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Objective: Unusual clinical course Background: Clinical management of intracranial transorbital penetrating injury (TOPI) is challenging and may require surgery. Both the trauma and surgery can result in neurovascular damage, bleeding, and infection. Low-speed injury may involve the superior orbital fissure (SOF) as the main point of entry into the skull and is associated with lower morbidity than high-speed injuries. This report describes a 19-year-old man with pontine and left cerebellar involvement from a TOPI with partial recovery without surgery. Case Report: We hereby report the case of a 19-year-old man who underwent a low-speed in-out (as the foreign body was immediately retrieved) deep transorbital pontine and left cerebellar penetrating injury. Despite transient loss of consciousness, his Glasgow Coma Scale at admission was 15. An intravenous antibiotic regimen was rapidly initiated. He had ophthalmic (V1) et maxillary (V2) nerves palsy, minor right pyramidal syndrome, and left kinetic cerebellar syndrome. Multi-modal imaging perfectly correlated with the clinical presentation. Neither surgical nor angiographic management was required. Clinical evolution was favorable, and the patient partially recovered. Conclusions: In case of penetration through the SOF, the clinical course tends to be benign. However, this case should not overshadow potential life-threatening complications of TOPIs. This report highlights the importance of a multidisciplinary approach for the diagnosis and management of traumatic transorbital penetrating intracranial injury. As illustrated, medical imaging may demonstrate the exact pathway of the offending object. [ABSTRACT FROM AUTHOR]

Intracerebral hemorrhage (ICH) is a severe condition characterized by bleeding within brain tissue. Primary brain injury in ICH results from a mechanical insult caused by blood accumulation, whereas secondary injury involves inflammation, oxidative stress, and disruption of brain physiology. miR-195-5p may participate in ICH pathology by regulating cell proliferation, oxidative stress, and inflammation. Therefore, we assessed the performance of miR-195-5p in alleviating ICH-induced secondary brain injury. ICH was established in male Sprague–Dawley rats (7 weeks old, 200–250 g) via the stereotaxic intrastriatal injection of type IV bacterial collagenase, after which miR-195-5p was administered intravenously. Neurological function was assessed using corner turn and forelimb grip strength tests. Protein expression was assessed by western blotting and ELISA. The miR-195-5p treatment significantly improved neurological function; modulated macrophage polarization by promoting anti-inflammatory marker (CD206 and Arg1) production and inhibiting pro-inflammatory marker (CD68 and iNOS) production; enhanced Akt signalling, reduced oxidative stress by increasing Sirt1 and Nrf2 levels, and attenuated inflammation by decreasing NF-κB activation; inhibited apoptosis via increased Bcl-2 and decreased cleaved caspase-3 levels; and regulated synaptic plasticity by modulating NMDAR2A, NMDAR2B, BDNF, and TrkB expression and ERK and CREB phosphorylation. In conclusion, miR-195-5p exerts neuroprotective effects in ICH by reducing inflammation and oxidative stress, inhibiting apoptosis, and restoring synaptic plasticity, ultimately restoring behavioral recovery, and represents a promising therapeutic agent that warrants clinical studies. [ABSTRACT FROM AUTHOR]

Objective: The objective of this study was to compare the severity of head injury in patients on an anticoagulant or antiplatelet agent and to look at the burden of these medications in patients 55 + years vs. younger. Methods: This was an observational cohort study of 2256 adult head trauma patients who presented to a Level I Trauma Center and were stratified by anticoagulant/antiplatelet medication use and age. Logistic regression analyses were performed to ascertain whether use of these medications resulted in worse outcomes. Results: Overall, elderly (>55yrs) patients had worse outcomes after TBI. Specifically, they were more likely to have an intracranial hemorrhage, be admitted to the hospital, have an ICU stay, be re-admitted within 30 days, die in the hospital and be dead within 3 months. Conclusion: Geriatric trauma patients along with their preexisting comorbidities are often on anticoagulants that increase their risk for complications, bleeding, mortality in the setting of even minor traumas.

Isolated cortical vein thrombosis (ICVT) is a rarer subtype of cerebral venous sinus thrombosis (CVST) that involves only the cortical veins without any thrombosis in the major cerebral veins or sinuses. Among the known causes of CVST are factors, such as being a young female or the use of hormonal preparations. This study presents a case of a 35-year-old female who underwent endometrial polyp removal 5 days before symptom onset and started using a transdermal estradiol patch. After 4 days of using the transdermal estradiol patch, the patient developed recurrent seizures and sustained sensory aphasia. The head computed tomography revealed hemorrhagic infarction. Given her young age and the use of hormonal therapy, CVST was suspected. However, the initial diagnosis with magnetic resonance imaging (MRI) was inconclusive, and no venous sinus thrombosis could be identified on additional cerebral angiography. Instead, stasis of venous flow in the temporal vein was noted. It was difficult to determine whether these findings were due to hemorrhage or ICVT. Upon re-evaluation with MRI, signal changes suggestive of thrombosis in a cortical vein in the parietal region, which is different from the stasis observed in cerebral angiography, led to the diagnosis of ICVT. This is the first study to link the use of transdermal estradiol patches to ICVT. In cases where ICVT leads to cerebral hemorrhage, cerebral angiography may not be useful. Instead, a comprehensive diagnosis should be made based on imaging findings from various MRI sequences and the patient's medical history.

Introduction: Early mobilization is key in neurologically impaired persons, limiting complications and improving long-term recovery. Self-balanced exoskeletons are used in rehabilitation departments to help patients stand and walk. We report the first case series of exoskeleton use in acute neurosurgery and intensive care patients, evaluating safety, clinical feasibility and patients' satisfaction. Methods: We report a retrospective observational study including individuals hospitalized in the neurosurgical intensive care and neurosurgery departments. We included patients with a medical prescription for an exoskeleton session, and who met no contraindication. Patients benefited from standing sessions using a self-balanced exoskeleton (Atalante, Wandercraft, France). Patients and sessions data were collected. Safety, feasibility and adherence were evaluated. Results: Seventeen patients were scheduled for 70 standing sessions, of which 27 (39%) were completed. They were typically hospitalized for intracranial hemorrhage (74%) and presented with unilateral motor impairments, able to stand but with very insufficient weight shifting to the hemiplegic limb, requiring support (MRC 36.2 ± 3.70, SPB 2.0 ± 1.3, SPD 0.7 ± 0.5). The average duration of standing sessions was 16 ± 9 min. The only side effect was orthostatic hypotension (18.5%), which resolved with returning to seating position. The most frequent reason for not completing a session was understaffing (75%). All patients were satisfied and expressed a desire to repeat it. Conclusions: Physiotherapy using the exoskeleton is safe and feasible in the acute neurosurgery setting, although it requires adaptation from the staff to organize the sessions. An efficacy study is ongoing to evaluate the benefits for the patients. [ABSTRACT FROM AUTHOR]

Introduction: The impact of intracerebral hemorrhage (ICH) on cognition and the determinants of cognitive recovery early after ICH remain elusive. In this post hoc analysis of the intracerebral hemorrhage deferoxamine (iDEF) trial, we examined the trajectories of cognitive impairment and the determinants of early cognitive recovery after ICH. Methods: We examined baseline factors associated with a 90-day cognitive outcome and constructed generalized linear mixed models to examine the trajectory of cognitive function over time among iDEF participants. Cognition was measured by the Montreal Cognitive Assessment (MoCA) scores on days 7, 30, and 90. Results: 291 were available for analysis under the trial’s modified intention-to-treat definition (38% female, mean age 60.3 ± 12.0 years, median NIHSS 13, IQR 8–18). The median baseline ICH volume was 12.9 IQR (6.4–26.0) mL; 59 (20%) of the ICH cases were lobar, 120 (41%) had intraventricular extension. There was an overall significant increase in total MOCA score with time (p < 0.0001). Total MOCA score increased by an estimated 3.9 points (95% CI: 3.1, 4.7) between the day 7 and day 30 assessments and by an additional 2.9 points (95% CI: 2.2, 3.6) between the day 30 and day 90 assessments. Despite the overall improvement, 134 of 205 (65%) patients with an available 90-day MoCA score remained cognitively impaired with a score <26 on day 90. Older age, higher NIHSS score, baseline ICH volume, intraventricular hemorrhage, and perihematoma edema had an adjusted negative impact on cognitive recovery. Conclusions: Although ICH survivors exhibit significant improvement of cognitive status over the first 3 months, cognitive performance remains impaired in the majority of patients. Among factors independently associated with worse cognitive recovery, higher baseline ICH, intraventricular blood and perihematomal edema volumes, are potential therapeutic targets that merit further exploration. [ABSTRACT FROM AUTHOR]

The Centers for Medicare & Medicaid Services (CMS) established a class‐based National Coverage Determination (NCD) for monoclonal antibodies directed against amyloid for Alzheimer's disease (AD) with patient access through Coverage with Evidence Development (CED) based on three questions. This review, focused on donanemab, answers each of these CED questions with quality evidence. TRAILBLAZER‐ALZ registration trials are presented with supporting literature and real‐world data to answer CED questions for donanemab. TRAILBLAZER‐ALZ registration trials demonstrated that donanemab significantly slowed cognitive and functional decline in amyloid‐positive early symptomatic AD participants, and lowered their risk of disease progression while key safety risks occurred primarily within the first 6 months and then declined. Donanemab meaningfully improved health outcomes with a manageable safety profile in an early symptomatic AD population, representative of Medicare populations across diverse practice settings. The donanemab data provide the necessary level of evidence for CMS to open a reconsideration of their NCD. Highlights: Donanemab meaningfully improved outcomes in trial participants with early symptomatic Alzheimer's disease.Comorbidities in trial participants were consistent with the Medicare population.Co‐medications in trial participants were consistent with the Medicare population.Risks associated with treatment tended to occur in the first 6 months.Risks of amyloid‐related imaging abnormalities were managed with careful observation and magnetic resonance imaging monitoring. [ABSTRACT FROM AUTHOR]

Leonidas D Panos,1,2 Panagiotis Bargiotas,2 Marcel Arnold,1 Georgios Hadjigeorgiou,2 Georgios D Panos3,4 1Department of Neurology, Bern University Hospital Inselspital, Bern, Switzerland; 2Department of Neurology, School of Medicine, University of Cyprus, Nicosia, Cyprus; 3Department of Ophthalmology, Queen’s Medical Centre, Nottingham University Hospitals (NUH), Nottingham, UK; 4Division of Ophthalmology and Visual Sciences, School of Medicine, University of Nottingham, Nottingham, UKCorrespondence: Leonidas D Panos, Department of Neurology, Bern University Hospital “Inselspital”, Freiburgstrasse 16, Bern, 3010, Switzerland, Tel +41 31 632 70 00, Email ldpanos@yahoo.gr Georgios D Panos, Department of Ophthalmology, Queen’s Medical Centre, NUH, Derby Road, Lenton, Nottingham, NG7 2UH, UK, Tel +44 115 924 9924, Email gdpanos@gmail.comAbstract: Stem cells, renowned for their unique regenerative capabilities, present significant hope in treating stroke, a major cause of disability globally. This review offers a detailed analysis of stem cell applications in stroke (ischemic and hemorrhagic) recovery. It examines therapies based on autologous (patient-derived), allogeneic (donor-derived), and Granulocyte-Colony Stimulating Factor (G-CSF) based stem cells, focusing on cell types such as Mesenchymal Stem/Stromal Cells (MSCs), Bone Marrow Mononuclear Stem Cells (BMMSCs), and Neural Stem/Progenitor Cells (NSCs). The paper compiles clinical trial data to evaluate their effectiveness and safety and addresses the ethical concerns of these innovative treatments. By explaining the mechanisms of stem cell-induced neurological repair, this review underscores stem cells’ potential in revolutionizing stroke rehabilitation and suggests avenues for future research.Keywords: stem cell therapy, stroke, brain hemorrhage, autologous stem cells transplantation, allogeneic stem cells transplantation, granulocyte-colony stimulating factor

Objective: Neurological adverse reactions to SARS-CoV-2 vaccines include a wide variety of central nervous system (CNS) disorders; however, the cause-and-effect relationship is unclear. Herein, we present a fatal case of extensive basal ganglia bleeding after mRNA-based SARS-CoV-2 vaccination and discuss the pathophysiological mechanisms of brain hemorrhage. Case presentation: A 66-year-old woman with cerebral palsy and a history of neonatal asphyxia suddenly presented with hypothermia and consciousness disturbance one day after the sixth dose of an mRNA-based SARS-CoV-2 vaccine (Moderna). Clinical investigations revealed a normal thrombocyte count, but stage 1 hypertension and mild prolongation of the prothrombin time and activated partial thromboplastin time. Urgent brain computed tomography (CT) revealed extensive left basal ganglia hemorrhage with global brain edema and downward herniation of the brainstem. The region of the large hematoma corresponded to the basal ganglia lesion which had been produced by neonatal asphyxia at birth. Because the neurosurgeons evaluated her state as inoperable, conservative therapy was continued, but the patient died on day 5 after the event. Conclusion: We hypothesized that two pathophysiological mechanisms were responsible for the brain hemorrhage in this case: disruption of focal cerebrovascular autoregulation in preexisting neonatal asphyxiated lesions and disturbance of coagulation pathways after mRNA-based SARS-CoV-2 vaccination.

Brain hemorrhage refers to a potentially fatal medical disorder that affects millions of individuals. The percentage of patients who survive can be significantly raised with the prompt identification of brain hemorrhages, due to image-guided radiography, which has emerged as the predominant treatment modality in clinical practice. A Computed Tomography Image has frequently been employed for the purpose of identifying and diagnosing neurological disorders. The manual identification of anomalies in the brain region from the Computed Tomography Image demands the radiologist to devote a greater amount of time and dedication. In the most recent studies, a variety of techniques rooted in Deep learning and traditional Machine Learning have been introduced with the purpose of promptly and reliably detecting and classifying brain hemorrhage. This overview provides a comprehensive analysis of the surveys that have been conducted by utilizing Machine Learning and Deep Learning. This research focuses on the main stages of brain hemorrhage, which involve preprocessing, feature extraction, and classification, as well as their findings and limitations. Moreover, this in-depth analysis provides a description of the existing benchmark datasets that are utilized for the analysis of the detection process. A detailed comparison of performances is analyzed. Moreover, this paper addresses some aspects of the above-mentioned technique and provides insights into prospective possibilities for future research.

Brain hemorrhages have become increasingly common and can be fatal if left untreated. Current methods for monitoring the progression of the disorder that rely on MRI and PET scans are inconvenient and costly for patients. This has spurred research toward portable and cost-effective techniques for predicting the current stage and malignancy of the hemorrhages. In this study, simulated S-parameter data obtained from a two-antenna system placed over the head is used in conjunction with machine learning to detect the dielectric changes in the brain caused by hemorrhage non-invasively. Several machine learning classifiers are used to analyze the data, and their performance metrics are compared to determine the optimal classifier for this case. The study revealed that Decision Tree, KNN, and Random Forest classifiers are better than SVM and MLP classifiers in terms of accuracy, precision, and recall in predicting Brain hemorrhage at the most probable locations. Contrary to conventional microwave imaging systems requiring several antennas for brain hemorrhage detection, this study demonstrates that integrating machine learning with microwave sensors enables accurate solutions with a reduced antenna count. The results present a transformative strategy for monitoring systems in clinics, where a simple, safe, and low-cost microwave antenna-based system can be intelligently integrated with machine learning to diagnose the presence of Brain hemorrhage.

Background: The 30‐day hospital re‐admission rate is a quality measure of hospital care to monitor the efficiency of the healthcare system. The hospital re‐admission of acute stroke (AS) patients is often associated with higher mortality rates, greater levels of disability and increased healthcare costs. The aim of our study was to identify predictors of unplanned 30‐day hospital re‐admissions after discharge of AS patients and define an early re‐admission risk score (RRS). Methods: This observational, retrospective study was performed on AS patients who were discharged between 2014 and 2019. Early re‐admission predictors were identified by machine learning models. The performances of these models were assessed by receiver operating characteristic curve analysis. Results: Of 7599 patients with AS, 3699 patients met the inclusion criteria, and 304 patients (8.22%) were re‐admitted within 30 days from discharge. After identifying the predictors of early re‐admission by logistic regression analysis, RRS was obtained and consisted of seven variables: hemoglobin level, atrial fibrillation, brain hemorrhage, discharge home, chronic obstructive pulmonary disease, one and more than one hospitalization in the previous year. The cohort of patients was then stratified into three risk categories: low (RRS = 0–1), medium (RRS = 2–3) and high (RRS >3) with re‐admission rates of 5%, 8% and 14%, respectively. Conclusions: The identification of risk factors for early re‐admission after AS and the elaboration of a score to stratify at discharge time the risk of re‐admission can provide a tool for clinicians to plan a personalized follow‐up and contain healthcare costs. [ABSTRACT FROM AUTHOR]

The molecular basis for circadian dependency in stroke due to subarachnoid hemorrhagic stroke (SAH) remains unclear. We reasoned that microglial erythrophagocytosis, crucial for SAH response, follows a circadian pattern involving carbon monoxide (CO) and CD36 surface expression. The microglial BV-2 cell line and primary microglia (PMG) under a clocked medium change were exposed to blood ± CO (250 ppm, 1 h) in vitro. Circadian dependency and the involvement of CD36 were analyzed in PMG isolated from control mice and CD36−/− mice and by RNA interference targeting Per-2. In vivo investigations, including phagocytosis, vasospasm, microglia activation and spatial memory, were conducted in an SAH model using control and CD36−/− mice at different zeitgeber times (ZT). In vitro, the surface expression of CD36 and its dependency on CO and phagocytosis occurred with changed circadian gene expression. CD36−/− PMG exhibited altered circadian gene expression, phagocytosis and impaired responsiveness to CO. In vivo, control mice with SAH demonstrated circadian dependency in microglia activation, erythrophagocytosis and CO-mediated protection at ZT2, in contrast to CD36−/− mice. Our study indicates that circadian rhythmicity modulates microglial activation and subsequent CD36-dependent phagocytosis. CO altered circadian-dependent neuroprotection and CD36 induction, determining the functional outcome in a hemorrhagic stroke model. This study emphasizes how circadian rhythmicity influences neuronal damage after neurovascular events. [ABSTRACT FROM AUTHOR]

Cerebral edema, characterized by abnormal fluid accumulation in brain tissue leading to increased intracranial pressure, poses significant challenges for anesthesiologists. This review delves into the pathophysiology, clinical manifestations, diagnostic approaches, pharmacological strategies, and anesthesiological considerations associated with cerebral edema. Disruptions in the blood-brain barrier, alterations in cerebral blood flow, cellular swelling, and aquaporin dysregulation contribute to the complexity of cerebral edema. Clinical presentations vary, encompassing cognitive changes, seizures, and neurological deficits. Accurate diagnosis relies on clinical assessments and neuroimaging, with MRI and CT scans playing pivotal roles. Pharmacological interventions, including osmotic agents, corticosteroids, diuretics, and barbiturates, target specific causes and symptoms. Anesthesiological challenges encompass ICP monitoring, choice of anesthetic agents, maintenance of cerebral perfusion, fluid management, temperature control, and collaboration with neurosurgical teams. This multidisciplinary approach ensures optimal patient care and emphasizes ongoing research collaboration for refining therapeutic strategies. This comprehensive review provides valuable insights for clinicians managing cerebral edema, offering a roadmap for tailored interventions and highlighting the need for continued advancements in understanding and treating this critical condition. Material and method: The literature review applied standard criteria and focused on PubMed articles using keywords: cerebral edema, pathophysiology, aquaporin, blood-brain barrier, anesthesiology, cerebral edema treatment, corticosteroids. [ABSTRACT FROM AUTHOR]

Intracranial hemorrhage (ICH) brain hemorrhages are life‐threatening medical conditions that require a prompt and accurate diagnosis to ensure timely intervention and treatment. Computed tomography (CT) scans play a vital role in diagnosing brain hemorrhages due to their ability to provide detailed cross‐sectional images of the brain. However, the manual interpretation of CT scans is time‐consuming and subjects to human error. To address these challenges, this study proposes a stacked deep model‐based classification approach for the automated identification and differentiation of multiclass brain hemorrhages in CT scans. The stacked deep model architecture consists of multiple layers of neural networks, each designed to learn specific levels of features, leading to enhanced representation learning and improved classification performance. Later, the stacked models are connected with the weighted approach that helps to get the ensemble models in the proper order based on their power of predicting correct samples. To build the stacked deep model, a large dataset of 7,52 000 annotated CT scans is utilized to train the model and optimize its parameters. Furthermore, transfer learning is employed to leverage pretrained models for feature extraction, which aids in handling limited data scenarios. Experimental results demonstrate that the stacked deep model achieves superior accuracy (98.56%), and other classification performance measures such as sensitivity (95.89%), specificity (99.58%), AUC‐ROC (98.47%), and weighted log loss (0.04967) as compared to conventional methods. The automated classification of multiclass brain hemorrhages in CT scans using the proposed model not only significantly reduces the time required for diagnosis but also enhances the reliability and consistency of results. This model has the potential to assist medical professionals in making more informed decisions and improve patient outcomes by enabling rapid and accurate diagnosis of brain hemorrhages. [ABSTRACT FROM AUTHOR]

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Background: The advent of computed tomography (CT) and magnetic resonance imaging (MRI) has revolutionized stereotactic brain interventions, which enabled precise targeting of deep brain structures and enhanced patient safety in modern neurosurgery. This study aims to investigate the risk factors associated with biopsy failure and hemorrhage in CT-guided brain stereotactic surgeries. Methods: In the current study, we present a retrospective descriptive analysis of cases that showed biopsy failures and hemorrhage after CT-guided stereotactic brain biopsy surgeries at our department from January 2019 to January 2021. Biopsies were obtained using a Sedan-type needle. Results: Out of the 80 patients who underwent CT-guided stereotactic surgeries, two patients (2.5 %) experienced biopsy failure, necessitating a repeat procedure. There was a notably higher risk of biopsy failure when fewer than four biopsy attempts were made (adjusted odds ratio = 6.4, 95 % CI 1.8 to 16.7). A postprocedural CT scan revealed intracranial hemorrhage in five patients (6.25 %); four of these cases were silent, with no accompanying neurological complications. Four out of the five hemorrhage cases were associated with astrocytoma. Conclusions: Stereotactic surgery provides a precise and minimally invasive approach to target lesions with a relatively low risk of biopsy failures and hemorrhage.

Abstract Background The heme oxygenase-1 (HO-1) enzyme pathway is of crucial importance in the removal of toxic blood components and regulation of neuroinflammation following hemorrhagic stroke. Although a circadian pattern dependency in the incidence and severity of hemorrhagic stroke exists, it is unknown whether the activity of the HO-1 system in the context of hemorrhagic injury also exhibits circadian dependency. We hypothesized that the circadian regulation of microglial HO-1 would determine the extent of neuroinflammation and neuronal injury in a murine model of subarachnoid hemorrhage (SAH). Methods In vitro expression patterns of HO-1 and circadian rhythm genes were analyzed in the microglial BV-2 cell line and primary microglia (PMG) using Western blot and qPCR. PMG isolated from Hmox1 fl/fl and LyzM-Cre-Hmox1 fl/fl mice were used to evaluate the role of microglial HO-1. We further investigated the in vivo relevance in a murine subarachnoid hemorrhage (SAH) model using Hmox1 fl/fl and LyzM-Cre-Hmox1 fl/fl mice with myeloid cell HO-1 deficiency, inducing SAH at different zeitgeber (ZT) times and analyzing the expression of HO-1 and the circadian control gene Period-2 (Per-2), respectively. Furthermore, we measured the inflammatory cytokine Monocyte Chemoattractant Protein-1 (MCP-1) in the cerebrospinal fluid of SAH patients in correlation with clinical outcome. Results HO-1 baseline expression and response to CO with blood exposure depended on ZT. In vitro expression of circadian control genes was de-synchronized in LyzM-Cre-Hmox1 fl/fl PMG and did not respond to exogenous CO exposure. We found that circadian rhythm plays a crucial role in brain damage after SAH. At ZT2, we observed less phagocytic function, more vasospasm and increased microglial activation. CO reduced mortality at ZT12 in HO-1 deficient mice and reduced the difference between ZT2 and ZT12 in the inflammatory response. Induction of MCP-1 in the CSF from SAH patients was time-dependent and correlated with the expression of circadian control genes, SAH severity, functional impairment and delirium. Conclusions Our data point towards a crucial role for the HO-1 enzyme system and circadian control in neuronal injury after a hemorrhagic stroke.

Ferroptosis is a caspase-independent, iron-dependent form of regulated necrosis extant in traumatic brain injury, Huntington disease, and hemorrhagic stroke. It can be activated by cystine deprivation leading to glutathione depletion, the insufficiency of the antioxidant glutathione peroxidase-4, and the hemolysis products hemoglobin and hemin. A cardinal feature of ferroptosis is extracellular signal-regulated kinase (ERK)1/2 activation culminating in its translocation to the nucleus. We have previously confirmed that the mitogen-activated protein (MAP) kinase kinase (MEK) inhibitor U0126 inhibits persistent ERK1/2 phosphorylation and ferroptosis. Here, we show that hemin exposure, a model of secondary injury in brain hemorrhage and ferroptosis, activated ERK1/2 in mouse neurons. Accordingly, MEK inhibitor U0126 protected against hemin-induced ferroptosis. Unexpectedly, U0126 prevented hemin-induced ferroptosis independent of its ability to inhibit ERK1/2 signaling. In contrast to classical ferroptosis in neurons or cancer cells, chemically diverse inhibitors of MEK did not block hemin-induced ferroptosis, nor did the forced expression of the ERK-selective MAP kinase phosphatase (MKP)3. We conclude that hemin or hemoglobin-induced ferroptosis, unlike glutathione depletion, is ERK1/2-independent. Together with recent studies, our findings suggest the existence of a novel subtype of neuronal ferroptosis relevant to bleeding in the brain that is 5-lipoxygenase-dependent, ERK-independent, and transcription-independent. Remarkably, our unbiased phosphoproteome analysis revealed dramatic differences in phosphorylation induced by two ferroptosis subtypes. As U0126 also reduced cell death and improved functional recovery after hemorrhagic stroke in male mice, our analysis also provides a template on which to build a search for U0126's effects in a variant of neuronal ferroptosis.SIGNIFICANCE STATEMENT Ferroptosis is an iron-dependent mechanism of regulated necrosis that has been linked to hemorrhagic stroke. Common features of ferroptotic death induced by diverse stimuli are the depletion of the antioxidant glutathione, production of lipoxygenase-dependent reactive lipids, sensitivity to iron chelation, and persistent activation of extracellular signal-regulated kinase (ERK) signaling. Unlike classical ferroptosis induced in neurons or cancer cells, here we show that ferroptosis induced by hemin is ERK-independent. Paradoxically, the canonical MAP kinase kinase (MEK) inhibitor U0126 blocks brain hemorrhage-induced death. Altogether, these data suggest that a variant of ferroptosis is unleashed in hemorrhagic stroke. We present the first, unbiased phosphoproteomic analysis of ferroptosis as a template on which to understand distinct paths to cell death that meet the definition of ferroptosis.

Cerebral edema, characterized by abnormal fluid accumulation in brain tissue leading to increased intracranial pressure, poses significant challenges for anesthesiologists. This review delves into the pathophysiology, clinical manifestations, diagnostic approaches, pharmacological strategies, and anesthesiological considerations associated with cerebral edema. Disruptions in the blood-brain barrier, alterations in cerebral blood flow, cellular swelling, and aquaporin dysregulation contribute to the complexity of cerebral edema. Clinical presentations vary, encompassing cognitive changes, seizures, and neurological deficits. Accurate diagnosis relies on clinical assessments and neuroimaging, with MRI and CT scans playing pivotal roles. Pharmacological interventions, including osmotic agents, corticosteroids, diuretics, and barbiturates, target specific causes and symptoms. Anesthesiological challenges encompass ICP monitoring, choice of anesthetic agents, maintenance of cerebral perfusion, fluid management, temperature control, and collaboration with neurosurgical teams. This multidisciplinary approach ensures optimal patient care and emphasizes ongoing research collaboration for refining therapeutic strategies. This comprehensive review provides valuable insights for clinicians managing cerebral edema, offering a roadmap for tailored interventions and highlighting the need for continued advancements in understanding and treating this critical condition. Material and method: ​​ The literature review applied standard criteria and focused on PubMed articles using keywords: cerebral edema, pathophysiology, aquaporin, blood-brain barrier, anesthesiology, cerebral edema treatment, corticosteroids

Background: The heme oxygenase-1 (HO-1) enzyme pathway is of crucial importance in the removal of toxic blood components and regulation of neuroinflammation following hemorrhagic stroke. Although a circadian pattern dependency in the incidence and severity of hemorrhagic stroke exists, it is unknown whether the activity of the HO-1 system in the context of hemorrhagic injury also exhibits circadian dependency. We hypothesized that the circadian regulation of microglial HO-1 would determine the extent of neuroinflammation and neuronal injury in a murine model of subarachnoid hemorrhage (SAH). Methods: In vitro expression patterns of HO-1 and circadian rhythm genes were analyzed in the microglial BV-2 cell line and primary microglia (PMG) using Western blot and qPCR. PMG isolated from Hmox1fl/fl and LyzM-Cre-Hmox1fl/fl mice were used to evaluate the role of microglial HO-1. We further investigated the in vivo relevance in a murine subarachnoid hemorrhage (SAH) model using Hmox1fl/fl and LyzM-Cre-Hmox1fl/fl mice with myeloid cell HO-1 deficiency, inducing SAH at different zeitgeber (ZT) times and analyzing the expression of HO-1 and the circadian control gene Period-2 (Per-2), respectively. Furthermore, we measured the inflammatory cytokine Monocyte Chemoattractant Protein-1 (MCP-1) in the cerebrospinal fluid of SAH patients in correlation with clinical outcome. Results: HO-1 baseline expression and response to CO with blood exposure depended on ZT. In vitro expression of circadian control genes was de-synchronized in LyzM-Cre-Hmox1fl/fl PMG and did not respond to exogenous CO exposure. We found that circadian rhythm plays a crucial role in brain damage after SAH. At ZT2, we observed less phagocytic function, more vasospasm and increased microglial activation. CO reduced mortality at ZT12 in HO-1 deficient mice and reduced the difference between ZT2 and ZT12 in the inflammatory response. Induction of MCP-1 in the CSF from SAH patients was time-dependent and correlated with the expression of circadian control genes, SAH severity, functional impairment and delirium. Conclusions: Our data point towards a crucial role for the HO-1 enzyme system and circadian control in neuronal injury after a hemorrhagic stroke. [ABSTRACT FROM AUTHOR]

Intracranial hemorrhages require an immediate diagnosis to optimize patient management and outcomes, and CT is the modality of choice in the emergency setting. We aimed to evaluate the performance of the first scanner-integrated artificial intelligence algorithm to detect brain hemorrhages in a routine clinical setting. This retrospective study includes 435 consecutive non-contrast head CT scans. Automatic brain hemorrhage detection was calculated as a separate reconstruction job in all cases. The radiological report (RR) was always conducted by a radiology resident and finalized by a senior radiologist. Additionally, a team of two radiologists reviewed the datasets retrospectively, taking additional information like the clinical record, course, and final diagnosis into account. This consensus reading served as a reference. Statistics were carried out for diagnostic accuracy. Brain hemorrhage detection was executed successfully in 432/435 (99%) of patient cases. The AI algorithm and reference standard were consistent in 392 (90.7%) cases. One false-negative case was identified within the 52 positive cases. However, 39 positive detections turned out to be false positives. The diagnostic performance was calculated as a sensitivity of 98.1%, specificity of 89.7%, positive predictive value of 56.7%, and negative predictive value (NPV) of 99.7%. The execution of scanner-integrated AI detection of brain hemorrhages is feasible and robust. The diagnostic accuracy has a high specificity and a very high negative predictive value and sensitivity. However, many false-positive findings resulted in a relatively moderate positive predictive value. [ABSTRACT FROM AUTHOR]

An intrasaccular flow diverter, the Woven EndoBridge device has emerged as an alternate intervention for complex aneurysms of the ACA, MCA, ICA, and basilar artery. However, few studies report the use of the WEB device in off-label locations. This case report aims to contribute to this limited collection of data. We present a case of a 53-year-old male presenting with occipital headaches, found to have vertebrobasilar junction aneurysm. The WEB device was successfully used to embolize a large aneurysm of the vertebrobasilar junction, a current off-label location. This represents a new use of the WEB device, as well as an approach that addresses the limitations of other techniques used for vertebrobasilar junction aneurysms.

A 61-year-old man was found dead on the terrace in front of his house. The body showed external signs of advanced (Grade 4) putrefaction. Routine post-mortem computed tomography (PMCT) was conducted prior to the forensic autopsy showing a radiological alteration index (RAI) of 100. Due to a suspicious hyperdense brain lesion seen in PMCT, additional post-mortem magnetic resonance imaging (PMMR) of the head was performed for research purpose. Compared to PMCT, the lesion appeared considerably more detailed in PMMR with a slightly hyperintense and focal hypointense signal in T2w images and an isointense and focal hyperintense signal in T1w images. Autoptic assessment of the brain lesion was considerably complicated due to softening and partial liquefaction of the brain. Considering post-mortem imaging and autopsy results, the lesion was determined as an acute brain hemorrhage. Case findings indicate that PMMR may be superior to autopsy in terms of diagnosis and localization of cerebral hemorrhage in putrefied brains.

Hemorrhagic complications arising from ventricular drainage procedures are typically asymptomatic and of low volume. A particular subset of these complications, known as delayed intracranial hemorrhage (DICH), is however recognized for its particularly poor prognosis. We primarily aimed to identify epidemiological characteristics associated with DICH, to shed light on its occurrence and potential risk factors. To do so, we performed a retrospective analysis of a series of ten patients who presented with DICH in the context of a ruptured brain arteriovenous malformation (bAVM) and a systematic literature review of all DICH cases reported in the literature. Our ten patients showed delayed neurological deterioration after a ventriculoperitoneal shunt (VPS) procedure, with a computed tomography (CT) scan revealing a DICH surrounding the ventricular catheter, distinct and away from the nidus of their previously ruptured bAVM. Four patients (40%) rapidly declined and passed away, three (30%) required surgical management and the remaining three (30%) demonstrated gradual clinical improvement with conservative management. In the literature, most patients presenting with DICH had hydrocephalus associated with neurovascular disorders (47% of cases), such as bAVM rupture in our present series. These constatations point out the significance of the underlying pathologies potentially being predisposed to these unusual complications. [ABSTRACT FROM AUTHOR]

Thanks to a more widespread knowledge of the disease, and improved diagnostic techniques, the clinical spectrum of cerebral amyloid angiopathy (CAA) is now broad. Sporadic CAA, hereditary CAA, CAA-related inflammation (CAA-ri) and iatrogenic CAA (iCAA) create a clinical and radiological continuum which is intriguing and only partially discovered. Despite being relatively rare, CAA-ri, an aggressive subtype of CAA with vascular inflammation, has gained growing attention also because of the therapeutic efficacy of anti-inflammatory and immunomodulating drugs. More recently, diagnostic criteria have been proposed for an unusual variant of CAA, probably related to an iatrogenic origin (iCAA), toward which there is mounting scientific interest. These atypical forms of CAA are still poorly known, and their recognition can be challenging and deserve to be pursued in specialized referral centres. The aim of this brief review is to focus current developments in the field of rare forms of CAA, its pathogenesis as well as clinical and biological features in order to increase awareness of these rare forms. [ABSTRACT FROM AUTHOR]

The third cause of morbidity and mortality in many countries is cerebrovascular accident (CVA), the incidence is higher in hemodialysis patients. The presence of hemorrhagic stroke is associated with worse results; early diagnosis and treatment are essential due to its rapid expansion, which causes neurological detriment, up to a fatal outcome. The case of a 52-year-old woman is presented, admitted for emergency service on 05/23/23 with a history of three-weekly renal replacement therapy, arterial hypertension, diabetes mellitus; clinical picture with sudden headache of moderate intensity, accompanied by drowsiness, numbness at the level of the cervicodorsal spine, paraparesis in the lower extremities and hypertension; skull tomography with pre-brain stem hemorrhagic stroke; he was admitted to the Intensive Care Unit (ICU) for monitoring and management, however despite the treatment he evolved torpidly and died on 06/11/2023. [ABSTRACT FROM AUTHOR]

BackgroundTraumatic brain injury (TBI) causes early seizures and is the leading cause of post-traumatic epilepsy. We prospectively assessed structural imaging biomarkers differentiating patients who develop seizures secondary to TBI from patients who do not.DesignMulticentre prospective cohort study starting in 2018. Imaging data are acquired around day 14 post-injury, detection of seizure events occurred early (within 1 week) and late (up to 90 days post-TBI).ResultsFrom a sample of 96 patients surviving moderate-to-severe TBI, we performed shape analysis of local volume deficits in subcortical areas (analysable sample: 57 patients; 35 no seizure, 14 early, 8 late) and cortical ribbon thinning (analysable sample: 46 patients; 29 no seizure, 10 early, 7 late). Right hippocampal volume deficit and inferior temporal cortex thinning demonstrated a significant effect across groups. Additionally, the degree of left frontal and temporal pole thinning, and clinical score at the time of the MRI, could differentiate patients experiencing early seizures from patients not experiencing them with 89% accuracy.Conclusions and relevanceAlthough this is an initial report, these data show that specific areas of localised volume deficit, as visible on routine imaging data, are associated with the emergence of seizures after TBI.

Cerebral microbleeds (CMB) are a common MRI finding, representing underlying cerebral microhemorrhages (CMH). The etiology of CMB and microhemorrhages is obscure. We conducted a pathological investigation of CMH, combining standard and immunohistological analyses of postmortem human brains. We analyzed 5 brain regions (middle frontal gyrus, occipital pole, rostral cingulate cortex, caudal cingulate cortex, and basal ganglia) of 76 brain bank subjects (mean age ± SE 90 ± 1.4 years). Prussian blue positivity, used as an index of CMH, was subjected to quantitative analysis for all 5 brain regions. Brains from the top and bottom quartiles (n = 19 each) were compared for quantitative immunohistological findings of smooth muscle actin, claudin-5, and fibrinogen, and for Sclerosis Index (SI) (a measure of arteriolar remodeling). Brains in the top quartile (i.e. with most extensive CMH) had significantly higher SI in the 5 brain regions combined (0.379 ± 0.007 vs 0.355 ± 0.008; p

Brain microbleeds are increased in chronic kidney disease (CKD) and their presence increases risk of cognitive decline and stroke. We examined the interaction between CKD and brain microhemorrhages (the neuropathological substrate of microbleeds) in mouse and cell culture models and studied progression of microbleed burden on serial brain imaging from humans. Mouse studies: Two CKD models were investigated: adenine-induced tubulointerstitial nephritis and surgical 5/6 nephrectomy. Cell culture studies: bEnd.3 mouse brain endothelial cells were grown to confluence, and monolayer integrity was measured after exposure to 5-15% human uremic serum or increasing concentrations of urea. Human studies: Progression of brain microbleeds was evaluated on serial MRI from control, pre-dialysis CKD, and dialysis patients. Microhemorrhages were increased 2-2.5-fold in mice with CKD independent of higher blood pressure in the 5/6 nephrectomy model. IgG staining was increased in CKD animals, consistent with increased blood-brain barrier permeability. Incubation of bEnd.3 cells with uremic serum or elevated urea produced a dose-dependent drop in trans-endothelial electrical resistance. Elevated urea induced actin cytoskeleton derangements and decreased claudin-5 expression. In human subjects, prevalence of microbleeds was 50% in both CKD cohorts compared with 10% in age-matched controls. More patients in the dialysis cohort had increased microbleeds on follow-up MRI after 1.5 years. CKD disrupts the blood-brain barrier and increases brain microhemorrhages in mice and microbleeds in humans. Elevated urea alters the actin cytoskeleton and tight junction proteins in cultured endothelial cells, suggesting that these mechanisms explain (at least in part) the microhemorrhages and microbleeds observed in the animal and human studies.

The objective of this study is to assess the effectiveness of a stroke clinic in stroke prevention and progression of cerebral microbleeds (CMB). We conducted a retrospective observational study of patients who visited a stroke clinic between January 2011 and March 2017. Susceptibility-weighted imaging (SWI) MRI studies were obtained at baseline and follow-up visits to identify new infarctions and CMB progression. Patients with CMB who also underwent brain computed tomography (CT) imaging were identified and their cerebral arterial calcification was quantified to evaluate the relationship between the extent of intracranial calcification and CMB burden. A total of 64 stroke patients (mean age 73.1 ± 11.0, 47% males) had CMB on baseline and follow-up MRI studies. During a mean follow-up period of 22.6 months, four strokes occurred (4/64, 6%; 3 ischemic, 1 hemorrhagic), producing mild neurological deficit. Progression of CMB was observed in 54% of patients with two MRIs and was significantly associated with length of follow-up. Subjects with intracranial calcification score > 300 cm3 had higher CMB count than those with scores

ObjectiveA high level of vascular endothelial growth factor (VEGF) has been implicated in brain arteriovenous malformation (bAVM) bleeding and rupture. However, direct evidence is missing. In this study the authors used a mouse bAVM model to test the hypothesis that elevation of focal VEGF levels in bAVMs exacerbates the severity of bAVM hemorrhage.MethodsBrain AVMs were induced in adult mice in which activin receptor-like kinase 1 (Alk1, a gene that causes AVM) gene exons 4-6 were floxed by intrabasal ganglia injection of an adenoviral vector expressing Cre recombinase to induce Alk1 mutation and an adeno-associated viral vector expressing human VEGF (AAV-VEGF) to induce angiogenesis. Two doses of AAV-VEGF (5 × 109 [high] or 2 × 109 [low]) viral genomes were used. In addition, the common carotid artery and external jugular vein were anastomosed in a group of mice treated with low-dose AAV-VEGF 6 weeks after the model induction to induce cerebral venous hypertension (VH), because VH increases the VEGF level in the brain. Brain samples were collected 8 weeks after the model induction. Hemorrhages in the bAVM lesions were quantified on brain sections stained with Prussian blue, which detects iron deposition. VEGF levels were quantified in bAVM tissue by enzyme-linked immunosorbent assay.ResultsCompared to mice injected with a low dose of AAV-VEGF, the mice injected with a high dose had higher levels of VEGF (p = 0.003) and larger Prussian blue-positive areas in the bAVM lesion at 8 or 9 weeks after model induction (p = 0.002). VH increased bAVM hemorrhage in the low-dose AAV-VEGF group. The overall mortality in the high-dose AAV-VEGF group was 26.7%, whereas no mouse died in the low-dose AAV-VEGF group without VH. In contrast, VH caused a mortality of 50% in the low-dose AAV-VEGF group.ConclusionsUsing mouse bAVM models, the authors provided direct evidence that elevation of the VEGF level increases bAVM hemorrhage and mouse mortality.

Intraparenchymal brain hemorrhage is not uncommon and results from a wide variety of causes ranging from trauma to tumor. Many a time, it is not possible to determine the exact cause of non-traumatic hemorrhage on conventional magnetic resonance imaging (MRI). Susceptibility-weighted imaging (SWI) is a high-resolution (3D) gradient-echo sequence. It is extremely sensitive to the inhomogeneity of the local magnetic field and highly useful in identifying the small amount of hemorrhage, which may be inapparent on other MR pulse sequences. In this review, we present different pattern of an intra-parenchymal brain hemorrhage on SWI with emphasis on differential diagnosis.

Abstract Background Limited studies have evaluated the use of ultrasound for detection of intracerebral hemorrhage (ICH) using diagnostic ultrasound Transcranial Doppler machines in adults. The feasibility of ICH detection using Point of care Ultrasound (POCUS) machines has not been explored. We evaluated the feasibility of using cranial POCUS B mode imaging performed using intensive care unit (ICU) POCUS device for ICH detection with a secondary goal of mapping optimal imaging technique and brain topography likely to affect sensitivity and specificity of ICH detection with POCUS. Materials and methods After obtaining IRB approval, a blinded investigator performed cranial ultrasound (Fujifilm, Sonosite® Xporte, transcranial and abdominal presets) through temporal windows on 11 patients with intracerebral pathology within 72 h of last CT/MRI (computed tomography scan/magnetic resonance imaging) brain after being admitted to a neurocritical care unit in Aug 2020 and Nov 2020–Mar 2021. Images were then compared to patient’s CT/MRI to inform topography. Inferential statistics were reported. Results Mean age was 57 (28–77 years) and 6/11 were female. Six patients were diagnosed with ICH, 3 with ischemic stroke, 1 subarachnoid hemorrhage, and 1 brain tumor. The sensitivity and specificity of point of care diagnosis of ICH compared to CT/MRI brain was 100% and 50%, respectively. Mean time between ultrasound scan and CT/MRI was 13.3 h (21 min–39 h). Falx cerebri, choroid calcification and midbrain-related artifacts were the most reproducible hyperechoic signals. Abdominal preset on high gain yielded less artifact than Transcranial Doppler preset for cranial B mode imaging. False positive ICH diagnosis was attributed to intracerebral tumor and midbrain-related artifact. Conclusions Our exploratory analysis yielded preliminary data on use of point of care cranial ultrasound for ICH diagnosis to inform imaging techniques, cranial topography on B mode and sample size estimation for future studies to evaluate sensitivity and specificity of cranial POCUS in adult patients. This pilot study is limited by small sample size and over representation of ICH in the study. Cranial POCUS is feasible using POCUS machines and may have potential as a screening tool if validated in adequately powered studies.

Stroke as one of the main problems in the medical field. From the three leading causes of death in the world including 13% are coronary heart disease and 12% are cancer. Stroke occurs mostly in developed countries such as Indonesia, of all deaths in Indonesia, the cause of stroke is 7.9%. One of the efforts to minimize the risk of stroke is take preventive measures in stroke patients, before and after an attack. Ways to overcome stroke are primary and secondary measures. Prevention of stroke symptoms can be avoided by prompt and appropriate treatment in stroke care according to medical service standards. This study applies texture analysis and improves the quality of CT-Scan or MRI brain images using the Hybrid Thresholding (HT) method, which combines edge detection and P-File methods. Differences the texture of the image a brain hemorrhage that is indicated by stroke and clarify the quality of the image of a brain hemorrhage that is indicated by a stroke with the parameters of contrast, correlation, energy, homogeneity. The results of segmentation and feature and texture extraction are then classified using the Backpropagation Neural Network (BNN) method with variations in the learning rate value, resulting in the best test at a learning rate of 0.1 with an error percentage of 2%. The results of the classification of the calculation of the area of brain bleeding and analysis of image quality in classifying brain strokes with an accuracy level are: 27 / 3 x 100% = 90.0%. [ABSTRACT FROM AUTHOR]

Artificial Intelligence (AI) refers to the ability to learn, remember, predict, and make an optimal judgment based on Computer-assisted Design (CAD) Systems. Traditional CAD algorithms and methods on head CT scans focused on the automatic recognition, segmentation, and classification of the abnormalities. But, these approaches were encountered with several limitations like (i) smaller dataset size, (ii) negative Transfer Learning, and (iii) improper localization. This paper proposed the new dense-layered deep neural model to classify brain hemorrhages using head CT scans. The proposed model is the ten-layered network having dense blocks with skip connections. It uses the cross-chained connection between dense blocks to minimize gradient loss while training. Later, the last layer of the model is extended with Grad-Cam for localization of the affected cell regions. The model performance is evaluated on a dataset of head CT scans of size 427.25GB. The dataset is partitioned into 752,800 images in the training set and 121,232 images in the testing set. The experimentation results achieved an accuracy of 98.32% with a mean logarithmic loss of 0.06487. The average classification accuracy of the proposed model on multiple-class hemorrhages is 98.27%. The experimentation results are found satisfactory having the best AUC-ROC accuracy of 98.32%. The comparative analysis of the model with other traditional deep neural networks proves the efficacy of the model in predicting results. Also, in comparison with other methods, the gained results are found satisfactory with an increase in the accuracy of 1.3%. [ABSTRACT FROM AUTHOR]

Thanks to a more widespread knowledge of the disease, and improved diagnostic techniques, the clinical spectrum of cerebral amyloid angiopathy (CAA) is now broad. Sporadic CAA, hereditary CAA, CAA-related inflammation (CAA-ri) and iatrogenic CAA (iCAA) create a clinical and radiological continuum which is intriguing and only partially discovered. Despite being relatively rare, CAA-ri, an aggressive subtype of CAA with vascular inflammation, has gained growing attention also because of the therapeutic efficacy of anti-inflammatory and immunomodulating drugs. More recently, diagnostic criteria have been proposed for an unusual variant of CAA, probably related to an iatrogenic origin (iCAA), toward which there is mounting scientific interest. These atypical forms of CAA are still poorly known, and their recognition can be challenging and deserve to be pursued in specialized referral centres. The aim of this brief review is to focus current developments in the field of rare forms of CAA, its pathogenesis as well as clinical and biological features in order to increase awareness of these rare forms.

The objective of this study is to assess the effectiveness of a stroke clinic in stroke prevention and progression of cerebral microbleeds (CMB). We conducted a retrospective observational study of patients who visited a stroke clinic between January 2011 and March 2017. Susceptibility-weighted imaging (SWI) MRI studies were obtained at baseline and follow-up visits to identify new infarctions and CMB progression. Patients with CMB who also underwent brain computed tomography (CT) imaging were identified and their cerebral arterial calcification was quantified to evaluate the relationship between the extent of intracranial calcification and CMB burden. A total of 64 stroke patients (mean age 73.1 ± 11.0, 47% males) had CMB on baseline and follow-up MRI studies. During a mean follow-up period of 22.6 months, four strokes occurred (4/64, 6%; 3 ischemic, 1 hemorrhagic), producing mild neurological deficit. Progression of CMB was observed in 54% of patients with two MRIs and was significantly associated with length of follow-up. Subjects with intracranial calcification score > 300 cm3 had higher CMB count than those with scores

ObjectiveA high level of vascular endothelial growth factor (VEGF) has been implicated in brain arteriovenous malformation (bAVM) bleeding and rupture. However, direct evidence is missing. In this study the authors used a mouse bAVM model to test the hypothesis that elevation of focal VEGF levels in bAVMs exacerbates the severity of bAVM hemorrhage.MethodsBrain AVMs were induced in adult mice in which activin receptor-like kinase 1 (Alk1, a gene that causes AVM) gene exons 4-6 were floxed by intrabasal ganglia injection of an adenoviral vector expressing Cre recombinase to induce Alk1 mutation and an adeno-associated viral vector expressing human VEGF (AAV-VEGF) to induce angiogenesis. Two doses of AAV-VEGF (5 × 109 [high] or 2 × 109 [low]) viral genomes were used. In addition, the common carotid artery and external jugular vein were anastomosed in a group of mice treated with low-dose AAV-VEGF 6 weeks after the model induction to induce cerebral venous hypertension (VH), because VH increases the VEGF level in the brain. Brain samples were collected 8 weeks after the model induction. Hemorrhages in the bAVM lesions were quantified on brain sections stained with Prussian blue, which detects iron deposition. VEGF levels were quantified in bAVM tissue by enzyme-linked immunosorbent assay.ResultsCompared to mice injected with a low dose of AAV-VEGF, the mice injected with a high dose had higher levels of VEGF (p = 0.003) and larger Prussian blue-positive areas in the bAVM lesion at 8 or 9 weeks after model induction (p = 0.002). VH increased bAVM hemorrhage in the low-dose AAV-VEGF group. The overall mortality in the high-dose AAV-VEGF group was 26.7%, whereas no mouse died in the low-dose AAV-VEGF group without VH. In contrast, VH caused a mortality of 50% in the low-dose AAV-VEGF group.ConclusionsUsing mouse bAVM models, the authors provided direct evidence that elevation of the VEGF level increases bAVM hemorrhage and mouse mortality.

Intraparenchymal brain hemorrhage is not uncommon and results from a wide variety of causes ranging from trauma to tumor. Many a time, it is not possible to determine the exact cause of non-traumatic hemorrhage on conventional magnetic resonance imaging (MRI). Susceptibility-weighted imaging (SWI) is a high-resolution (3D) gradient-echo sequence. It is extremely sensitive to the inhomogeneity of the local magnetic field and highly useful in identifying the small amount of hemorrhage, which may be inapparent on other MR pulse sequences. In this review, we present different pattern of an intra-parenchymal brain hemorrhage on SWI with emphasis on differential diagnosis. [ABSTRACT FROM AUTHOR]