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AbstractIntroductionMethodsResultsDiscussionConclusionsDelayed neurological sequelae is a common complication following carbon monoxide poisoning, which significantly affects the quality of life of patients with the condition. We aimed to develop a machine learning-based prediction model to predict the frequency of delayed neurological sequelae in patients with carbon monoxide poisoning.A single-center retrospective analysis was conducted in an emergency department from January 01, 2018, to December 31, 2023. We analyzed data from patients with carbon monoxide poisoning, which were divided into training and test sets. We developed and evaluated sixteen machine learning models, using accuracy, sensitivity, specificity, and other relevant metrics. Threshold adjustments were performed to determine the most accurate model for predicting patients with carbon monoxide poisoning at risk of delayed neurological sequelae.A total of 360 patients with carbon monoxide poisoning were investigated in the present study, of whom 103 (28.6%) were diagnosed with delayed neurological sequelae, and two (0.6%) died. After threshold adjustment, the synthetic minority oversampling technique-random forest model demonstrated superior performance with an area under the receiver operating characteristic curve of 0.89 and an accuracy of 0.83. The sensitivity and specificity of the model were 0.9 and 0.8, respectively.The study developed a machine learning-based synthetic minority oversampling technique-random forest model to predict delayed neurological sequelae in patients with carbon monoxide poisoning, achieving an area under the receiver operating characteristic curve of 0.89. This technique was used to handle class imbalance, and shapley additive explanations analysis helped explain the model predictions, highlighting important factors such as the Glasgow Coma Scale, hyperbaric oxygen therapy, kidney function, immune response, liver function, and blood clotting.The machine learning-based synthetic minority oversampling technique-random forest model developed in this study effectively identifies patients with carbon monoxide poisoning at high risk for delayed neurological sequelae. [ABSTRACT FROM AUTHOR]

Background: Little is known about extracorporeal membrane oxygenation (ECMO)-related spinal cord infarction (SCI), and reports regarding this rare and catastrophic complication are rare. Here, we report two cases of ECMO-related SCI that occurred between April and December 2023. Data were collected from patients' medical records, with SCI as the endpoint. We reviewed previously published reports by searching PubMed and summarizing the findings. Case summary: One female patient presenting with multiple traumas required oxygenation support through veno-venous ECMO (VV ECMO) due to pulmonary hemorrhage, while one male patient required circulatory support via veno-arterial ECMO (VA ECMO) concurrently with an intra-aortic balloon pump due to cardiac arrest. Neither patient had preexisting neurological deficits; however, upon weaning from ECMO, they presented with severe neurological deficits of uncertain etiology, subsequently confirmed as SCI using magnetic resonance imaging. Conclusion: ECMO-related SCI remains elusive and intricate, and this is the first report of adult VV ECMO-related SCI. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to investigate the safety of induction chemotherapy (IC) for patients with sinonasal malignancies with brain invasion or a neurological deficit. Methods We conducted a retrospective analysis of patients who underwent IC for sinonasal malignancies with intracranial invasion or a neurological deficit at a single tertiary cancer center from 1992 to 2020. Results In total, 460 patients with sinonasal malignancies were included in the study. Of the patients reviewed, 341 underwent IC and within this group 40 had brain invasion (BI) and 31 had a neurological deficit (ND) at presentation. The most prevalent malignancy was sinonasal undifferentiated carcinoma (BI 40%, ND 41.9%), followed by esthesioneuroblastoma (BI 27.5%, ND 9.7%). All tumors were stage T4 with the majority lacking nodal metastases (BI N0: 72.5%, ND N0: 77.5%). All patients completed at least two cycles of IC. Partial or complete response to IC was seen in 80% of BI and 71% of ND patients. No patients had cessation of treatment due to neurologic decline and none required urgent surgery. Five patients (12.5%) with BI and 2 (6.5%) with ND had interruption of IC for reasons other than neurological decline. In patients with ND, IC led to improvement of 54.5% NDs. Conclusion In patients with sinonasal malignancies with BI or ND who underwent IC, no patients had cessation of treatment due to neurologic decline. In contrast, most patients had improvement of neurologic symptoms with IC. IC was safely administered without interruption due to neurological decline or symptom progression. [ABSTRACT FROM AUTHOR]

Background: Small artery occlusion (SAO) is a common ischemic stroke subtype. However, its clinical outcome can be more severe than commonly understood. The severity of SAO can vary, ranging from mild to moderate. Iron deposition has been associated with the development and progression of stroke. However, its specific distribution and relationship with stroke severity in SAO remain unclear. The study's purpose is to investigate the differences in iron deposition between mild stroke with SAO (SAO-MiS) and moderate stroke with SAO (SAO-MoS) through quantitative susceptibility mapping (QSM) and its association with neurological deficits. Methods: Sixty-eight SAO participants within 24 hours of first onset were enrolled and separated into SAO-MiS and SAO-MoS according to the National Institutes of Health Stroke Scale (NIHSS) scores. QSM helped calculate the susceptibility maps, reflecting the iron content within the brain. The susceptibility maps were analyzed using voxel-wise statistical analysis to compare the iron deposition between SAO-MiS and SAO-MoS. Then, differentially distributed iron deposition helped differentiate between mild and moderate stroke using support vector machine (SVM) methods. Results: Compared with SAO-MiS, SAO-MoS depicted elevated iron deposition in the left pallidum, parahippocampal gyrus, and superior frontal gyrus medial region, and is lower in the right superior/middle frontal gyrus and bilateral supplementary motor area. Based on iron deposition, the SVM classifier's analysis revealed a high power to discriminate SAO-MoS from SAO-MiS. In addition, fibrinogen, triglyceride (TG), and total cholesterol (TC) were linked with QSM values in specific brain regions. Conclusions: Our study first revealed the brain iron distribution after SAO and differently distributed iron deposition in SAO-MiS and SAO-MoS. The results indicate that iron deposition could play a role in the pathophysiology of SAO and its correlation with stroke severity. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage (SAH) is the deadliest form of hemorrhagic stroke; however, effective therapies are still lacking. Perfluorocarbons (PFCs) are lipid emulsion particles with great flexibility and their much smaller size as compared to red blood cells (RBCs) allows them to flow more efficiently within the blood circulation. Due to their ability to carry oxygen, a specific PFC-based emulsion, PFC-Oxygent, has been used as a blood substitute; however, its role in cerebral blood flow regulation is unknown. Adult C57BL/6 wildtype male mice were subjected to an endovascular perforation model of SAH followed by an intravenous (i.v.) injection of 9 ml/kg PFC-Oxygent or no treatment at 5 h after SAH. At 48 h after SAH, functional and anatomical outcomes were assessed. We found that SAH resulted in significant neurologic and motor deficits which were prevented by PFC-Oxygent treatment. We found that SAH-induced vasospasm, reduced RBC deformability, and augmented endothelial dysfunction were also restricted by PFC-Oxygent treatment. Moreover, mitochondrial activity and fusion proteins were also markedly decreased as assessed by oxidative phosphorylation (OXPHOS) after SAH. Interestingly, PFC-Oxygent treatment brought the mitochondrial activity close to the basal level. Moreover, SAH attenuated the level of phosphorylated AMP-activated protein kinase (pAMPK), whereas PFC treatment improved pAMPK levels. These data show the beneficial effects of PFC-Oxygent in limiting the severity of SAH. Further studies are needed to fully understand the mechanism through which PFC-Oxygent exerts its beneficial effects in limiting SAH severity. [ABSTRACT FROM AUTHOR]

Abstract Subarachnoid hemorrhage (SAH) is the deadliest form of hemorrhagic stroke; however, effective therapies are still lacking. Perfluorocarbons (PFCs) are lipid emulsion particles with great flexibility and their much smaller size as compared to red blood cells (RBCs) allows them to flow more efficiently within the blood circulation. Due to their ability to carry oxygen, a specific PFC-based emulsion, PFC-Oxygent, has been used as a blood substitute; however, its role in cerebral blood flow regulation is unknown. Adult C57BL/6 wildtype male mice were subjected to an endovascular perforation model of SAH followed by an intravenous (i.v.) injection of 9 ml/kg PFC-Oxygent or no treatment at 5 h after SAH. At 48 h after SAH, functional and anatomical outcomes were assessed. We found that SAH resulted in significant neurologic and motor deficits which were prevented by PFC-Oxygent treatment. We found that SAH-induced vasospasm, reduced RBC deformability, and augmented endothelial dysfunction were also restricted by PFC-Oxygent treatment. Moreover, mitochondrial activity and fusion proteins were also markedly decreased as assessed by oxidative phosphorylation (OXPHOS) after SAH. Interestingly, PFC-Oxygent treatment brought the mitochondrial activity close to the basal level. Moreover, SAH attenuated the level of phosphorylated AMP-activated protein kinase (pAMPK), whereas PFC treatment improved pAMPK levels. These data show the beneficial effects of PFC-Oxygent in limiting the severity of SAH. Further studies are needed to fully understand the mechanism through which PFC-Oxygent exerts its beneficial effects in limiting SAH severity.

Introduction: Ischemic brain injury remains one of the main causes of disability and mortality worldwide. Protection of cellular population, depriving from oxygen supply and nutrients, is of extreme importance for further both clinical and health outcomes of timely implemented intravascular intervention. The aim: to assess anti-ischemic activity of 3-hydroxypyridine ascorbate in the in vitro and in vivo models of brain cell and tissue response to ischemia and reoxygenation. Materials and Methods: 3-hydroxypyridine ascorbate (laboratory code 3-EA) was assessed as chemical substance (purity 99.8%) diluted in sterile phosphate-buffered saline. Intracellular Ca2+ response to glutamate excitotoxicity (GluTox), ischemia and reoxygenation as well as cellular viability was evaluated on NMRI murine fresh cortical neuro-glial cell culture incubated with 2-EA by registering intracellular Fura-2 and propidium iodide fluorescence respectively. Expression of apoptosis regulating genes BCL-2, STAT3, SOCS3, inflammation regulating genes TRAIL, MLKL, Cas-1, Cas-3, IL-1β и TNFα, and genes MAO-A and MAO-B was determined by real-time PCR. The substance neuroprotection was studied in male Sprague-Dawley rats with intraluminal middle cerebral artery (MCA) occlusion/reperfusion treated with 18 mg/kg of 2-EA along with neurological deficiency evaluation and morphological assessment of brain sections. Results: Preincubation of cortical cells with 10-100 μM of 3-EA leads to inhibition of [Ca2+]i in cytosol of neurons and astrocytes under GluTox and oxygen-glucose deprivation (OGD) conditions. Reducing [Ca2+]i inhibits necrotic cell death in an acute experiment. Incubation of cerebral cortex cells with 3-EA leads to an overexpression of anti-apoptotic genes BCL-2, STAT3, SOCS3, along with downregulation of genes TRAIL, MLKL, Cas-1, Cas-3, IL-1β and TNFα. Intraperitoneal administration of 3-EA reduces the volume of necrotic areas, perinecrotic edema, cell damage, and neurological deficits in rats with MCA occlusion. Conclusion: 3-EA dose-dependently suppresses the death of cerebral cortex cells under the excitotoxic effects of glutamate and ischemia/reoxygenation. Cell-protective effect of 3-EA involves changes in the basal and ischemia/reoxygenation-induced expression of genes encoding anti-apoptotic proteins and oxidative status proteins, which leads to inhibition of the late irreversible stages of apoptosis. A course administration of 3-hydroxypyridine ascorbate at a dose of 18 mg/kg per day reduces the severity of damage both by preserving the population of neurons in the penumbra zone and by limiting the local stress response.

Background: The neurological assessment plays a crucial role in evaluating stroke patients and is a skill that has been practiced by physicians for a long time, and further refined by practitioners. The purpose of the current study was to systematically review and synthesize the evidence-based neurological assessment of the different methods of treadmill-related training protocols in stroke patients. Evidence Acquisition: In this study, the appropriate studies were documented (N = 1270) using PubMed as the sole electronic database. Moreover, subgroup studies were provided based on training intensity and duration, categorized as low intensity-low duration, low intensity-high duration, high intensity-low duration, and high intensity-high duration. Training intensities were standardized to meters per second (m/s), and the training duration was calculated in terms of minutes per session, the number of sessions per week, and the total number of training weeks, which were then converted into minutes. The assessment of neurological recovery following stroke was conducted using standard neurological assessment scales. Results: This meta-analysis in humans found a notably positive standardized mean difference in protocols with high intensity and high duration (1.792; 95% CI = 0.566 to 3.02). Conclusions: In conclusion, the current meta-analysis suggests that practitioners using the high intensity-high duration protocol should regularly monitor the neurological outcomes, as they may be negatively impacted by the intensity and duration of the protocol. [ABSTRACT FROM AUTHOR]

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Surgical resection of glioblastoma multiforme (GBM) often results in tumor recurrence and mild neurologic deficits. Here, a 3D asynchronous drug delivery system is innovatively developed to address the dual challenges of GBM recurrence and postoperative neurological deficit. Based on transcriptome analysis of tumor cells and tumor microenvironment (TME) cells between primary and recurrent mouse GBM tissues, a novel dual‐targeting approach is developed to combine mTOR pathway inhibition with microglia/macrophage repolarization. Then, in situ injectable methacrylated gelatin (GelMA) is constructed to perfectly fit into the tumor resection cavity and achieve direct delivery of dual‐targeted drugs, exhibiting outstanding postoperative GBM inhibitory effects in vivo. At the same time, neurotrophic factor‐saturated 3D‐printed GelMA patches are used to construct a 3D asynchronous drug delivery system, allowing gradual penetration of the neurotrophic factors into the underlying hydrogel to promote axonal sprouting after GBM suppression. Notably, this 3D asynchronous drug delivery system promotes neurological recovery without weakening the efficacy of inhibiting tumor recurrence. Therefore, this study not only proposes a new dual‐targeted GBM treatment strategy but also pioneers the construction of a 3D asynchronous drug delivery system for the comprehensive treatment of GBM. This study is expected to improve the poor prognosis of patients with GBM. [ABSTRACT FROM AUTHOR]

Cardiopulmonary arrest (CA) is a major cause of death/disability in the U.S. with poor prognosis and survival rates. Current therapeutic challenges are physiologically complex because they involve hypoperfusion (decreased cerebral blood flow), neuroinflammation, and mitochondrial dysfunction. We previously discovered novel serum/glucocorticoid-regulated kinase 1 (SGK1) is highly expressed in brain of neurons that are susceptible to ischemia (hippocampus and cortex). We inhibited SGK1 and utilized pharmacological (specific inhibitor, GSK650394) and neuron-specific genetic approaches (shRNA) in rodent models of CA to determine if SGK1 is responsible for hypoperfusion, neuroinflammation, mitochondrial dysfunctional, and neurological deficits after CA. Inhibition of SGK1 alleviated cortical hypoperfusion and neuroinflammation (via Iba1, GFAP, and cytokine array). Treatment with GSK650394 enhanced mitochondrial function (via Seahorse respirometry) in the hippocampus 3 and 7 days after CA. Neuronal injury (via MAP2, dMBP, and Golgi staining) in the hippocampus and cortex was observed 7 days after CA but ameliorated with SGK1-shRNA. Moreover, SGK1 mediated neuronal injury by regulating the Ndrg1-SOX10 axis. Finally, animals subjected to CA exhibited learning/memory, motor, and anxiety deficits after CA, whereas SGK1 inhibition via SGK1-shRNA improved neurocognitive function. The present study suggests the fundamental roles of SGK1 in brain circulation and neuronal survival/death in cerebral ischemia-related diseases. [ABSTRACT FROM AUTHOR]

Introduction: Ischemic brain injury remains one of the main causes of disability and mortality worldwide. Protection of cellular population, depriving from oxygen supply and nutrients, is of extreme importance for further both clinical and health outcomes of timely implemented intravascular intervention. The aim: to assess anti-ischemic activity of 3-hydroxypyridine ascorbate in the in vitro and in vivo models of brain cell and tissue response to ischemia and reoxygenation. Materials and Methods: 3-hydroxypyridine ascorbate (laboratory code 3-EA) was assessed as chemical substance (purity 99.8%) diluted in sterile phosphate-buffered saline. Intracellular Ca2+ response to glutamate excitotoxicity (GluTox), ischemia and reoxygenation as well as cellular viability was evaluated on NMRI murine fresh cortical neuro-glial cell culture incubated with 2-EA by registering intracellular Fura-2 and propidium iodide fluorescence respectively. Expression of apoptosis regulating genes BCL-2, STAT3, SOCS3, inflammation regulating genes TRAIL, MLKL, Cas-1, Cas-3, IL-1β и TNFα, and genes MAO-A and MAO-B was determined by real-time PCR. The substance neuroprotection was studied in male Sprague-Dawley rats with intraluminal middle cerebral artery (MCA) occlusion/reperfusion treated with 18 mg/kg of 2-EA along with neurological deficiency evaluation and morphological assessment of brain sections. Results: Preincubation of cortical cells with 10-100 μM of 3-EA leads to inhibition of [Ca2+]i in cytosol of neurons and astrocytes under GluTox and oxygen-glucose deprivation (OGD) conditions. Reducing [Ca2+]i inhibits necrotic cell death in an acute experiment. Incubation of cerebral cortex cells with 3-EA leads to an overexpression of anti-apoptotic genes BCL-2, STAT3, SOCS3, along with downregulation of genes TRAIL, MLKL, Cas-1, Cas-3, IL-1β and TNFα. Intraperitoneal administration of 3-EA reduces the volume of necrotic areas, perinecrotic edema, cell damage, and neurological deficits in rats with MCA occlusion. Conclusion: 3-EA dose-dependently suppresses the death of cerebral cortex cells under the excitotoxic effects of glutamate and ischemia/reoxygenation. Cell-protective effect of 3-EA involves changes in the basal and ischemia/reoxygenation-induced expression of genes encoding anti-apoptotic proteins and oxidative status proteins, which leads to inhibition of the late irreversible stages of apoptosis. A course administration of 3-hydroxypyridine ascorbate at a dose of 18 mg/kg per day reduces the severity of damage both by preserving the population of neurons in the penumbra zone and by limiting the local stress response. [ABSTRACT FROM AUTHOR]

Objectives: To research the connection between the indexes of the indexes of triglyceride-glucose (TyG) combined with obesity indices and the initial neurological severity and short-term outcome of new-onset acute ischemic stroke. Methods: Data of patients with acute ischemic stroke admitted to the Stroke Ward of the Affiliated Hospital of Beihua University from November 2021 to October 2023, were collected. The two indexes were calculated by combining TyG and obesity indices: TyG-body mass index (TyG-BMI) and TyG-waist circumference (TyG-WC). The National Institute of Health Stroke Scale (NIHSS) was used to assess and group patients with neurological deficits within 24 hours of admission: mild stroke (NIHSS ≤5) and moderate-severe stroke (NIHSS >5). Short-term prognosis was evaluated using the modified Rankin Scale (mRS) at discharge or 14 days after onset of the disease and grouped: good outcome (mRS ≤2) and poor outcome (mRS >2). According to the quartiles of TyG-BMI and TyGWC, the patients were placed into four groups: Q1, Q2, Q3 and Q4. Multi-factor logistic regression analysis was utilized to evaluate the correlation of TyG-BMI and TyG-WC with the severity and short-term outcome. Results: The study included 456 patients. After adjusting for multiple variables, the results showed that compared with the quartile 1, patients in quartile 4 of TyG-BMI had a reduced risk of moderate-severe stroke [Q4: OR: 0.407, 95%CI (0.185-0.894), P = 0.025]; Patients in quartiles 2, 3 and 4 of TyG-BMI had sequentially lower risk of short-term adverse outcomes [Q2: OR: 0.394, 95%CI (0.215-0.722), P = 0.003; Q3: OR: 0.324, 95%CI (0.163-0.642), P = 0.001; Q4: OR: 0.158, 95%CI (0.027-0.349), P <0.001]; Patients in quartiles 3 and 4 of TyG-WC had sequentially lower risk of moderate-severe stroke [Q3: OR: 0.355, 95%CI (0.173-0.728), P = 0.005; Q4: OR: 0.140, 95%CI (0.056-0.351), P <0.001]; Patients in quartiles 3 and 4 of TyG-WC had sequentially lower risk of short-term adverse outcomes [Q3: OR: 0.350, 95%CI (0.175-0.700), P = 0.003; Q4: OR: 0.178, 95%CI (0.071-0.451), P <0.001]. Conclusions: TyG-WC and TyG-BMI were correlated with the severity and shortterm outcome of new-onset acute ischemic stroke. As TyG-WC and TyG-BMI increased, stroke severity decreased and short-term outcome was better. [ABSTRACT FROM AUTHOR]

Objectives: The study aimed to determine the clinical relevance of cortical vein thrombosis (CVT) accompanying cerebral venous sinus thrombosis (CVST) and to investigate the risk factors. Patients and methods: This retrospective study included 176 patients (52 males, 124 females; mean age: 41.8±14.5 years; range, 16 to 72 years) with CVST between January 2015 and January 2021. The radiological, demographic, and clinical features and risk factors of patients with and without CVT were com-pared. Results: When the clinical demographic and radiological features associated with CVT were evaluated; there was a significant relationship between age, clinical onset symptom, connective tissue disease, post-partum period, presence of hypercoagulopathy, superior sagittal sinus (SSS) thrombosis, transverse sinus thrombosis, sigmoid sinus thrombosis, non-hemorrhagic venous infarct, small juxtacortical hemorrhage and large parenchymal hematomas, time to diagnosis (days), and poor clinical outcome. When significant risk factors for CVT were analyzed by binary logistic regression, the post-partum period and SSS thrombosis were independent risk factors. Conclusion: In this study, the rate of CVT accompanying CVST was 30.7%, which is higher than the studies in the literature. Cortical vein thrombosis accompanying CVST is associated with parenchymal lesions and poor clinical outcome; SSS thrombosis and the postpartum period are independent risk factors. Multicenter prospective studies are recommended for more precise information. [ABSTRACT FROM AUTHOR]

The efficacy of surgical intervention in ameliorating long-term prognosis for moderate volume of cerebral hemorrhage in the thalamus-internal capsule region remains unsubstantiated by clinical investigations. Consequently, the acquisition of credible evidence is imperative to authenticate the effectiveness of these methodologies. One hundred and three eligible patients with moderate-volume thalamus-internal capsule region cerebral hemorrhage. Twenty-seven pairs of successful matches after using the 1:1 propensity score matching method, totaling 54 patients, were analyzed. The short- and long-term treatment outcomes of patients in the stereotactic surgery and conservative treatment groups were compared. The prognosis of the 2 groups of patients was analyzed by logistic regression analysis and model comparison. The primary outcome of this study was to assess the assessment of daily living scores after 6 months of treatment. Based on the analysis of this study, the assessment of daily living of the surgical group were significantly higher than those of the conservative treatment group after 6 months of treatment (P < 0.001), and the difference was statistically significant. The amount of residual hematoma was significantly lower in the stereotactic surgery group than in the conservative treatment group at 3 days, 7 days, and 2 weeks after the onset of the disease (P < 0.001), and the complication rate was lower than the conservative treatment group (P < 0.05). Univariate logistic regression showed that the risk of severe neurological dysfunction for patients in the surgery group was (odds ratio -0.27, 95% confidence interval: 0.08–0.86, P < 0.05). In multivariate logistic regression analysis, the odds ratio was 0.29 (95% confidence interval: 0.09–0.96, P < 0.05) after adjusting for all covariates. For moderate-volume thalamus-internal capsule region cerebral hemorrhage, stereotactic paracentesis has the advantage of a shorter hospital stay and a lower complication rate than conservative treatment. Moreover, it yields superior outcomes in terms of daily living assessment scores after six months of treatment and enhanced neurological recovery. [ABSTRACT FROM AUTHOR]

We aimed to investigate whether the consumption of Egg White Hydrolysate (EWH) acts on nervous system disorders induced by exposure to Cadmium (Cd) in rats. Male Wistar rats were divided into (a) Control (Ct): H2O by gavage for 28 days + H2O (i.p. − 15th − 28th day); (b) Cadmium (Cd): H2O by gavage + CdCl2 − 1 mg/kg/day (i.p. − 15th − 28th day); (c) EWH 14d: EWH 1 g/kg/day by gavage for 14 days + H2O (i.p.- 15th − 28th day); (d) Cd + EWH cotreatment (Cd + EWHco): CdCl2 + EWH for 14 days; (e) EWH 28d: EWH for 28 days; (f) EWHpre + Cd: EWH (1st − 28th day) + CdCl2 (15th − 28th day). At the beginning and the end of treatment, neuromotor performance (Neurological Deficit Scale); motor function (Rota-Rod test); ability to move and explore (Open Field test); thermal sensitivity (Hot Plate test); and state of anxiety (Elevated Maze test) were tested. The antioxidant status in the cerebral cortex and the striatum were biochemically analyzed. Cd induces anxiety, and neuromotor, and thermal sensitivity deficits. EWH consumption prevented anxiety, neuromotor deficits, and alterations in thermal sensitivity, avoiding neuromotor deficits both when the administration was performed before or during Cd exposure. Both modes of administration reduced the levels of reactive species, and the lipid peroxidation increased by Cd and improved the striatum's antioxidant capacity. Pretreatment proved to be beneficial in preventing the reduction of SOD activity in the cortex. EWH could be used as a functional food with antioxidant properties capable of preventing neurological damage induced by Cd. Highlights: EWH prevented neurological damage induced by Cd exposure. EWH prevented anxiety and neuromotor, and thermal sensitivity deficits before or during Cd exposure. EWH improved the redox balance before or during Cd exposure. [ABSTRACT FROM AUTHOR]

Compressive vertebral hemangiomas with neurological deficits (CVHND) form a rare, unique subset of lesions comprising of differing clinico-imaging findings, pathologic behavior and treatment, when compared to the commoner and usually incidental intra-osseus vertebral hemangiomas (VH). Though various surgical strategies and a broad array of adjuncts have evolved and changed over the years, there is paucity of comprehensive data from sizeable series of such patients treated surgically with long term follow up. The purpose of this study is to device an optimum management strategy in CVHND based on our surgical experience. The data from electronic medical records of 26 consecutive patients operated in our department from 2009 to 2019 were retrospectively analyzed. There were 11 males and 15 females with a mean age of 34.7 years. Neurological examination revealed paraparesis or paraplegia with myelopathy in all patients with Frankel score of B, C and D in 1 (3.9%), 11 (42.3%) and 14 (53.8%) patients respectively. Sixteen patients (61%) underwent laminectomy and gross total excision of extradural soft tissue component, 7 (27%) laminectomy with posterolateral fusion, three (12%) underwent additional anterior interbody support. The mean follow up was 72.4 months and at last follow-up 24 patients (92%) were Frankel E. Symptomatic recurrence was seen in two patients operated early in the series, they underwent re-surgery, gross total excision with posterolateral fusion, remaining neurologically intact at last follow up. Pre-operative embolization, surgical excision of extradural component and intra-operative vertebroplasty form the mainstay of treatment for CVHND. Instrumented posterolateral fusion with optional anterior interbody support accomplished through the same approach is required only in a minority of cases. The long-term outcome following timely and appropriate treatment is excellent. Anterior or anterolateral approaches for intervertebral support and radical procedures like total en-bloc spondylectomy (TES) are not usually required. [ABSTRACT FROM AUTHOR]

Simple Summary: The study investigates the impact of preoperative anticoagulant and antiplatelet use on bleeding risks in patients undergoing surgery for spinal metastases, particularly focusing on the elderly population. Due to advancements in cancer treatments, more patients over 65 require such surgeries to address neurological deficits and spinal instability. Conducted retrospectively from 2010 to 2023, the study analyzed 290 patients' data, including demographics, neurological status, surgical details, anticoagulant use, and coagulation management. Among the patients, 24.1% were on anticoagulants or antiplatelets preoperatively, and the rebleeding rate within 30 days was 4.5%, which was not significantly related to anticoagulant use. A significant correlation was found between preoperative neurological deficits and rebleeding risk, and fewer surgical levels treated correlated with higher postoperative bleeding. The study concludes that surgery for spinal metastases is generally safe regardless of anticoagulation status, but it emphasizes the need for individualized preoperative planning and risk assessment to optimize patient outcomes. Introduction: The age of patients requiring surgery for spinal metastasis, primarily those over 65, has risen due to improved cancer treatments. Surgical intervention targets acute neurological deficits and instability. Anticoagulants are increasingly used, especially in the elderly, but pose challenges in managing bleeding complications. The study examines the correlation between preoperative anticoagulant/antiplatelet use and bleeding risks in spinal metastasis surgery, which is crucial for optimizing patient outcomes. Material and Methods: In a retrospective study at our department from 2010 to 2023, spinal tumor surgery patients were analyzed. Data included demographics, neurological status, surgical procedure, preoperative anticoagulant/antiplatelet use, intra-/postoperative coagulation management, and the incidence of rebleeding. Coagulation management involved blood loss assessment, coagulation factor administration, and fluid balance monitoring post-surgery. Lab parameters were documented at admission, preop, postop, and discharge. Results: A cohort of 290 patients underwent surgical treatment for spinal metastases, predominantly males (63.8%, n = 185) with a median age of 65 years. Preoperatively, 24.1% (n = 70) were on oral anticoagulants or antiplatelet therapy. Within 30 days, a rebleeding rate of 4.5% (n = 9) occurred, unrelated to preoperative anticoagulation status (p > 0.05). A correlation was found between preoperative neurologic deficits (p = 0.004) and rebleeding risk and the number of levels treated surgically, with fewer levels associated with a higher incidence of postoperative bleeding (p < 0.01). Conclusions: Surgical intervention for spinal metastatic cancer appears to be safe regardless of the patient's preoperative anticoagulation status. However, it remains imperative to customize preoperative planning and preparation for each patient, emphasizing meticulous risk–benefit analysis and optimizing perioperative care. [ABSTRACT FROM AUTHOR]

Abstract Background Currently, there is still a lack of valuable neuroimaging markers to assess the clinical severity of stroke patients with small artery occlusion (SAO). Quantitative susceptibility mapping (QSM) is a quantitative processing method for neuroradiological diagnostics. Gray matter (GM) volume changes in stroke patients are also proved to be associated with neurological deficits. This study aims to explore the predictive value of QSM and GM volume in neurological deficits of patients with SAO. Methods As neurological deficits, the National Institutes of Health Stroke Scale (NIHSS) was used. Sixty‐six SAO participants within 24 h of first onset were enrolled and divided into mild and moderate groups based on NIHSS. QSM values of infarct area and GM volume were calculated from magnetic resonance imaging (MRI) data. Two‐sample t‐tests were used to compare differences in QSM value and GM volume between the two groups, and the diagnostic efficacy of the combination of QSM value and GM volume was evaluated. Results The results revealed both the QSM value and GM volume within the infarct area of the moderate group were lower compared to the mild group. Moderate group exhibited lower GM volume in some specific gyrus compared with mild group in the case of voxel‐wise GM volume on whole‐brain voxel level. The support vector machine (SVM) classifier's analysis showed a high power for the combination of QSM value, GM volume within the infarct area, and voxel‐wise GM volume. Conclusion Our research first reported the combination of QSM value, GM volume within the infarct area, and voxel‐wise GM volume could be used to predict neurological impairment of patients with SAO, which provides new insights for further understanding the SAO stroke.

Background: Electroacupuncture (EA) has been shown to promote functional recovery after cerebral ischemia–reperfusion (I/R) injury. However, the contribution of mitochondrial dynamics to recovery remains unclear. The aim of this study was to investigate whether mitochondrial dynamics are involved in the effects of EA on cerebral I/R injury. Methods: The rats with cerebral I/R injury were established by the middle cerebral artery occlusion/reperfusion. Subsequently, EA was applied to Baihui (GV20) and Dazhui (GV14) acupoints, with 2 Hz/5 Hz in frequency, 1.0 mA in intensity, 20 min each time, once a day for seven consecutive days. The therapeutic outcomes were assessed by modified neurological severity score (mNSS), 2,3,5-Triphenyte-trazolium chloride (TTC) staining, and hematoxylin-eosin (HE) staining. Mitochondrial morphology was observed under transmission electron microscopy. Adenosine triphosphate (ATP) content and ATP synthases (ATPases) activity were evaluated to measure mitochondrial function using ELISA. Finally, mitochondrial dynamics-related molecules, including dynamin-related protein 1 (Drp1), fission 1 (Fis1), mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and optic atrophy 1 (OPA1), were detected by Western blot and immunofluorescence staining. Results: Cerebral I/R injury induced neurological dysfunction, cerebral infarction and neuronal injury, all of which were ameliorated by EA. And EA improved mitochondrial morphology and function. Moreover, EA altered the balance of mitochondrial dynamics. Specifically, the data showed a significant decrease in the expression of Drp1 and Fis1, leading to the inhibition of mitochondrial fission. Additionally, Mfn1, Mfn2 and Opa1, which are related to mitochondrial fusion, were effectively promoted after EA treatment. However, sham EA did not show any neuroprotective effects in rats with cerebral I/R injury. Conclusions: In summary, our study indicates that the balance of mitochondrial dynamics is crucial for EA therapy to treat cerebral I/R injury.

ObjectivesTo research the connection between the indexes of the indexes of triglyceride-glucose (TyG) combined with obesity indices and the initial neurological severity and short-term outcome of new-onset acute ischemic stroke.MethodsData of patients with acute ischemic stroke admitted to the Stroke Ward of the Affiliated Hospital of Beihua University from November 2021 to October 2023, were collected. The two indexes were calculated by combining TyG and obesity indices: TyG-body mass index (TyG-BMI) and TyG-waist circumference (TyG-WC). The National Institute of Health Stroke Scale (NIHSS) was used to assess and group patients with neurological deficits within 24 hours of admission: mild stroke (NIHSS ≤5) and moderate-severe stroke (NIHSS >5). Short-term prognosis was evaluated using the modified Rankin Scale (mRS) at discharge or 14 days after onset of the disease and grouped: good outcome (mRS ≤2) and poor outcome (mRS >2). According to the quartiles of TyG-BMI and TyG-WC, the patients were placed into four groups: Q1, Q2, Q3 and Q4. Multi-factor logistic regression analysis was utilized to evaluate the correlation of TyG-BMI and TyG-WC with the severity and short-term outcome.ResultsThe study included 456 patients. After adjusting for multiple variables, the results showed that compared with the quartile 1, patients in quartile 4 of TyG-BMI had a reduced risk of moderate-severe stroke [Q4: OR: 0.407, 95%CI (0.185-0.894), P = 0.025]; Patients in quartiles 2, 3 and 4 of TyG-BMI had sequentially lower risk of short-term adverse outcomes [Q2: OR: 0.394, 95%CI (0.215-0.722), P = 0.003; Q3: OR: 0.324, 95%CI (0.163-0.642), P = 0.001; Q4: OR: 0.158, 95%CI (0.027-0.349), P

Introduction. Intraoperative neuromonitoring consists in current stimulation of the laryngeal nerve located near the thyroid gland. The intensity is usually set in the range of 1–2 mA in order to give the desired effect, but also to give the selectivity of the controlled nerves. The charge is designed to stimulate the vocal cords and motor innervation within the larynx, especially in the area of tissues subjected to surgery. Aim. The aim of the study was to present intraoperative monitoring of the recurrent laryngeal nerve as a method of reducing the incidence of side effects associated with damage to the laryngeal nerve and to compare the quality of life of patients who were neuromonitored during procedures with those who underwent surgery without the use of intraoperative neuromonitoring. Material and Methods. The study was conducted in two research groups. The first group consisted of 100 patients from CentroMedica Sp. z o. o. from all over Poland, who underwent surgery to remove a thyroid tumor with the help of neuromonitoring. The second research group consisted of 100 patients of the same company. They also underwent thyroid tumor excision, but in their case without the use of neuromonitoring. In the study described in this paper, the diagnostic survey method was used using the HAQ health questionnaire and the analysis of medical records. Results. In patients after procedures without the use of intraoperative monitoring, postoperative complications were observed more often than in patients with monitoring. Patients after procedures without neuromonitoring more often had hoarseness as a complication after the procedure. Conclusions. Based on the conducted research, it can be concluded that intraoperative neuromonitoring during thyroid surgery has an impact on the better quality of life of patients after surgery. (JNNN 2023;12(3):112–119)

Abstract Background Previous studies on thoracolumbar fractures with neurological symptoms have focused on how to achieve satisfactory fracture reduction, adequate nerve decompression, and stable spinal alignment. With the development of the minimally invasive spine surgery technique, achieving satisfactory treatment results and reducing iatrogenic trauma at the same time has become a new goal of spinal surgery. This research used percutaneous transpedicular screw distraction to partially reduce the fractured vertebrae, followed by completing nerve decompression and reducing residual displacement bone fragments with the assistance of the unilateral biportal endoscopic (UBE) technique to achieve full protection of bone-ligament tissue and obtain good clinical efficacy. Methods Guide wires were safely inserted into the fractured vertebra and adjacent upper and lower vertebra under the surveillance of anteroposterior and lateral X-ray fluoroscopy. Transpedicular screws were implanted via guide wires on the side with mild neurological deficits or bone fragment compression (the opposite side of the endoscopic operation). A titanium rod was installed and moderately distracted to reduce the fractured vertebra. Then, under the guidance of the endoscopic view, the laminectomy and ligamentum flavum resection were completed according to the position of the protruding bone fragment into the spinal canal, and the compressed dural sac or nerve root was fully exposed and decompressed. An L-shaped replacer was used to reduce residual bone fragments. The ipsilateral transpedicular screws and rod were installed and adjusted to match the contralateral side. The drainage tube was indwelled, and the incision was closed. The preoperative and postoperative images of the patients were evaluated, and the recovery of neurological symptoms was observed. Results Surgery was successfully completed on all six patients, and no intraoperative conversion to open surgery was performed. Postoperative images showed good reduction of the protruding bone fragment and good placement of all screws. At the last follow-up, the neurological symptoms of all patients returned to normal. Conclusion The UBE technique combined with percutaneous transpedicular screw fixation in the treatment of thoracolumbar fractures with neurological symptoms can effectively achieve the reduction of displaced bone fragments, improve damaged nerve function, stabilize spinal alignment, and protect the integrity of bone-ligament tissue.

Abstract Background Bone overgrowth after decompressive surgery for lumbar stenosis resulting in recurrence of neurological signs has not been reported in veterinary literature. However, there are few cases described in human medicine. Case presentation A 13-month-old entire female dog, a crossbreed between a Springer Spaniel and a Border Collie, weighing 24 kg, was referred with a 5-day history of progressive spastic paraplegia, indicative of a T3-L3 myelopathy. Magnetic resonance (MR) imaging revealed a right-sided L2-L3 compressive extradural lesion, compatible with epidural haemorrhage, which was confirmed by histopathology. The lesion was approached via right-sided L2-L3 hemilaminectomy and was successfully removed. One-year postoperatively the dog re-presented with pelvic limb ataxia. MR and computed tomography (CT) images demonstrated excessive vertebral bone formation affecting the right articular processes, ventral aspect of the spinous process of L2-L3, and contiguous vertebral laminae, causing spinal cord compression. Revision surgery was performed, and histopathology revealed normal or reactive osseous tissue with a possible chondroid metaplasia and endochondral ossification, failing to identify a definitive reason for the bone overgrowth. Nine-month postoperatively, imaging studies showed a similar vertebral overgrowth, resulting in minimal spinal cord compression. The patient remained stable with mild proprioceptive ataxia up until the last follow-up 18 months post-revision surgery. Conclusion This is the first report in the veterinary literature of bone overgrowth after lumbar hemilaminectomy which resulted in neurological deficits and required a revision decompressive surgery.

Cerebral ischemia is one reason for death and loss of movement ability of people, which imposes a large and significant cost on the global health system. Niosomes, as useful tools, can increase drug delivery to the brain. The purpose of this research is to investigate the effect of niosomes containing saponin (NS) on stroke- induced damage in the hippocampus of an animal model. The physicochemical characteristics of nanocarriers, such as zeta potential, size, and release test were investigated after the fabrication of thin film method. In this study, Wistar rats were divided into five experimental groups including sham group, stroke group, stroke group with empty niosome injection, stroke group with saponin injection, and stroke group with niosome saponin injection. The study examined various aspects of ischemia including stroke volume, blood-brain barrier (BBB) damage, neurological defects, levels of inflammatory cytokines, and cellular damage in the hippocampus. The findings indicate that NS, with a size of 85.92nm, zeta potential of -34.7 mv, and an entrapment efficiency (EE%) of 85.70% effectively reduced stroke volume, cerebral edema, BBB damage, expression level of TNF-α, and NF-kB genes and inflammation in hippocampal cells. Additionally, NS improved sensory and motor performance in rats. These results demonstrate that NS can mitigate strokeinduced damage in the hippocampus of the rat model by effectively crossing the BBB. [ABSTRACT FROM AUTHOR]

Background: Learning curves (LC) are typically defined by the number of different spinal procedures surgeons must perform before becoming "proficient," as demonstrated by reductions in operative times, estimated blood loss (EBL), length of hospital stay (LOS), adverse events (AE), fewer conversions to open procedures, along with improved outcomes. Reviewing 12 studies revealed LC varied widely from 10-44 cases for open vs. minimally invasive (MI) lumbar diskectomy, laminectomy, transforaminal lumbar interbody fusion (TLIF), anterior lumbar interbody fusion (ALIF), and oblique/extreme lateral interbody fusions (OLIF/XLIF). We asked whether the risks of harm occurring during these LC could be limited if surgeons routinely utilized in-person/intraoperative mentoring (i.e., via industry, academia, or well-trained colleagues). Methods: We evaluated LC for multiple lumbar operations in 12 studies Results: These studies revealed no LC for open vs. MI lumbar diskectomy. LC required 29 cases for MI laminectomy, 10-44 cases for MI TLIF, 24-30 cases for MI OLIF, and 30 cases for XLIF. Additionally, the LC for MI ALIF was 30 cases; one study showed that 32% of major vascular injuries occurred in the first 25 vs. 0% for the next 25 cases. Shouldn't the risks of harm to patients occurring during these LC be limited if surgeons routinely utilized in-person/intraoperative mentoring? Conclusions: Twelve studies showed that the LC for at different MI lumbar spine operations varied markedly (i.e., 10-44 cases). Wouldn't and shouldn't spine surgeons avail themselves of routine in-person/intraoperative mentoring to limit patients' risks of injury during their respective LC for these varied spine procedures? [ABSTRACT FROM AUTHOR]

Background Hyperlactatemia, is common in patients undergoing neurosurgical procedures. Several studies have identified potential risk factors for developing hyperlactatemia in neurosurgical patients, including body mass index, surgery duration, tumour volume, and certain drugs such as volatile anesthetic agents and corticosteroids. This systematic review and meta-analysis examined the evidence of the association between perioperative lactate levels in patients undergoing brain surgery and postoperative morbidity and mortality.

Acute neurologic deficits in the postoperative period after carotid endarterectomy (CEA) can prompt extensive diagnostic evaluation. Reversible cerebral vasoconstriction syndrome (RCVS) is an underrecognized cause of acute neurologic deficit after CEA. We present the case of RCVS in an 84-year-old male patient who had experienced left limb weakness after CEA, prompting multiple code stroke activations. The present case is novel because the obtained computed tomography perfusion imaging studies demonstrated abnormalities that have not been previously described in patients with RCVS. These findings, combined with the cerebral angiography findings, led to the rapid diagnosis and delivery of intra-arterial vasodilator therapy. He experienced subsequent resolution of his symptoms and radiologic abnormalities.

Progressive Multifocal Leukoencephalopathy (PML), primarily affecting immunocompromised individuals due to the John Cunningham virus (JC), is common in HIV-positive adults but rare in paediatrics. We present a unique case of a 14-year-old female with PML as the initial manifestation of HIV, with MRI lesions isolated to the posterior fossa. Initial symptoms included fever and rash, progressing to neurological deficits and ataxia. Severe immune suppression due to HIV and JC virus in the cerebrospinal fluid were confirmed. Management included immune reconstitution therapy (antiretroviral treatment) and supportive care. Despite interventions, the patient had a slow recovery with significant residual neurological sequelae. Timely recognition of Immune Reconstitution Inflammatory Syndrome (IRIS) and steroid initiation proved helpful. Antiretroviral therapy improved the survival rate of HIV-related PML, but long-term neurological sequelae, especially in posterior fossa cases, significantly impact the patient's quality of life. This case highlights diagnostic and treatment challenges in paediatric PML, particularly with atypical lesions location.

Clinically, it is nearly impossible to differentiate between high-grade glioma, specifically Glioblastoma Multiforme (GBM), and Tumefactive Demyelination (TMD). Radiologically, distinguishing between GBM and TMD is challenging since they show similar findings on Computed Tomography (CT) and Magnetic Resonance Imaging (MRI). To avoid invasive procedures that may increase patient morbidity, the use of MR perfusion imaging is highlighted in these case reports. We present two cases of young adult females with neurological deficits. The first case involves an 18-year-old female who presented with a dull, intermittent, holocephalic headache for eight months, along with heaviness and recent onset of pain in the right upper limb. MR spectroscopy revealed an increased choline/creatinine ratio at the margins of the lesion, measuring approximately 2.4, with a decrease in N-Acetylaspartate (NAA) and NAA/Creatinine. Based on these findings, the possibility of either high-grade glioma or TMD was considered. Further evaluation using perfusion imaging showed a substantial increase in the mean relative Cerebral Blood Volume (rCBV) within the lesion, suggesting a higher likelihood of high-grade glioma rather than TMD. Biopsy confirmed the diagnosis as high-grade glioma (GBM), revealing marked mitotic changes with nuclear pleomorphism and multinucleated cells. The second case involves a 22-year-old female who presented with left upper limb and lower limb weakness for 10 days. MR spectroscopy showed reduced NAA values and an elevated choline peak with small lactate at a few places. A choline/creatine ratio of 1.9 was obtained. On perfusion imaging, the observed mean rCBV values were substantially low (rCBV measuring approximately 1.07). Consequently, a final radiological diagnosis of TMD was considered. A biopsy confirmed the presence of inflammatory demyelination.

Background: Stroke is the major cause of mortality and permanent disability and is associated with an astonishing economic burden worldwide. In the past few decades, accumulated evidence has indicated that Xuesaitong (XST) has therapeutic benefits in cases of acute ischemic stroke (AIS). Our study aimed to provide the best current body of evidence of the efficacy and safety of XST for patients with AIS. Methods: This is a systematic review and meta-analysis of randomized controlled trials (RCTs). We searched eight electronic databases from inception to 17 July 2023 for relevant RCTs. The investigators independently screened trials, extracted data, and assessed the risk of bias. A meta-analysis was conducted using RevMan 5.3 and STATA 16.0 software. Results: In total, 46 RCTs involving 7,957 patients were included. The results showed that XST improved the long-term functional outcomes with lower modified Rankin Scale (mRS) scores (MD = -0.67; 95% CI [-0.92 to -0.42]; p < 0.00001) and a higher proportion of functional independence (mRS ≤2) (RR = 1.08; 95% CI [1.05 to 1.12]; p < 0.00001). Low-quality evidence indicated that XST improved the activities of daily living (MD = 10.17; 95% CI [7.28 to 13.06]; p < 0.00001), improved the neurological impairment (MD = -3.39; 95% CI [-3.94 to -2.84]; p < 0.00001), and enhanced the total efficiency rate (RR = 1.19; 95% CI [1.15 to 1.23]; p < 0.00001). No significant difference was found in the all-cause mortality or incidence of adverse events between the XST and control groups. The certainty of evidence was estimated as moderate to very low. Conclusion: Presently, the administration of XST within 14 days of AIS is associated with favorable long-term functional outcomes. In addition, XST can improve activities of daily living, alleviate neurological deficits, and has shown good tolerability. However, the current evidence is too weak, and the confidence of evidence synthesis was restricted by the high risk of bias. Given the insufficient evidence, appropriately sized and powered RCTs investigating the efficacy and safety of XST for patients with AIS are warranted. [ABSTRACT FROM AUTHOR]

Background: Bone overgrowth after decompressive surgery for lumbar stenosis resulting in recurrence of neurological signs has not been reported in veterinary literature. However, there are few cases described in human medicine. Case presentation: A 13-month-old entire female dog, a crossbreed between a Springer Spaniel and a Border Collie, weighing 24 kg, was referred with a 5-day history of progressive spastic paraplegia, indicative of a T3-L3 myelopathy. Magnetic resonance (MR) imaging revealed a right-sided L2-L3 compressive extradural lesion, compatible with epidural haemorrhage, which was confirmed by histopathology. The lesion was approached via right-sided L2-L3 hemilaminectomy and was successfully removed. One-year postoperatively the dog re-presented with pelvic limb ataxia. MR and computed tomography (CT) images demonstrated excessive vertebral bone formation affecting the right articular processes, ventral aspect of the spinous process of L2-L3, and contiguous vertebral laminae, causing spinal cord compression. Revision surgery was performed, and histopathology revealed normal or reactive osseous tissue with a possible chondroid metaplasia and endochondral ossification, failing to identify a definitive reason for the bone overgrowth. Nine-month postoperatively, imaging studies showed a similar vertebral overgrowth, resulting in minimal spinal cord compression. The patient remained stable with mild proprioceptive ataxia up until the last follow-up 18 months post-revision surgery. Conclusion: This is the first report in the veterinary literature of bone overgrowth after lumbar hemilaminectomy which resulted in neurological deficits and required a revision decompressive surgery. [ABSTRACT FROM AUTHOR]

Neuroblastoma (NB) is a leading cause of death in children. It usually occurs in the adrenal gland and rarely in the spinal canal. Here, we report the case of a 48-year-old male patient with abnormal thickening of the cauda equina nerve as revealed by lumbosacral magnetic resonance imaging. The patient’s main clinical manifestations were numbness and pain in both lower limbs. The patient underwent surgical treatment; however, intraoperatively, an unclear border was observed between the cauda equina nerve and the tumor; therefore, the tumor was not forcibly excised. The postoperative pathological results were reported as NB. The disease known as NB, which is extremely rare. We believe that a pathological biopsy is extremely vital for diagnosing NB, and aggressive postoperative radio-chemotherapy could potentially prolong the patient’s survival time. [ABSTRACT FROM AUTHOR]

Background: Previous studies on thoracolumbar fractures with neurological symptoms have focused on how to achieve satisfactory fracture reduction, adequate nerve decompression, and stable spinal alignment. With the development of the minimally invasive spine surgery technique, achieving satisfactory treatment results and reducing iatrogenic trauma at the same time has become a new goal of spinal surgery. This research used percutaneous transpedicular screw distraction to partially reduce the fractured vertebrae, followed by completing nerve decompression and reducing residual displacement bone fragments with the assistance of the unilateral biportal endoscopic (UBE) technique to achieve full protection of bone-ligament tissue and obtain good clinical efficacy. Methods: Guide wires were safely inserted into the fractured vertebra and adjacent upper and lower vertebra under the surveillance of anteroposterior and lateral X-ray fluoroscopy. Transpedicular screws were implanted via guide wires on the side with mild neurological deficits or bone fragment compression (the opposite side of the endoscopic operation). A titanium rod was installed and moderately distracted to reduce the fractured vertebra. Then, under the guidance of the endoscopic view, the laminectomy and ligamentum flavum resection were completed according to the position of the protruding bone fragment into the spinal canal, and the compressed dural sac or nerve root was fully exposed and decompressed. An L-shaped replacer was used to reduce residual bone fragments. The ipsilateral transpedicular screws and rod were installed and adjusted to match the contralateral side. The drainage tube was indwelled, and the incision was closed. The preoperative and postoperative images of the patients were evaluated, and the recovery of neurological symptoms was observed. Results: Surgery was successfully completed on all six patients, and no intraoperative conversion to open surgery was performed. Postoperative images showed good reduction of the protruding bone fragment and good placement of all screws. At the last follow-up, the neurological symptoms of all patients returned to normal. Conclusion: The UBE technique combined with percutaneous transpedicular screw fixation in the treatment of thoracolumbar fractures with neurological symptoms can effectively achieve the reduction of displaced bone fragments, improve damaged nerve function, stabilize spinal alignment, and protect the integrity of bone-ligament tissue. [ABSTRACT FROM AUTHOR]

Forebrain ischemia-reperfusion (IR) injury causes neurological impairments due to decreased cerebral autoregulation, hypoperfusion, and edema in the hours to days following the restoration of spontaneous circulation. This study aimed to examine the protective and/or therapeutic effects of cerebrolysin (CBL) in managing forebrain IR injury and any probable underlying mechanisms. To study the contribution of reperfusion to forebrain injury, we developed a transient dual carotid artery ligation (tDCAL/IR) mouse model. Five equal groups of six BLC57 mice were created: Group 1: control group (no surgery was performed); Group 2: sham surgery (surgery was performed without IR); Group 3: tDCAL/IR (surgery with IR via permanently ligating the left CA and temporarily closing the right CA for 30 min, followed by reperfusion for 72 h); Group 4: CBL + tDCAL/IR (CBL was given intravenously at a 60 mg/kg BW dose 30 min before IR); and Group 5: tDCAL/IR + CBL (CBL was administered i.v. at 60 mg/kg BW three hours after IR). At 72 h following IR, the mice were euthanized. CBL administration 3 h after IR improved neurological functional recovery, enhanced anti-inflammatory and antioxidant activities, alleviated apoptotic neuronal death, and inhibited reactive microglial and astrocyte activation, resulting in neuroprotection after IR injury in the tDCAL/IR + CBL mice group as compared to the other groups. Furthermore, CBL reduced the TLRs/NF-kB/cytokines while activating the Keap1/Nrf2/antioxidant signaling pathway. These results indicate that CBL may improve neurologic function in mice following IR. [ABSTRACT FROM AUTHOR]

Study Design. Retrospective database analysis. Objective. To elucidate trends in the utilization of intraoperative neurophysiological monitoring (IONM) during elective lumbar surgery procedures and to investigate the association between the use of IONM and surgical outcomes. Background. The routine use of IONM in elective lumbar spine procedures has recently been called into question due to longer operative time, higher cost, and other substitute advanced technologies. Methods. The Statewide Planning and Research Cooperative System database was accessed to perform this retrospective study. The trends of IONM use for lumbar decompression and fusion procedures were investigated from 2007 to 2018. The association between IONM use and surgical outcomes was investigated from 2017 to 2018. Multivariable logistic regression analyses, as well as propensity score matching (PS-matching), were conducted to assess IONM association in neurological deficits reduction. Results. The utilization of IONM showed an increase in a linear fashion from 79 cases in 2007 to 6201 cases in 2018. A total of 34,592 (12,419 monitored and 22,173 unmonitored) patients were extracted, and 210 patients (0.6%) were reported for postoperative neurological deficits. Unadjusted comparisons demonstrated that the IONM group was associated with significantly fewer neurological complications. However, the multivariable analysis indicated that IONM was not a significant predictor of neurological injuries. After the PS-matching of 23,642 patients, the incidence of neurological deficits was not significantly different between IONM and non-IONM patients. Conclusion. The utilization of IONM for elective lumbar surgeries continues to gain popularity. Our results indicated that IONM use was not associated with a reduction in neurological deficits and will not support the routine use of IONM for all elective lumbar surgery. [ABSTRACT FROM AUTHOR]

Introduction: The incidence and pattern of neurological complications after congenital cardiac surgery have been changing over the years due to improvement in surgical technique and perioperative management. The aim of this study was to evaluate the incidence and pattern of neurological injury in our institute. Materials and Methods: We retrospectively reviewed all pediatric patients who underwent noncontrast computed tomography of the brain for suspected postoperative neurological injury occurring during the 1st week after pediatric cardiac surgery between April 2016 and February 2020. We identified neurological injury as patients having ischemic infarct and intracranial hemorrhage. Results: A total of 2971 pediatric cardiac surgeries were performed at our institute. Sixty-seven patients (2.25%) developed neurological injury. Fifty-five patients (82%) developed ischemic infarct while 12 patients (18%) had intracranial hemorrhagic. Pattern of ischemic infarct included global hypoxic injury in 30 patients (54.5%), posterior cerebral artery territory in 9 patients (16.3%), middle cerebral artery territory in 8 patients (14.5%), multiterritory involvement in 5 patients (9.0%), and anterior cerebral artery territory in 3 patients (5.4%). In patients with intracranial hemorrhage, 5 patients (7.4%) developed subarachnoid hemorrhage (SAH), 4 patients (5.9%) developed subdural hemorrhage, and 3 patients (4.4%) developed intraparenchymal hemorrhage. Conclusions: Neurological complication accounts for significant morbidity and mortality after congenital cardiac surgery. In our study, ischemic infarct accounted for 82% cases. In ischemic infarct, global ischemia was the most common type and carried high risk of mortality. In hemorrhage group, SAH was the most common finding. Nevertheless, the aim of this study was to characterize the current incidence of acute clinically evident neurologic complications in children undergoing congenital cardiac surgery in a tertiary hospital, although acute neurologic morbidity appears to be appreciably lower than in the past at our institution.

A reduction in fluid absorption or an obstruction of normal outflow is a common cause of hydrocephalus. It typically requires medical attention, which frequently entails the placement of a ventriculoperitoneal shunt (VPS) to lower intracranial pressure. We intend to list the few, documented examples of neurological impairments resulting from the installation of a VPS in this systematic study. Two search engines (PubMed and Cochrane) were used to conduct a systematic review from 1975 to December 12, 2021. The following search terms were employed: neurological deficits or neurological injury or palsies or thalamus or tract or longitudinal fasciculus or somatotropy or fasciculus or hearing loss or hemisensory or cortico AND ventriculoperitoneal shunt or VPS AND hydrocephalus. The inclusion criteria included VPS, neurological deficits, and human participants. The exclusion criteria included ventriculoarterial shunt, lumboperitoneal shunt, nonhuman subjects, and infection. Twenty trials in total, including a total of 25 patients, were included. There were 17 case report studies. A total of 35/785 patients (4.46%) experienced neurological impairments. In 9/25 (36%) of shunt cases had one of the three recognized causes: trapped fourth ventricle, dandy walker, or syringomyelia. Most of the patients developed VI, VII nerve palsies 11/25 (44%) followed by weakness, cerebellar symptoms, and VI nerve palsy. The brainstem was seen to be the most often injured structure (15/25; 60%), followed by deep brain structures (thalamus, basal ganglia, and white matter tracts; 20%). Even though ventriculoperitoneal shunting is a routine and straightforward treatment, issues can still arise. Although rare, there have been reports of cranial nerve impairments, therefore care should be taken. [ABSTRACT FROM AUTHOR]

Background Hyperlactatemia, is common in patients undergoing neurosurgical procedures. Several studies have identified potential risk factors for developing hyperlactatemia in neurosurgical patients, including body mass index, surgery duration, tumour volume, and certain drugs such as volatile anesthetic agents and corticosteroids. This systematic review and meta-analysis examined the evidence of the association between perioperative lactate levels in patients undergoing brain surgery and postoperative morbidity and mortality. Methods Using PubMed, Scopus, Web of Science, Embase, CINAHL, Medline, Google Scholar, and the Cochrane Central Register of Controlled Trials databases, a systematic literature search was conducted for studies examining the association between perioperative hyperlactatemia and postoperative outcomes in patients undergoing brain surgery. Two authors independently evaluated the full-text papers for eligibility, and then data extraction and meta-analyses of similar studies were conducted (using a random effect model for each outcome measure). The Newcastle Ottawa Scale was used to evaluate the risk of bias (NOS scale). Results Seven observational studies were included, and a total of 1,832 patients were assessed in the systematic review and meta-analysis. The quality of the included studies ranged from poor to high quality according to the NOS quality assessment tool. Meta-analysis results revealed no significant association between perioperative hyperlactatemia and postoperative new neurological deficits (five studies: odds ratio [OR] = 0.97, 95% confidence interval [CI] [0.50–1.87], p = 0.92; heterogeneity: I2 = 38%, p = 0.18). Similarly, perioperative hyperlactatemia was neither significantly associated with increased 30-day postoperative mortality (two studies; OR = 0.20, 95% CI [0.02–2.00], p = 0.17; heterogeneity: I2 = 0%, p = 0.59) nor 6 months survival rate (three studies; OR = 1.05, 95% CI [0.75–1.47], p = 0.79; heterogeneity: I2 = 0%, p = 0.51). Moreover, there was no difference in the length of hospital stay between the two groups (four studies: mean difference = –0.85, 95% CI [–1.73 to 0.03], p = 0.06). Pooled studies were not homogenous (I2 = 68%, p = 0.03). Conclusion Perioperative hyperlactatemia is benign in neurosurgical patients and is not associated with significant postoperative outcomes, such as developing new postoperative neurological deficit, 30-day mortality, 6-month survival, or prolonged hospital stay. [ABSTRACT FROM AUTHOR]

The aim of this study is to introduce surgical technique of endoscopic decompression combined with percutaneous pedicle screw fixation (PPSF) for thoracolumbar burst fractures (TLBFs) with neurological deficits and evaluate its efficacy. A total of 32 patients with TLBFs and neurological deficits who were treated by endoscopic decompression combined with PPSF from June 2018 to August 2019 were included in this study. The effect of decompression was analyzed using canal encroachment ratio, while deformity correction was assessed using the sagittal Cobb angle and the percentage of anterior vertebral height. We also analyzed other clinical outcomes such as visual analog scale, Oswestry Disability Index, and American Spinal Injury Association impairment scale dose. The patients were followed up for an average of 16 months. Our data showed that the patients' mean operation time was 153.75 minutes, the mean intraoperative blood loss was 48.84 mL, and the mean incision length was 7.78 cm. The canal encroachment ratio decreased from 55.91% ± 12.27% to 12.44% ± 3.91% (P < 0.05), sagittal Cobb angle decreased from 17.09° ± 5.46° to 5.72° ± 3.68° (P < 0.05), while the percentage of anterior vertebral height increased from 53.72% ± 8.99% to 83.22% ± 8.21% (P < 0.05). In addition, there was a significant improvement in the visual analog scale score, Oswestry Disability Index, and American Spinal Injury Association impairment scale classification (P < 0.05). Screw fracture occurred only in one patient during follow-up. Endoscopic decompression combined with PPSF in the treatment of TLBFs with neurological deficits is safe and effective, which is a new minimally invasive method for the treatment of such diseases. [ABSTRACT FROM AUTHOR]

Based on accumulating evidence, cholesterol metabolism dysfunction has been suggested to contribute to the pathophysiological process of traumatic brain injury (TBI) and lead to neurological deficits. As a key transporter of cholesterol that efflux from cells, the ATP‐binding cassette (ABC) transporter family exerts many beneficial effects on central nervous system (CNS) diseases. However, there is no study regarding the effects and mechanisms of ABCG1 on TBI. As expected, TBI resulted in the different time‐course changes of cholesterol metabolism‐related molecules in the injured cortex. Considering ABCG1 is expressed in neuron and glia post‐TBI, we generated nestin‐specific Abcg1 knockout (Abcg1‐KO) mice using the Cre/loxP recombination system. These Abcg1‐KO mice showed reduced plasma high‐density lipoprotein cholesterol levels and increased plasma lower‐density lipoprotein cholesterol levels under the base condition. After TBI, these Abcg1‐KO mice were susceptible to cholesterol metabolism turbulence. Moreover, Abcg1‐KO exacerbated TBI‐induced pyroptosis, apoptosis, neuronal cell insult, brain edema, neurological deficits, and brain lesion volume. Importantly, we found that treating with retinoid X receptor (RXR, the upstream molecule of ABCG1) agonist, bexarotene, in Abcg1‐KO mice partly rescued TBI‐induced neuronal damages mentioned above and improved functional deficits versus vehicle‐treated group. These data show that, in addition to regulating brain cholesterol metabolism, Abcg1 improves neurological deficits through inhibiting pyroptosis, apoptosis, neuronal cell insult, and brain edema. Moreover, our findings demonstrate that the cerebroprotection of Abcg1 on TBI partly relies on the activation of the RXRalpha/PPARgamma pathway, which provides a potential therapeutic target for treating TBI. [ABSTRACT FROM AUTHOR]