Development Of Brain Edema Research Articles

Convexity Meningioma, Parasagittal Meningioma, Falx Meningioma

During surgery for meningioma, basic surgical techniques and strategies required for the removal of the tumor are common, particularly for tumors located superficially, such as convexity, parasagittal, and falx meningiomas. Four basic surgical techniques, including detachment; devascularization; debulking; and dissection should be combined and repeated in appropriate sequence, tailored to the specific conditions of each tumor. This eventually enables the total circumferential dissection of the tumor from the surrounding tissues. It is essential to retract the tumor towards the space created at the tumor center through internal debulking, rather than retracting the normal brain, to avoid damage to the surrounding brain tissue. During surgery for parasagittal meningioma with venous sinus occlusion, it is crucial to preserve the cortical veins that have developed as collateral pathways to prevent venous complications. During surgery for falx meningioma, the selection of a surgical approach including a contralateral approach based on factors such as the development of bridging veins and significant peritumoral brain edema is required. In this article, detailed surgical procedures for convexity meningioma, parasagittal meningioma, and falx meningioma were described focusing on the application of fundamental surgical techniques tailored to each tumor type.

Glymphatic System Impairment Contributes to the Formation of Brain Edema After Ischemic Stroke.

Blood-brain barrier damage has traditionally been considered to determine the occurrence and development of poststroke brain edema, a devastating and life-threatening complication. However, no treatment strategy targeting blood-brain barrier damage has been proven clinically effective in ameliorating brain edema. In mice with stroke models induced by transient middle cerebral artery occlusion (MCAO), the changes in glymphatic system (GS) function impairment were detected by ex vivo fluorescence imaging, 2-photon in vivo imaging, and magnetic resonance imaging within 1 week after MCAO, and the effects of GS impairment and recovery on the formation and resolution of brain edema were evaluated. In addition, in patients with ischemic stroke within 1 week after onset, changes in GS function and brain edema were also observed by magnetic resonance imaging. We found that the extravasation of protein-rich fluids into the brain was not temporally correlated with edema formation after MCAO in mice, as brain edema reabsorption preceded blood-brain barrier closure. Strikingly, the time course of edema progression matched well with the GS dysfunction after MCAO. Pharmacological enhancement of the GS function significantly alleviated brain edema developed on day 2 after MCAO, accompanied by less deposition of Aβ (amyloid-β) and better cognitive function. Conversely, functional suppression of the GS delayed the absorption of brain edema on day 7 after MCAO. Moreover, patients with ischemic stroke revealed a consistent trend of GS dysfunction after reperfusion as MCAO mice, which was correlated with the severity of brain edema and functional outcomes. GS is a key contributor to the formation of brain edema after ischemic stroke, and targeting the GS may be a promising strategy for treating brain edema in ischemic stroke. URL: https://www.chictr.org.cn/showproj.html?proj=162857; Unique identifier: NFEC-2019-189.

Diffusion MRI in Intracranial Hypertension: Quantitative Assessment

Intracranial hypertension (IH) is a neurological disease characterized by increased intracranial pressure. Idiopathic intracranial hypertension (IIH) is characterized by increased intracranial pressure without an underlying neuroradiological cause (1-3). The IH associated with a reason such as a mass, hydrocephalus, or drug use, is referred to as secondary intracranial hypertension (SIH). We aimed to detect and determine whether the increased intracranial pressure causes a change in the diffusion values of the brain in the diffusion MRI images. The study includes 24 consecutive patients diagnosed with IIH and 18 consecutive patients diagnosed with secondary intracranial hypertension (SIH). The control group included 24 patients. Measurement of apparent diffusion coefficient (ADC) was performed using DWI sections obtained from subcortical white matter and the cortex of the frontal lobe in the basal ganglia plane, caudate nucleus head, thalamus, the posterior leg of the internal capsule, corpus callosum splenium; in the centrum semiovale plane, from the central white matter region. with 1.5T MRI using b=500s/mm2 and b=1000s/mm2 values both in patients and control groups. Mean ADC values were compared between IIH, SIH patients and control groups. The ADC values from the head of the caudate nucleus and the cortex were significantly higher in the IIH group compared to the control group. When the ADC values of the SIH and control groups were compared, it was found that some of the ADC measurements (subcortical white matter, cortex and semioval center) were significantly different. The comparison of the IIH and the SIH groups revealed that the ADC measurements of central white matter in the centrum semiovale, the subcortical white matter and the posterior leg of the internal capsule were significantly different. We have found increased diffusion of IIH and SIH patients, which supports the development of brain edema. Even though the mechanism of the brain edema in IIH is not entirely clear, it is thought that the mechanism is different from the brain edema caused by a mass or a sinus thrombosis.

TAK-3 Inhibits Lipopolysaccharide-Induced Neuroinflammation in Traumatic Brain Injury Rats Through the TLR-4/NF-κB Pathway.

The activation of the inflammatory response is regarded as a pivotal factor in the pathogenesis of TBI. Central nervous system infection often leads to the exacerbation of neuroinflammation following TBI, primarily caused by Gram-negative bacteria. This study aims to elucidate the effects of the novel anti-inflammatory drug TAK-3 on LPS-induced neuroinflammation in TBI rats. In conjunction with the rat controlled cortical impact model, we administered local injections of Lipopolysaccharide to the impact site. Subsequently, interventions were implemented through intraperitoneal injections of TAK-3 and NF-κB activitor2 to modulate the TLR4/NF-κB axis The impact of LPS on neurological function was assessed using mNSS, open field test, and brain water content measurement. Inflammatory markers, including TNF-α, IL-1β, IL-6 and IL-10 were assessed to evaluate the condition of neuritis by Elisa. The activation of the TLR-4/NF-κB signaling pathway was detected by immunofluorescence staining and Western blot to assess the anti-inflammatory effects of TAK-3. The administration of LPS exacerbated neurological damage in rats with TBI, as evidenced by a reduction in motor activity and an increase in anxiety-like behavior. Furthermore, LPS induced disruption of the blood-brain barrier integrity and facilitated the development of brain edema. The activation of microglia and astrocytes by LPS at the cellular and molecular levels has been demonstrated to induce a significant upregulation of neuroinflammatory factors. The injection of TAK-3 attenuated the neuroinflammatory response induced by LPS. The present study highlights the exacerbating effects of LPS on neuroinflammation in TBI through activation of the TLR-4/NF-κB signaling pathway. TAK-3 can modulate the activity of this signaling axis, thereby attenuating neuroinflammation and ultimately reducing brain tissue damage.

Effect of Bevacizumab on traumatic penumbra brain edema in rats at different time points

ABSTRACT Traumatic penumbra (TP) is a secondary injury area located around the core area of traumatic brain injury after brain trauma, and is an important factor affecting the outcome of traumatic brain injury (TBI). The main pathological change caused by TP is brain edema, including (cellular brain edema and vascular brain edema). The formation and development of brain edema in the TP area are closely related to the blood-brain barrier (BBB) and vascular endothelial growth factor (VEGF). VEGF is a vascular permeability factor that can promote angiogenesis and increase BBB permeability, and there is a debate on the pros and cons of its role in early TBI. Therefore, in the early stage of TBI, when using the VEGF inhibitor bevacizumab to treat TP area brain edema, the timing of bevacizumab administration is particularly important, and there are currently no relevant literature reports. This article explores the treatment time window and optimal treatment time point of bevacizumab in the treatment of cerebral edema in the TP area by administering the same dose of bevacizumab at different time points after brain injury in rats. The results showed that there was traumatic brain edema in TP area, BBB structure and function were damaged, VEGF expression and angiogenesis were increased. Compared with TBI + NS Group, after Bevacizumab treatment, brain edema in TP area was alleviated, BBB structure and function were improved, VEGF expression and angiogenesis were decreased in each treatment group, and the effect of TBI + Bevacizumab 1 h group was the most significant. Bevacizumab can be used as a targeted therapy for traumatic brain edema. The therapeutic time window of bevacizumab for traumatic brain edema is within 12 hours after TBI, and 1 h is the optimal therapeutic time point.

Intracranial dynamics biomarkers at traumatic cerebral vasospasm

IntroductionPatients who suffer severe traumatic brain injury (sTBI) and cerebral vasospasm (CVS) frequently have posttraumatic cerebral ischemia (PCI). The research questionwas to study changes in cerebral microcirculatory bed parameters in sTBI patients with CVS and with or without PCI. Material and methodsA total of 136 severe TBI patients were recruited in the study. All patients underwent perfusion computed tomography, intracranial pressure monitoring, and transcranial Doppler. The levels of cerebrovascular resistance (CVR), cerebral arterial compliance (CAC), cerebrovascular time constant (CTC), and critical closing pressure (CCP) were measured using the neuromonitoring complex. Statistical analysis was performed using parametric and nonparametric methods and factor analysis. The patients were dichotomized into PCI-positive (n = 114) and PCI-negative (n = 22) groups. Data are presented as mean values (standard deviations). ResultsCVR was significantly increased, whereas CAC, CTC, and CCP were significantly decreased in sTBI patients with CVS and PCI development (p < 0.05). Factor analyses revealed that all studied microcirculatory bed parameters were significantly associated with the development of PCI (p < 0.05). Discussion and conclusionThe changes in all studied microcirculatory bed parameters in TBI patients with CVS were significantly associated with PCI development, which enables us to regard them as the biomarkers of CVS and PCI development. The causes of the described microcirculatory bed parameters changes might include complex (cytotoxic and vasogenic) brain edema development, regional microvascular spasm, and dysfunction of pericytes. A further prospective study is warranted.

Surface-Tailored Nanoplatform for the Diagnosis and Management of Stroke: Current Strategies and Future Outlook.

Stroke accounts for one of the top leading reasons for neurological mortality and morbidity around the globe. Both ischemic and hemorrhagic strokes lead to local hypoxia and are brought about by the occlusion or rupturing of the blood vessels. The events taking place after the onset of a stroke include membrane ion pump failure, calcium and glutamate-mediated excitotoxicity, increased ROS production causing DNA damage, mitochondrial dysfunction, oxidative stress, development of brain edema, and microvascular dysfunction. To date, tissue plasminogen activator (tPA) therapy and mechanical removal of blood clots are the only clinically available stroke therapies, approved by Food and Drug Administration (FDA). But because of the narrow therapeutic window of around 4.5h for tPA therapy and complications like systemic bleeding and anaphylaxis, more clinical trials are ongoing in the same field. Therefore, using nanocarriers with diverse physicochemical properties is a promising strategy in treating and diagnosing stroke as they can efficiently bypass the tight blood-brain barrier (BBB) through mechanisms like receptor-mediated transcytosis and help achieve controlled and targeted drug delivery. In this review, we will mainly focus on the pathophysiology of stroke, BBB alterations following stroke, strategies to target BBB for stroke therapies, different types of nanocarriers currently being used for therapeutic intervention of stroke, and biomarkers as well as imaging techniques used for the detection and diagnosis of stroke.

Cerebroprotective effect of sitagliptin and aminoguanidine combination in disorders of cerebral circulation

The aim of the study was to evaluate a cerebroprotective activity of the sitagliptin and aminoguanidine combination in rats with an acute and chronic cerebral circulation insufficiency, as well as with a traumatic brain injury.Materials and methods. The study was carried out on male Wistar rats in 3 stages using, respectively, a model of a chronic pathology: a chronic cerebral circulation insufficiency (CCCI), as well as 2 models of the acute brain injury (BI): an acute cerebral circulation insufficiency (ACCI), and a traumatic brain injury (TBI). А CCCI was modeled by a bilateral stenosis of the common carotid arteries (by 50%), a model of a hemorrhagic stroke caused by an intracerebral injection of the autologous blood was used as a stroke, a TBI was modeled by a mechanical damage to the brain tissue. To assess the pathology course severity, the following tests were used: Adhesion test, Open field, Morris water maze test, as well as Garcia and Combs&amp;D’Alecy scales. In the animals with an acute damage to the brain at the end of the experiment, the severity of edema of the affected hemisphere was also determined. The treatment was with sitagliptin (10 mg/kg), aminoguanidine (25 mg/kg), or a combination thereof. The obtained data were subjected to the statistical processing.Results. In the course of the study, it was found out that the administration of a sitagliptin and aminoguanidine combination, unlike each of the components, had a cerebroprotective effect in the animals with a chronic or acute damage to the brain, reducing the severity of psychoneurological (cognitive and sensory-motor) disorders, as well as the brain edema.Conclusion. Aminoguanidine, as an iNOS blocker, enhances the action of sitagliptin, preventing the brain edema development and reducing the neurological deficit severity (the severity of cognitive and sensory-motor impairments) in the animals with an acute and chronic cerebral circulation insufficiency.

Bobbing, weaving, collapsing and dying-preventing boxing deaths in the ring

Background: Professional boxing is a popular combat sport around the world. It is unfortunately also a sport which carries a very high risk of concussion and more severe forms of traumatic brain injury (TBI). In a sport where every punch thrown to the opponent’s head is thrown with the intention of winning by causing a knockout (KO), TBI is an omnipresent danger. Traumatic subdural hematoma is the most common cause of boxing related mortality. The boxer either collapses in the ring during the fight or in the immediate aftermath of the fight. Discussion: Boxers with traumatic epidural and subdural hematoma often have a lucid interval and then exhibit rapid at times precipitous neurological deterioration as the hematoma expands. Rapid loss of consciousness follows leading to a comatose state. Development of brain edema and secondary ischemic injury are the other substrates of delayed neurological deterioration. Conclusion: Both the referee and the ringside physician (s) should be aware of this clinical presentation of acute TBI so that the fights can be stopped in a timely fashion, neither too early but certainly never too late! Innovate solutions can help present tragedies in the ring.

Basic principle in the management of brain edema and elevated intracranial pressure

Background: Brain edema is a well-recognized pathophysiological secondary change after primary brain injury. The mechanism of brain edema may differ based on the types of brain edema. However, numerous ion channels are involved in its development and are therefore currently a hot target for anti-edema therapy. Here, this paper reviews the clinically important differences among the types of brain edema and a step-wise management strategy for brain edema and elevated intracranial pressure (ICP).Current Concepts: Brain edema can be classified as cytotoxic, ionic, vasogenic, and interstitial edema. Although the underlying mechanisms may differ among the various types of brain edema, multiple ion channels and the integrity of tight junctions are associated with the development of brain edema. If brain edema aggravates, the intracranial volume expands and leads to an elevation of ICP. A basic principle in the management of ICP includes proper positioning, screening for a need for extraventricular drainage, proper sedation, transient hyperventilation, assessing the intracranial water status with the serum sodium level, optimization of cerebral perfusion pressure, hyperosmolar therapy, targeted temperature management, and induction of a pharmacological coma with sedatives.Discussion and Conclusion: Stepwise treatment strategies are recommended in the management of patients with ICP crisis. Based on the principle, detailed management plans need to be adjusted based on the status of an individual patient.

Spikenet, a targeted therapeutic agent for covid-19, reverses severe lung and brain dysfunction in mice

We established a murine hepatitis virus-1 (MHV-1) coronavirus model, to study disease mechanisms of Covid-19 (Viruses, 2021). With the goal of creating a therapeutic for pregnancy, using advanced imaging techniques, computational modeling, molecular dynamics and spectroscopy, we invented and tested a small peptide, SPIKENET (SPK) with high binding affinity to spike protein of MHV-1. SPK significantly reduced acute (7 days) and long term (1 year) consequences (mortality, pathology, and weight loss) (Front. Pharmacol, 2022, Mol Neurobiol 2022). Since we discovered the role of aquaporins (AQP) water channels in edema development, and that SPK reversed such an effect, we examined the molecular events in the development of lung and brain edema. Using our MHV-1 model (non-pregnant), we examined the involvement of factors known to modulate volume changes in lung and brain, namely [N-Methyl-D-Aspartate receptors (NMDAR1/2), and surfactant A]. Mice were inoculated with 5000 PFU intranasally, and divided into 5 groups (n=5/group): control (no infusion); control with Dulbecco’s Modified Eagle Medium; MHV-1; SPK 5mg/kg/d subcutaneous (s.c.) on days 2,4,6; MHV-1 plus SPK 5mg/kg/d s.c. on days 2,4,6. Mice were sacrificed 7 days post inoculation. Data were subjected to ANOVA and Tukey’s test with a level of significance p< 0.05. Lung NMDAR1/2 levels are increased (160.3 and 124.6%, respectively, p< 0.05) (Fig. 1). Similarly, brain NMDAR1 levels are increased (109.4%, p< 0.05), while brain NMDAR2 level are decreased (42.8%, p< 0.05) (Fig. 1). Surfactant A level decreased in the brain post-infection (57.4%, p< 0.05) while its level increased in the lung after infection (187.2%, p< 0.05) (Fig. 2). SPK normalized NMDAR1/2 and surfactant A levels in lung and brain. We report for the first time that lung and brain NMDA receptors and surfactant A are involved in the development of COVID-19 disease progression. Our invention, SPIKENET, abrogates these critical events, and together with our AQP findings, strongly suggest the potential therapeutic benefit of SPK in counteracting COVID-19.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Management of a Case of Acute Ischaemic Stroke with Large Vessel Occlusion in an LVAD Patient; A UK Secondary Medical Center Experience

Introduction: Left ventricular assist devices (LVADs) are getting more popular in managing advanced heart failure patients. The implantation of LVADs is associated with neurological complications, including ischemic stroke or intracranial hemorrhage. There are no current guidelines on how to manage these neurological complications. In this report, we presented an LVAD patient with a large ischemic cerebral infarct and subarachnoid hemorrhage simultaneously and outlined our approach to managing these complications without affecting the LVAD function. Case presentation: A 34- year-old gentleman with an LVAD to bridge him to heart transplantation presented with acute left-sided body weakness of an undetermined time of onset. His CT head showed a large right middle cerebral artery infarct. He was not a thrombolysis candidate due to the undetermined onset of his stroke, the anticoagulation he was on for the LVAD, and the signs of infarct maturation in the CT head. We managed him in a multidisciplinary team approach holding the Aspirin and Warfarin he was taking and doing serial CT imaging of his brain to monitor the development of brain edema. The patient developed a small subarachnoid hemorrhage on day 2, that spontaneously resolved on day 5. We started him on unfractionated heparin on day 7 and Warfarin on day 10. We made an excellent recovery of his neurological function without impairment of the function on the LVAD. Conclusion: Simultaneous ischemic stroke and brain hemorrhage are a challenge in LVAD patients. A closely monitored stoppage of antithrombotics and serial brain imaging can guide the treatment. Regular assessment of LVAD function is mandated. Antithrombotics could be carefully reintroduced under surveillance brain scanning to maintain the LVAD function.

Determination of brain water content by dry/wet weight measurement for the detection of experimental brain edema.

Brain edema is a fatal pathological state in which brain volume increases as a result of abnormal accumulation of fluid within the brain parenchyma. A key attribute of experimentally induced brain edema - increased brain water content (BWC) - needs to be verified. Various methods are used for this purpose: specific gravimetric technique, electron microscopic examination, magnetic resonance imaging (MRI) and dry/wet weight measurement. In this study, the cohort of 40 rats was divided into one control group (CG) and four experimental groups with 8 rats in each group. The procedure for determining BWC using dry/wet weight measurement was initiated 24 h after the completion of edema induction by the water intoxication method (WI group); after the intraperitoneal administration of Methylprednisolone (MP) together with distilled water during edema induction (WI+MP group); 30 min after osmotic blood brain barrier disruption (BBBd group); after injection of MP via the internal carotid artery immediately after BBBd (BBBd + MP group). While induction of brain edema (WI, BBBd) resulted in significantly higher BWC, there was no increase in BWC in the MP groups (WI+MP, BBBd+MP), suggesting a neuroprotective effect of MP in the development of brain edema.

Serum S-100B adds incremental value for the prediction of symptomatic intracranial hemorrhage and brain edema after acute ischemic stroke.

Early identification of patients developing symptomatic intracranial hemorrhage and symptomatic brain edema after acute ischemic stroke is essential for clinical decision-making. Astroglial protein S-100B is a marker of blood-brain barrier disruption, which plays an important role in the formation of intracranial hemorrhage and brain edema. In this study, we assessed the prognostic value of serum S-100B for the development of these complications. Serum S-100B levels were measured within 24 h from symptom onset in 1749 consecutive acute ischemic stroke patients from the prospective, observational, multicenter BIOSIGNAL cohort study (mean age 72.0 years, 58.3% male). To determine symptomatic intracranial hemorrhage or symptomatic brain edema, follow-up neuroimaging was performed in all patients receiving reperfusion therapy or experiencing clinical worsening with an NIHSS increase of ⩾4. Forty six patients (2.6%) developed symptomatic intracranial hemorrhage and 90 patients (5.2%) developed symptomatic brain edema. After adjustment for established risk factors, log10S-100B levels remained independently associated with both symptomatic intracranial hemorrhage (OR 3.41, 95% CI 1.7-6.9, p = 0.001) and symptomatic brain edema (OR 4.08, 95% CI 2.3-7.1, p < 0.001) in multivariable logistic regression models. Adding S-100B to the clinical prediction model increased the AUC from 0.72 to 0.75 (p = 0.001) for symptomatic intracranial hemorrhage and from 0.78 to 0.81 (p < 0.0001) for symptomatic brain edema. Serum S-100B levels measured within 24 h after symptom onset are independently associated with the development of symptomatic intracranial hemorrhage and symptomatic brain edema in acute ischemic stroke patients. Thus, S-100B may be useful for early risk-stratification regarding stroke complications.

The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury.

Astrocytic Aquaporin 4 (AQP4) and Transient receptor potential vanilloid 4 (TRPV4) channels form a functional complex that likely influences cell volume regulation, the development of brain edema, and the severity of the ischemic injury. However, it remains to be fully elucidated whether blocking these channels can serve as a therapeutic approach to alleviate the consequences of having a stroke. In this study, we used in vivo magnetic resonance imaging (MRI) to quantify the extent of brain lesions one day (D1) and seven days (D7) after permanent middle cerebral artery occlusion (pMCAO) in AQP4 or TRPV4 knockouts and mice with simultaneous deletion of both channels. Our results showed that deletion of AQP4 or TRPV4 channels alone leads to a significant worsening of ischemic brain injury at both time points, whereas their simultaneous deletion results in a smaller brain lesion at D1 but equal tissue damage at D7 when compared with controls. Immunohistochemical analysis 7 days after pMCAO confirmed the MRI data, as the brain lesion was significantly greater in AQP4 or TRPV4 knockouts than in controls and double knockouts. For a closer inspection of the TRPV4 and AQP4 channel complex in the development of brain edema, we applied a real-time iontophoretic method in situ to determine ECS diffusion parameters, namely volume fraction (α) and tortuosity (λ). Changes in these parameters reflect alterations in cell volume, and tissue structure during exposure of acute brain slices to models of ischemic conditions in situ, such as oxygen-glucose deprivation (OGD), hypoosmotic stress, or hyperkalemia. The decrease in α was comparable in double knockouts and controls when exposed to hypoosmotic stress or hyperkalemia. However, during OGD, there was no decrease in α in the double knockouts as observed in the controls, which suggests less swelling of the cellular components of the brain. Although simultaneous deletion of AQP4 and TRPV4 did not improve the overall outcome of ischemic brain injury, our data indicate that the interplay between AQP4 and TRPV4 channels plays a critical role during neuronal and non-neuronal swelling in the acute phase of ischemic injury.

Does Vitamin D Administration Increase the Neuroprotective Effect of Estrogen in Male Rats with Traumatic Brain Injury?

Background: In our previous studies, the effect of sex hormones on brain edema reduction after traumatic brain injury (TBI) was demonstrated. In the current study, alone and combined effects of 17-β estradiol (E2) and vitamin D (Vit D) on TBI in male rats were investigated.Methods: Male rats were divided into six groups, including sham, TBI, vehicle, E2, Vit D, and E2+Vit D. In all groups except sham, moderate-intensity diffuse TBI was induced by the Marmarou’s method. Vehicle, E2, Vit D and their combination were intramusculary injected one and 12 hours after the TBI. The brain water content, permeability of blood brain barrier (BBB) and histopathological outcome were assessed 24h after TBI. The neurological outcome score was determined using the veterinary coma scale (VCS).Results: Significant reductions in brain water content (P<0.001, P<0.05 and P<0.01, respectively) and BBB permeability (P<0.001) appeared in the treated groups with E2, Vit D, and E2+Vit D compared to the vehicle group. Twenty-four hours after the injury, the neurological scores in the E2, Vit D, and E2+Vit D groups increased significantly compared to the vehicle group (P<0.05). Dramatic improvement in histopathological outcome was also observed in the treated groups compared to the vehicle group.Conclusion: Alone and combined consumption of estrogen and vitamin D may similarly decrease the development of brain edema and improve the neurological and histopathological consequences of TBI. Therefore, consumption of vitamin D did not enhance the neuroprotective effect of estrogen in TBI.

The ACORNS grading scale: a novel tool for the prediction of malignant brain edema after endovascular thrombectomy

BackgroundTo develop and validate a novel tool for predicting the development of malignant brain edema (MBE) in large vessel occlusion stroke patients after endovascular thrombectomy (EVT).MethodsWe used a prospectively registered...

Blood-Brain Barrier Alterations and Edema Formation in Different Brain Mass Lesions.

Differential diagnosis of brain lesion pathologies is complex, but it is nevertheless crucial for appropriate clinical management. Advanced imaging methods, including diffusion-weighted imaging and apparent diffusion coefficient, can help discriminate between brain mass lesions such as glioblastoma, brain metastasis, brain abscesses as well as brain lymphomas. These pathologies are characterized by blood-brain barrier alterations and have been extensively studied. However, the changes in the blood-brain barrier that are observed around brain pathologies and that contribute to the development of vasogenic brain edema are not well described. Some infiltrative brain pathologies such as glioblastoma are characterized by glioma cell infiltration in the brain tissue around the tumor mass and thus affect the nature of the vasogenic edema. Interestingly, a common feature of primary and secondary brain tumors or tumor-like brain lesions characterized by vasogenic brain edema is the formation of various molecules that lead to alterations of tight junctions and result in blood-brain barrier damage. The resulting vasogenic edema, especially blood-brain barrier disruption, can be visualized using advanced magnetic resonance imaging techniques, such as diffusion-weighted imaging and apparent diffusion coefficient. This review presents a comprehensive overview of blood-brain barrier changes contributing to the development of vasogenic brain edema around glioblastoma, brain metastases, lymphomas, and abscesses.

Diabetic ketoacidosis fluid management in children: systematic review and meta-analyses

ImportanceDiabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes mellitus, which may lead to significant morbidity and mortality.ObjectivesTo compare the safety and efficacy of liberalised versus conservative intravenous...

Hypernatremia is associated with poor long-term neurological outcomes in out-of-hospital cardiac arrest survivors

BackgroundBrain oedema after cardiac arrest is strongly associated with poor neurological outcomes. Excessive sodium supplementation may increase serum osmolarity and facilitate brain oedema development in cardiac arrest survivors. We aimed to investigate the association of serum sodium levels with long-term neurological outcomes in out-of-hospital cardiac arrest (OHCA) survivors. MethodsThis retrospective observational study used a multicentre prospective cohort registry of OHCA survivors collected between December 2013 and February 2018. We analyzed the association of serum sodium levels at the return of spontaneous circulation (ROSC) (Sodium 0H) and at 24 h after ROSC (Sodium 24H) with 1-year neurological outcomes in OHCA survivors. Patients with 1-year cerebral performance categories (CPC) 1 and 2 were included in the good outcome group while those with CPC 3, 4, and 5 were included in the poor outcome group. ResultsAmong 277 patients, 84 (30.3%) and 193 (69.7%) were in the good and poor outcome groups, respectively. Compared with the good outcome group, the poor outcome group showed significantly higher Sodium 24H levels (140 mEq/L vs. 137.4 mEq/L, p < 0.001). Increased serum sodium levels per 1 mEq/L increased the risk of poor 1-year CPC by 13% (adjusted odds ratio = 1.13; 95% CI, 1.04⎼1.23; p = 0.004). ConclusionsRelatively high Sodium 24H levels showed a strong and independent association with poor long-term neurological outcomes in OHCA survivors. These findings may be applied in therapeutic strategies for improving neurological outcomes in OHCA survivors.