026. Studies in adult aSAH patients reporting PK and/or PD outcomes after intravenous or enteral nimodipine were included. Data were synthesized qualitatively. Results: Twenty studies were included. Intravenous administration provided higher and more consistent systemic exposure, whereas enteral administration showed low and highly variable bioavailability, particularly via nasogastric tubes. Despite these differences, pharmacodynamic effects were not clearly related to systemic concentrations, and hypotension occurred similarly across routes. Evidence on cerebral physiology was limited. Randomized studies showed no significant differences in delayed cerebral ischemia, infarction, or functional outcomes between routes. Conclusions: Pharmacokinetic advantages of intravenous nimodipine do not consistently translate into pharmacodynamic or clinical benefits, although available evidence is limited and heterogeneous. The PK–PD relationship appears weak, and further research is needed to guide optimized administration strategies. Full article

Delayed cerebral ischemia (DCI) is a major complication of aneurysmal subarachnoid hemorrhage (aSAH), strongly associated with neurological deterioration and poor outcomes. Its pathophysiology remains incompletely understood and involves multiple interacting processes. Increasing evidence highlights the role of redox imbalance triggered by hemoglobin breakdown and the subsequent generation of reactive species, leading to vascular dysfunction, impaired nitric oxide signaling, and inflammatory activation This review aims to summarize current knowledge on redox-related mechanisms involved in DCI and to explore the potential role of the peroxiredoxin (PRDX) family in this setting. A narrative review of experimental and preclinical studies was performed, focusing on molecular pathways associated with vascular regulation, cellular injury, and antioxidant defense. Particular attention was given to the distribution and biological functions of PRDX isoforms within the central nervous system. This work addresses a topic not previously systematically discussed, the potential involvement of PRDX proteins in aSAH-related complications. By integrating available data, it provides a conceptual framework linking PRDX to mechanisms relevant for DCI. The manuscript serves as a starting point for future research, particularly translational and clinical studies in humans, which are necessary to verify the relevance of these findings and to better understand their potential clinical implications. Full article

Background: Temporary arterial occlusion (TAO) is a key adjunct in microsurgical clipping of middle cerebral artery (MCA) aneurysms, but its safe duration and impact on perioperative ischemia—particularly in subarachnoid hemorrhage (SAH)—remain uncertain. Methods: A retrospective cohort of 245 patients undergoing microsurgical clipping of MCA aneurysms (154 incidental, 91 SAH) at a tertiary neurovascular center (2010–2020) was analyzed. TAO use, cumulative duration (>5, >8, >10, >15 min), number of applications, and occlusion site were extracted alongside clinical, radiographic, and outcome data. The primary endpoint was perioperative ischemia within 48 h; secondary endpoints included clinically relevant cerebral vasospasm (CVS), intraoperative rupture, and functional outcome (mRS) at discharge and 6 months. Multivariable logistic and ordinal regression models adjusted for demographic, aneurysmal, and treatment covariates. Results: TAO was used in 134 cases (54.7%; mean total duration 10.4 ± 8.7 min). In the overall cohort, TAO (presence or duration) was not independently associated with perioperative ischemia or CVS. In the SAH subgroup, cumulative TAO > 5 min conferred an approximately sixfold higher odds of ischemia (p = 0.012; OR 6.33), whereas no threshold was significant in incidental aneurysms. Female sex, M2 location, SAH at admission, and initial GCS < 9 independently predicted ischemia; female sex, higher ASA grade, larger size, irregular morphology, and SAH predicted CVS. SAH and aneurysm wall calcification were associated with worse 6-month mRS. Conclusions: TAO appears safe in elective clipping of incidental MCA aneurysms when applied judiciously, but cumulative durations beyond 5 min substantially increase ischemia risk in SAH patients. TAO management should therefore be individualized by rupture status, neurological grade, and aneurysm morphology rather than a single universal time limit. Full article

Aneurysmal subarachnoid hemorrhage (SAH) remains a devastating cerebrovascular disorder with high morbidity and mortality, despite advances in aneurysm securing and neurocritical care. Clinical outcomes are determined by early brain injury (EBI), delayed cerebral ischemia (DCI), hydrocephalus, and long-term cognitive impairment, extending beyond the traditional focus on large-vessel vasospasm alone. Emerging evidence identifies the dysfunction of the glymphatic system and meningeal lymphatic pathway, the brain’s primary clearance pathways, as a central and unifying mechanism linking acute hemorrhagic injury to delayed and chronic neurological sequelae. Following SAH, acute intracranial pressure elevation, subarachnoid blood clot burden, loss of arterial pulsatility, venous congestion, astrocytic aquaporin-4 perivascular depolarization, and neuroinflammation converge to suppress cerebrospinal fluid–interstitial fluid exchange and outflow in glymphatic system and subsequent meningeal lymphatic drainage. Persistent clearance failure promotes the retention of blood breakdown products, inflammatory mediators, and metabolic waste, amplifying microvascular dysfunction, cortical spreading depolarizations, blood–brain barrier disruption, and secondary ischemic injury. Importantly, accumulating data highlight venous pathology and meningeal lymphatic impairment as critical, yet underappreciated, contributors to delayed injury and post-SAH hydrocephalus. In this review, we synthesize the current knowledge of the physiological organization of glymphatic and meningeal lymphatic systems, delineate the mechanistic and molecular drivers of their dysfunction after SAH, and discuss clinical implications for EBI, DCI, hydrocephalus, and long-term cognitive outcomes. We further outline future directions, including translational imaging, biomarker development, and therapeutic strategies targeting clearance pathways, to advance disease-modifying approaches in SAH. Full article

Objective: Cerebral cavernous malformations (CCMs) are usually occult but can present with a symptomatic hemorrhage. Treatment recommendations for CCMs are still controversially discussed, as all CCMs have signs of chronic hemorrhage. The distinction of acute hemorrhage can be difficult, especially when patients only present with mild symptoms. Because of emerging evidence supporting inflammatory burden as a main avenue in the disease pathogenesis of CCMs, the aim of the present study was to investigate routine inflammatory parameters to support decision-making in ambiguous cases. Methods: A total of 87 patients who underwent CCM resection at the authors’ institution between 2008 and 2021 were included in this study. Data were recorded retrospectively. Patients were dichotomized into two groups: those with acute hemorrhage and those without, as a control group (e.g., resection for seizure control). Inflammatory parameters included C-reactive Protein (CrP), White Blood Cell Count (WBC), Red Cell Distribution Width (RDW), and Mean Platelet Volume/Platelet Count Ratio (MPV/PC). Results: The receiver operating characteristic curve demonstrated moderate diagnostic accuracy for predicting acute hemorrhage from CCM based on WBC at admission (AUC: 0.74, 95%-CI: 0.63–0.84) with a cut-off of ≥6.595 G/L. The multivariable analysis confirmed that having a WBC > 6.595 G/L is an independent predictor for acute hemorrhage of CCM (adjusted odds ratio: 4.5, 95%-CI: 1.8–11.2, p < 0.001). Conclusions: A white blood cell count >6.595 G/L was significantly associated with acute hemorrhage in CCMs and appears to be a quick-to-use biomarker in controversial cases. Moreover, leukocytosis emphasizes the involvement of neuroinflammation in acute hemorrhage of CCM. Further investigations are needed to analyze the precise role of inflammation in CCM pathogenesis and its impact on treatment strategies. Full article

Background: Contemporary aneurysm surgery increasingly requires the management of complex lesions with limited physiological reserve. A growing “physiology-first” paradigm emphasizes that optimizing cerebrovascular dynamics during aneurysm treatment is essential for favorable neurological outcomes. Methods: This narrative review synthesizes current evidence and expert perspectives on cerebrovascular physiology relevant to aneurysm surgery, including cerebral perfusion, autoregulation, ischemia tolerance, neuroprotection, and intraoperative monitoring. Results: Key themes include individualized blood pressure management, recognition of impaired autoregulation—particularly after subarachnoid hemorrhage—safe application of temporary arterial occlusion, and the use of multimodal neuromonitoring to detect ischemia in real time. The strengths and limitations of neuroprotective adjuncts are critically discussed in the context of available clinical evidence. Conclusions: Integrating cerebrovascular physiology into aneurysm surgery supports informed intraoperative decision-making, minimizes ischemic injury, and enhances patient outcomes. A physiology-first approach complements technical expertise and represents a cornerstone of modern neurovascular practice. Full article

The aim of this study was to assess long-term outcomes in patients with different vascular types of childhood stroke. Methods: Data for children with childhood stroke (aged 29 days to 18 years) were collected from the Estonian Pediatric Stroke Database. Outcomes (death, recurrent stroke, epilepsy, neurodevelopmental outcome by pediatric stroke outcome measure (PSOM)) were assessed at a minimum of two years after stroke. Results: Long-term outcome data were available for 44 patients with childhood stroke (including three patients who died of stroke). According to the PSOM, based on gender, age, location of stroke and epilepsy, there were no differences in outcomes, but patients with a Pediatric NIH Stroke Scale (PedNIHSS) score of ≥6 had worse outcomes compared to patients with a score of <6. Children with arterial hemorrhagic stroke (AHS) were more likely to die, suffer from epilepsy and develop problems in the cognition/behavior PSOM subscale compared to children with arterial ischemic stroke (AIS). Combined poor outcomes (epilepsy, PSOM ≥ 1, recurrent stroke, mortality) occurred in 75% (33/44) of all patients with long-term outcome data. Conclusions: Combined poor outcomes occurred in 75% of the patients with childhood stroke. Patients with AHS showed higher mortality and worse long-term outcomes compared to patients with AIS in certain neurodevelopmental domains. Full article