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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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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: 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]

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]

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]

COVID-19, Fatigue, Long COVID, Neurological deficits, Neuropsychological assessment, Post-COVID, Somatization Of note, we have in the meantime examined more than 1000 people with post-COVID-19 syndrome in our post-COVID outpatient center, and the diagnostic results gathered so far are very similar to those published here. Keywords: COVID-19; Fatigue; Long COVID; Neurological deficits; Neuropsychological assessment; Post-COVID; Somatization EN COVID-19 Fatigue Long COVID Neurological deficits Neuropsychological assessment Post-COVID Somatization 333 336 4 01/16/23 20230201 NES 230201 This reply refers to the comment available at DOI https://doi.org/10.1007/s40120-022-00426-9 To the Editors We thank Vink and colleagues [[1]] for their critical appraisal of our study [[2]]. [Extracted from the article]

Study Design: Delphi study Objective: The objective of this study was to identify risk factors associated with the development and/or progression of neurological deficits in patients with metastatic spinal disease. Methods: A three-round Delphi study was conducted between January-May 2023 including AO Spine members, comprising mainly neurosurgeons and orthopedic surgeons. In round 1, participants listed radiological factors, patient characteristics, tumor characteristics, previous cancer-related treatment factors and additional factors. In round 2, participants ranked the factors on importance per category and selected a top 9 from all factors. Kendall's W coefficient of concordance was calculated as a measure of consensus. In the final round, participants provided feedback on the rankings resulting from round 2. Lastly, the highest-ranking factors were more clearly defined and operationalized by an expert panel. Results: Over two hundred physicians and researchers participated in each round. The factors listed in the first round were collapsed into 12 radiological factors, 14 patient characteristics, 6 tumor characteristics and 12 previous cancer-related treatment factors. High agreement was found in round 3 on the top-half lists in each category and the overall top 9, originating from round 2. Kendall's W indicated strong agreement between the participants. 'Epidural spinal cord compression', 'aggressive tumor behavior' and 'mechanical instability' were deemed most influential for the development of neurological deficits. Conclusion: This study provides factors that may be related to the development and/or progression of neurological deficits in patients with metastatic spinal disease. This list can serve as a basis for future directions in prognostication research. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the predictive value of motor evoked potentials (MEP) in the resection of pediatric intradural extramedullary (IDEM) tumors. Additionally, we aimed to assess the impact of MEP alerts on the extent of tumor resection. Medical records of pediatric patients who underwent resection of IDEM tumors with the assistance of MEP between March 2011 and October 2020 were reviewed. The occurrence of postoperative motor deficits was correlated with intraoperative MEP alerts. Sixteen patients were included. MEP alerts appeared in 2 patients (12.5%), being reflective of new postoperative motor deficits. Among the remaining 14 patients without any intraoperative MEP alerts, no motor decline was found. Accordingly, MEP significantly predicted postoperative motor deficits, reaching sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of 100% (p < 0.001). In the absence of MEP alerts, 11 out of 14 patients (78.6%) underwent GTR, while no patient with intraoperative IONM alerts underwent GTR (p = 0.025). Although MEP alerts limit the extent of tumor resection, the high sensitivity and PPV of MEP underline its importance in avoiding iatrogenic motor deficits. Concurrently, high specificity and NPV ensure safer tumor excision. Therefore, MEP can reliably support surgical decisions in pediatric patients with IDEM tumors. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Osteoporosis is the property of Chinese Journal of Osteoporosis and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: We aimed to evaluate the feasibility and performance of myocardial work echocardiography in assessing the severity of acute stroke and neurological deficits in patients with acute ischemic stroke. Methods: A total of 176 patients were examined by echocardiography within 24-48 hours of symptom onset with the measurement of global and regional myocardial work. The National Institutes of Health Stroke Scale score of each patient was documented. Results: With the increase of the National Institutes of Health Stroke Scale score, myocardial constructive work or positive work decreased (P < .05), while myocardial wasted work or negative work increased (P < .05). Except for global constructive work, global positive work, and global systolic constructive work, other myocardial work parameters all correlated with the National Institutes of Health Stroke Scale score (P < .05). Moreover, global wasted work, global negative work and global systolic wasted work had the strongest correlation with the National Institutes of Health Stroke Scale score (P < .001). Among these parameters, the ratio of global positive work/global negative work had the largest area (0.969, 0.938-1.001) under receiver operating characteristic curve in discriminating if the National Institutes of Health Stroke Scale score >15 or not. The optimal cutoff value was 3.89, with a sensitivity of 100%, a specificity of 93.0%, a positive predictive value of 84.9%, a negative predictive value of 100%, and an accuracy of 95.7%. Conclusion: Noninvasive myocardial work is highly competent in assessing the severity of acute stroke and neurological deficits, which can be used as a powerful supplement to the conventional scoring system. [ABSTRACT FROM AUTHOR]

Introduction: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can affect multiple organs. Reports of persistent or newly emergent symptoms, including those related to the nervous system, have increased over the course of the pandemic, leading to the introduction of post-COVID-19 syndrome. However, this novel syndrome is still ill-defined and structured objectification of complaints is scarce. Therefore, we performed a prospective observational cohort study to better define and validate subjective neurological disturbances in patients with post-COVID-19 syndrome. Methods: A total of 171 patients fulfilling the post-COVID-19 WHO Delphi consensus criteria underwent a comprehensive neurological diagnostic work-up including neurovascular, electrophysiological, and blood analysis. In addition, magnetic resonance imaging (MRI) and lumbar puncture were conducted in subgroups of patients. Furthermore, patients underwent neuropsychological, psychosomatic, and fatigue assessment. Results: Patients were predominantly female, middle-aged, and had incurred mostly mild-to-moderate acute COVID-19. The most frequent post-COVID-19 complaints included fatigue, difficulties in concentration, and memory deficits. In most patients (85.8%), in-depth neurological assessment yielded no pathological findings. In 97.7% of the cases, either no diagnosis other than post COVID-19 syndrome, or no diagnosis likely related to preceding acute COVID-19 could be established. Sensory or motor complaints were more often associated with a neurological diagnosis other than post-COVID-19 syndrome. Previous psychiatric conditions were identified as a risk factor for developing post-COVID-19 syndrome. We found high somatization scores in our patient group that correlated with cognitive deficits and the extent of fatigue. Conclusions: Albeit frequently reported by patients, objectifiable affection of the nervous system is rare in post-COVID-19 syndrome. Instead, elevated levels of somatization point towards a pathogenesis potentially involving psychosomatic factors. However, thorough neurological assessment is important in this patient group in order to not miss neurological diseases other than post-COVID-19. [ABSTRACT FROM AUTHOR]

Hypoxic–ischemic brain injury is an important cause of neonatal neurological deficits. Our previous study demonstrated that dexmedetomidine (Dex) provided neuroprotection against neonatal hypoxic brain injury; however, the underlying mechanisms remain incompletely elucidated. Overactivation of NADPH oxidase 2 (NOX2) can cause neuronal apoptosis and neurological deficits. Hence, we aimed to investigate the role of neuronal NOX2 in Dex-mediated neuroprotection and to explore its potential mechanisms. Hypoxic injury was modeled in neonatal rodents in vivo and in cultured hippocampal neurons in vitro. Our results showed that pre- or post-treatment with Dex improved the neurological deficits and alleviated the hippocampal neuronal damage and apoptosis caused by neonatal hypoxia. In addition, Dex treatment significantly suppressed hypoxia-induced neuronal NOX2 activation; it also reduced oxidative stress, as evidenced by decreases in intracellular reactive oxygen species (ROS) production, malondialdehyde, and 8-hydroxy-2-deoxyguanosine, as well as increases in the antioxidant enzymatic activity of superoxide dismutase and glutathione peroxidase in neonatal rat hippocampi and in hippocampal neurons. Lastly, the posthypoxicneuroprotective action of Dex was almost completely abolished in NOX2-deficient neonatal mice and NOX2-knockdown neurons. In conclusion, our data demonstrated that neuronal NOX2-mediated oxidative stress is involved in the neuroprotection that Dex provides against apoptosis and neurological deficits in neonates following hypoxia. [ABSTRACT FROM AUTHOR]

Bromodomain-containing protein 4 (BRD4), a member of the bromodomain and extra-terminal domain (BET) protein family, plays a crucial role in regulating inflammation and oxidative stress that are tightly related to stroke development and progression. Consequently, BRD4 blockade has attracted increasing interest for associated neurological diseases, including stroke. dBET1 is a novel and effective BRD4 degrader through the proteolysis-targeting chimera (PROTAC) strategy. We hypothesized that dBET1 protects against brain damage and neurological deficits in a transient focal ischemic stroke mouse model by reducing inflammation and oxidative stress and preserving the blood–brain barrier (BBB) integrity. Post-ischemic dBET1 treatment starting 4 h after stroke onset significantly ameliorated severe neurological deficits and reduced infarct volume 48 h after stroke. dBET1 markedly reduced inflammation and oxidative stress after stroke, indicated by multiple pro-inflammatory cytokines and chemokines including IL-1β, IL-6, TNF-α, CCL2, CXCL1 and CXCL10, and oxidative damage markers 4-hydroxynonenal (4-HNE) and gp91phox and antioxidative proteins SOD2 and GPx1. Meanwhile, stroke-induced BBB disruption, increased MMP-9 levels, neutrophil infiltration, and increased ICAM-1 were significantly attenuated by dBET1 treatment. Post-ischemic dBET1 administration also attenuated ischemia-induced reactive gliosis in microglia and astrocytes. Overall, these findings demonstrate that BRD4 degradation by dBET1 improves acute stroke outcomes, which is associated with reduced neuroinflammation and oxidative stress and preservation of BBB integrity. This study identifies a novel role of BET proteins in the mechanisms resulting in ischemic brain damage, which can be leveraged to develop novel therapies. [ABSTRACT FROM AUTHOR]

Background: Nodular plexiform neurofibromas in individuals with neurofibromatosis type 1 often cause significant symptoms and are treated with surgical excision despite the potential risk of complications. This study aimed to clarify the surgical outcomes of deep-seated nodular plexiform neurofibromas and identify the factors associated with postoperative complications. Methods: We retrospectively reviewed patients with neurofibromatosis type 1 who underwent surgical excision for deep-seated nodular plexiform neurofibromas in our hospital from 2015 to 2021. Enucleation while preserving the nerve fascicles was attempted first, and en bloc resection, ligating the nerve origin in cases in which the parent nerve was entrapped by the tumor, making the tumor difficult to dissect, was performed. Results: In 15 patients, 24 nodular plexiform neurofibromas received surgical excision. Sixteen tumors were enucleated, and eight were en bloc resected. The symptoms of all 10 patients with preoperative symptoms resolved after surgery. Four patients developed new neurological deficits immediately after surgery, two of whom had retained neurological symptoms at the last visit, but these symptoms were mild. Conclusions: The present study demonstrates that surgical treatment of nodular plexiform neurofibromas, even deep-seated neurofibromas, is safe with a low risk of severe complications and improvement in preoperative symptoms. [ABSTRACT FROM AUTHOR]

Background: Multimodal intraoperative monitoring (MIOM) is a useful tool to warn surgeons to intervene for intraoperative spinal cord injury in cervical spine surgery. However, the value of MIOM remains controversial before cervical spine surgery.Objective: To explore the value of MIOM in early detecting spinal cord injury associated with neck extension before cervical spine surgery.Methods and Materials: Data of 191 patients receiving cervical spine surgery with the MIOM were enrolled from June 2014 to June 2020. The subjects were divided into a group of evoked potentials (EP) changes and a group of no EP changes for analysis according to the monitoring alerts or not.Results: Five (2.62%) patients showed EP changes associated with neck extension during intubation or positioning. After early different interventions, such as repositioning and timely surgical decompression, none or transient postoperative neurological deficits were observed in four cases, and only one case was with permanent neurological deficits. The average preoperative Japanese Orthopaedic Association (JOA) scores of the group with EP changes were lower than those of the group with no EP changes (P = 0.037 < 0.05). There was no statistical significance in gender, average age, mean Pavlov ratio, and the minimum Palov ratio between the two groups (P > 0.05).Conclusions: The MIOM could identify spinal cord injury associated with neck extension before cervical spine surgery. Active and effective interventions could prevent or reduce permanent postoperative neurological deficits. Severe spinal cord compression might be a risk factor for EP changes. [ABSTRACT FROM AUTHOR]

Background: Edaravone alleviates neurological deficits among patients with intracerebral hemorrhage; however, its effects on mortality and long-term functional outcomes remain unknown. Objective: To assess clinical outcomes associated with edaravone initiated within 7 days of symptoms onset in intracerebral hemorrhage. Methods: We systematically searched PubMed, Embase, Cochrane Library, CiNii, China National Knowledge Infrastructure, Chinese VIP information, Wanfang Data, and SinoMed for relevant randomized controlled trials from their inception to 1 May 2021 and conducted a comprehensive systematic review and meta-analysis (PROSPERO registration number: CRD42019147801). All-cause mortality and long-term functional outcomes were taken as the primary outcomes. Results: A total of 38 randomized controlled trials including 3,454 participants with acute intracerebral hemorrhage were included. The selected articles were of poor quality. Meta-analysis revealed that edaravone could not reduce allcause mortality [relative risk (RR) = 0.51; 95% confidence interval (CI) (0.11-2.32); p = 0.38]. No studies reported on long-term functional outcomes in those trials. In addition, edaravone alleviated neurological deficits [mean difference (MD) = -5.44; 95% CI (-6.44 to -4.44); p<0.00001], improved the activities of daily living [MD = 8.44; 95% CI (7.65-9.23); p<0.00001], reduced the hematoma volume [MD = -4.71; 95% CI (-5.86 to -3.56); p<0.00001], and increased treatment response [RR = 1.26; 95% CI (1.22-1.31); p<0.00001]. In terms of safety outcome, there was no significant difference between the edaravone group and the control groups [RR = 1.67; 95% CI (0.92 to 3.06); p = 0.09]. Conclusion: Till date, edaravone does not associate with mortality reduction when initiated within 7 days of intracerebral hemorrhage onset. The effect of edaravone on long-term functional outcomes remains unknown due to lack of data. Although edaravone alleviated neurological deficits, improved activities of daily living, and reduced hematoma volume, we cautiously interpreted the results owing to the overall poor quality and high heterogeneity of the included trials. Presently, the results are insufficient to support edaravone as a routine treatment option for acute intracerebral hemorrhage. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Neurosurgery / Linchuang Shenjingwaike Zazhi is the property of Editorial Board of Journal of Clinical Neurosurgery and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: To investigate the association of serum high-sensitivity C-reactive protein (hs-CRP) with the severity of neurological deficits and prognosis in patients with acute cerebral infarction (ACI). Patients and Methods: In this retrospective analysis, 119 patients with ACI were recruited from January to December 2020. The serum hs-CRP level was measured by a latex-enhanced immunoturbidimetric assay. The severity of neurological deficits and prognosis of ACI patients were assessed using the National Institutes of Health Stroke Scale (NIHSS) and the modified Rankin Scale (mRS). Multivariate logistic analysis was performed and receiver operating characteristic (ROC) curves were plotted to evaluate the value of hs-CRP in predicting the prognosis of ACI. Results: The patients with a more favorable prognosis (mRS score 0– 2) had a lower median serum hs-CRP level than those with a worse prognosis (mRS score 3– 6) (3.32 IQR: 1.51, 8.04 to 17.93 IQR:16.02, 19.01; P< 0.001). After adjusting for potential confounders, multivariable linear regression showed that serum hs-CRP level was independently associated with NIHSS score (Beta = 0.952, P< 0.001) and mRS score (Beta=0.878, P< 0.001). Multivariate logistic analysis revealed that high hs-CRP level was an independent predictor of the poor prognosis in patients with ACI (adjusted1 OR = 1.995; 95% CI = 1.499– 2.655; adjusted2 OR = 2.75; 95% CI = 1.015– 7.457). ROC curve analysis indicated that the area under the curve for hs-CRP to predict poor prognosis was 0.986. The cutoff value, sensitivity, and specificity were 11.835 mg/L, 95%, and 92.5%, respectively. In terms of ischemic stroke subtypes, the serum hs-CRP level was higher in large-artery atherosclerosis (LAA) patients than in those with small-artery occlusion (SAO) and cardioembolism (CE). In addition, the patients with LAA had higher scores of NIHSS and mRS than those with SAO and CE. Conclusion: Serum hs-CRP level is an independent predictor of prognosis, and an efficient index to discriminate patients with ACI, especially for those with LAA. [ABSTRACT FROM AUTHOR]

Introduction: Nonketotic hyperglycemic hyperosmolar state (NKHHS) is associated with a wide spectrum of neurological syndromes including acute stroke-like deficits. Clinical features and etiology have not been established yet. Methods: Here we provide a case illustration and systematic review on non-epileptic acute neurological deficits in NKHSS. The systematic literature search followed PRISMA guidelines and a predefined protocol, including cases of NKHSS with acute stroke-like presentation. Results: The database search yielded 18 cases. Hemianopia was the most common clinical presentation (73%), followed by partial or total anterior circulation syndrome (26%). Patients with symptoms of acute anterior circulation infarct were significantly older (69.5 ± 5.1 vs. 52.2 ± 13.9 years; p = 0.03) and showed higher mean glucose levels at the admission vs. those with hemianopia (674.8 ± 197.2 vs. 529.4 ± 190.8 mg/dL; p = 0.16). Brain MRI was performed in 89% of patients, resulting abnormal in 71% of them, especially hemianopic (91%). Subcortical hypointensities in T2-FLAIR MR sequences were present in all the analyzed cases. Cortical DWI hyperintensities were also common (64%). EEG showed diffuse or focal slow wave activity in 68% of patients, especially with visual hallucinations (85%). Neurological symptoms completely resolved in 78% of patients within 6 (IQR 3–10) days, following aggressive treatment and glucose normalization. Conclusions: Our results suggest neuronal dysfunction on a metabolic basis as the leading cause of acute neurological deficits in NKHHS. Despite the generally favorable prognosis, prompt identification and aggressive treatment are crucial to avoid irreversible damage. Larger cohort studies are needed to confirm our findings. [ABSTRACT FROM AUTHOR]

Introduction: Acute high‐altitude hypoxia exposure causes multiple adverse neurological consequences. However, the exact mechanisms are still unclear, and there is no targeted treatment with few side effects. Excessive cerebral formaldehyde (FA) impairs numerous functions, and can be eliminated by nano‐packed coenzyme Q10 (CoQ10). Aims: In this study, we aimed to investigate whether cerebral FA was accumulated after hypobaric hypoxia exposure, and further explored the preventative effect of CoQ10 through FA elimination. Results: Accumulated cerebral FA was found in C57BL/6 mice after acute high‐altitude hypoxia exposure, which resulted in FA metabolic disturbance with the elevation of semicarbazide‐sensitive amine oxidase, and declination of aldehyde dehydrogenase‐2. Excessive FA was also found to induce neuronal ferroptosis in vivo. Excitingly, administration with CoQ10 for 3 days before acute hypobaric hypoxia reduced cerebral FA accumulation, alleviated subsequent neuronal ferroptosis, and preserved neurological functions. Conclusion: Cerebral FA accumulation mediates neurological deficits under acute hypobaric hypoxia, and CoQ10 supplementation may be a promising preventative strategy for visitors and sojourners at plateau. [ABSTRACT FROM AUTHOR]

Bromodomain-containing protein 4 (BRD4), a member of the bromodomain and extra-terminal domain (BET) protein family, plays a crucial role in regulating inflammation and oxidative stress that are tightly related to stroke development and progression. Consequently, BRD4 blockade has attracted increasing interest for associated neurological diseases, including stroke. dBET1 is a novel and effective BRD4 degrader through the proteolysis-targeting chimera (PROTAC) strategy. We hypothesized that dBET1 protects against brain damage and neurological deficits in a transient focal ischemic stroke mouse model by reducing inflammation and oxidative stress and preserving the blood-brain barrier (BBB) integrity. Post-ischemic dBET1 treatment starting 4 h after stroke onset significantly ameliorated severe neurological deficits and reduced infarct volume 48 h after stroke. dBET1 markedly reduced inflammation and oxidative stress after stroke, indicated by multiple pro-inflammatory cytokines and chemokines including IL-1β, IL-6, TNF-α, CCL2, CXCL1 and CXCL10, and oxidative damage markers 4-hydroxynonenal (4-HNE) and gp91phox and antioxidative proteins SOD2 and GPx1. Meanwhile, stroke-induced BBB disruption, increased MMP-9 levels, neutrophil infiltration, and increased ICAM-1 were significantly attenuated by dBET1 treatment. Post-ischemic dBET1 administration also attenuated ischemia-induced reactive gliosis in microglia and astrocytes. Overall, these findings demonstrate that BRD4 degradation by dBET1 improves acute stroke outcomes, which is associated with reduced neuroinflammation and oxidative stress and preservation of BBB integrity. This study identifies a novel role of BET proteins in the mechanisms resulting in ischemic brain damage, which can be leveraged to develop novel therapies. [ABSTRACT FROM AUTHOR]

Introduction: The morbidity associated with metastatic spinal disease is significant because of spinal cord and/or nerve root compression. The purpose of this paper is to define a diagnostic-therapeutic path for patients with vertebral metastases and from this path to build an algorithm to reduce the devastating consequences of spinal cord compression. Materials and Methods: The algorithm is born from the experience of a primary care center. A spine surgeon, an emergency room (ER) physician, a neuroradiologist, a radiation oncologist, and an oncologist form the multidisciplinary team. The ER physician or the oncologist intercept the patient with symptoms and signs of a metastatic spinal cord compression. Once the suspicion is confirmed, the following steps of the flow-chart must be triggered. The spine surgeon takes charge of the patient and, on the base of the anamnestic data and neurological examination, defines the appropriate timing for magnetic resonance imaging (MRI) in collaboration with the neuroradiologist. From the MRI outcome, the spine surgeon and the radiation oncologist consult each other to define further therapeutic alternatives. If indicated, surgical treatment should precede radiation therapy. The oncologist gets involved after surgery for systemic therapy. Results: In 2021, the Spine and Spinal Cord Surgery department evaluated 257 patients with vertebral metastasis. Fifty-three patients presented with actual or incipient spinal cord compression. Among these, 27 were admitted due to rapid progression of symptoms, neurological deficits and/or spine instability signs. The level was thoracic in 21 cases, lumbar in 4 cases, cervical in 1 case, sacral in 1 case. Fifteen were operated on, 10 of these programmed and 5 in emergency. Discussion: Patients with a history of malignancy can present to the ER or to the oncology department with symptoms that must be correctly framed in the context of a metastatic involvement. Even when there is no previous cancer history, the patient's pain characteristics and clinical signs must be interpreted to yield the correct diagnosis of vertebral metastasis with incipient or current spinal cord compression. The awareness of the alert symptoms and the application of an integrated paradigm consent to frame the patients with spinal cord compression, obtaining the benefits of a homogeneous step-by-step diagnostic and therapeutic path. Early surgical or radiation therapy treatment gives the best hope for preventing the worsening, or even improving, the deficits. Conclusions: Metastatic spinal cord compression can cause neurological deficits compromising quality of life. Treatment strategies should be planned comprehensively. A multidisciplinary approach and the application of the proposed algorithm is of paramount importance to optimize the outcomes of these patients. [ABSTRACT FROM AUTHOR]

Cardiopulmonary arrest (CA) can greatly impact a patient's life, causing long-term disability and death. Although multi-faceted treatment strategies against CA have improved survival rates, the prognosis of CA remains poor. We previously reported asphyxial cardiac arrest (ACA) can cause excessive activation of the sympathetic nervous system (SNS) in the brain, which contributes to cerebral blood flow (CBF) derangements such as hypoperfusion and, consequently, neurological deficits. Here, we report excessive activation of the SNS can cause enhanced neuropeptide Y levels. In fact, mRNA and protein levels of neuropeptide Y (NPY, a 36-amino acid neuropeptide) in the hippocampus were elevated after ACA-induced SNS activation, resulting in a reduced blood supply to the brain. Post-treatment with peptide YY3-36 (PYY3-36), a pre-synaptic NPY2 receptor agonist, after ACA inhibited NPY release and restored brain circulation. Moreover, PYY3-36 decreased neuroinflammatory cytokines, alleviated mitochondrial dysfunction, and improved neuronal survival and neurological outcomes. Overall, NPY is detrimental during/after ACA, but attenuation of NPY release via PYY3-36 affords neuroprotection. The consequences of PYY3-36 inhibit ACA-induced 1) hypoperfusion, 2) neuroinflammation, 3) mitochondrial dysfunction, 4) neuronal cell death, and 5) neurological deficits. The present study provides novel insights to further our understanding of NPY's role in ischemic brain injury. [ABSTRACT FROM AUTHOR]

Infection is a major reason for poor stroke outcomes, and sepsis is a major cause of stroke-elated deaths. We herein examined whether NMDA receptor blockade, which was reported to exert anti-inflammatory actions, protects against the deleterious consequences of lipopolysaccharide (LPS)-induced sepsis-like state in adult male NMRI mice exposed to transient intraluminal middle cerebral artery occlusion (MCAO). At 24 h post-ischemia, vehicle or Escherichia coli LPS (2 or 4 mg/kg) was intraperitoneally administered, whereas 30 min later vehicle or ketamine (10 mg/kg), which is a non-competitive NMDA receptor antagonist, was intraperitoneally applied. Delivery of LPS at a dosage of 4 mg/kg induced a sepsis-like state characterized by a rectal temperature reduction by ∼4.0°C, increased neurological deficits in Clark score, cylinder and open-field tests, increased brain infarct volume and reduced neuronal survival in the previously ischemic tissue. Notably, additional treatment with ketamine (10 mg/kg) significantly attenuated the sepsis-associated rectal temperature reduction by ∼1.5°C, reduced neurological deficits, reduced infarct volume, and promoted neuronal survival. Ketamine alone did not influence infarct volume or neurological deficits. Real-time PCR data analysis showed that GFAP , CD86 , CD206 , IL-1 β, and IL-10 mRNA levels were significantly increased in ischemic brains of LPS-treated compared with vehicle-treated mice. Additional treatment with ketamine significantly decreased IL-1 β and IL-10 , but not GFAP , CD86 , and CD206 mRNA levels. Our data show that ketamine at a dose that on its own does not confer neuroprotection reverses the adverse effects of LPS-induced sepsis-like state post-ischemia, presumably via immunomodulatory actions. [ABSTRACT FROM AUTHOR]

Background: Magnetic resonance imaging (MRI) is widely used in the diagnosis of tuberculous meningitis (TBM) and its complications. We aimed to explore the relationship between MRI features and neurological deficits and TBM patients' prognosis. Methods: patients diagnosed with TBM were subjected to a neurological evaluation on admission and divided into groups based on the Medical Research Council (MRC) scale. After several years of follow-up, the patients were further divided into groups according to the Modified Rankin Score (MRS). Their MR images were analyzed for meningeal enhancement, tuberculomas, infarction, hydrocephalus, and abscess, including the location and size of the lesion. Any changes in MRI features during the follow-up were recorded. MRI features between groups were compared, and the relationship between dynamic changes in images and Rankin grading was explored. Results: We found significant differences in acute cerebral infarction (ACI) and old cerebral infarctions (OCI) between the MRC groups, and the ORs of ACI and OCI were 21.818 (95% CI: 2.440–195.075) and 6.788 (95% CI: 1.516–30.392), respectively. There were significant differences in ACI, OCI, and Evan's ratio between the MRS groups (p < 0.05), and the ORs of ACI, OCI, and hydrocephalus were 6.375 (95% CI: 1.501–27.080), 5.556 (95% CI: 1.332–23.177), and 9.139 (95% CI: 2.052–40.700), respectively. The changes of Evan's ratio were related to the MRS grading (r = 0.335, p = 0.040). Conclusions: For patients with TBM, the presence of ACI or OCI is associated with neurological deficits, and ACI, OCI, and hydrocephalus can be regarded as poor prognostic predictors. Changes in Evan's ratio will affect the outcome. [ABSTRACT FROM AUTHOR]

Background: The mechanisms, leading to depression development in multiple sclerosis (MS) include progressive demyelination and axonal degeneration along with neurological deficit and a certain similarity of mechanisms leading to the development of immunological disorders and neuroinflammation involved in the pathogenesis of MS and depression.Objective: The objective of the study was to examine the specifics of relationships within a complex of neurological deficit, depression, and quality of life in MS.Materials and Methods: For purposes of integral quantification of neurologic disability in various functional systems, the "Expanded Disability Status Scale" (EDSS) is used. The severity of depression was measured using the Beck Depression Inventory (BDI). The level of quality of life was measured through the MS Quality of Life (MSQOL)-54 Instrument and Physical Health Composite Score MSQOL-54. The study was conducted among patients with relapsing-remitting (RRMS (n = 52) and secondary-progressive (SPMS, n = 51) phenotypes of MS.Results: The study shows a positive correlation of depression with various indicators of the physical and mental components of the QOL of patients per course and progression of MS phenotypes. It was revealed that in SPMS patients' correlation is significant compared to patients with RRMS. It's proven that the risk of developing depression in patients with RRMS and SPMS depends on the level of neurological deficit.Conclusions: The infrastructure of the target parameters study evidenced that regardless of the type of MS course, depression was found to have a stable connection with neurological impairment (per EDSS scale), especially in the secondary-progressive course of MS (SPMS). [ABSTRACT FROM AUTHOR]

An awake craniotomy is a common neurosurgical procedure for excising brain tumor(s) located near or in eloquent areas. The use of benzodiazepine (BZD) for sedation in some patients with neuropathological conditions (e.g., stroke, brain tumors) has been previously linked with re-appearance of neurological deficits including limb incoordination, ataxia, and motor weakness, resulting in complications for the patient along with procedural challenges. Whether or not these findings can be extrapolated to patients undergoing brain tumor resection is largely unknown. The current work primarily sought to compare neurological outcome(s) in the immediate postoperative period between BZD-free and BZD-based sedation techniques in patients undergoing awake craniotomy. Using a database composed of awake craniotomies conducted within a single center and by a single surgeon, patients were retrospectively classified based on midazolam administration into BZD-free sedation (n=125) and BZD-based sedation (n=416) groups. Patients from each group were matched based on age, sex, tumor location, tumor grade, preoperative neurological deficits, non-operative BZD use, and Karnofsky Performance Scale scores, resulting in 108 patients within each group. Postoperative neurological deficits were recorded. Logistic regression analyses were conducted comparing postoperative neurological deficits between the matched groups. Postoperative neurological deficits were more prevalent within the BZD-based sedation group compared to the BZD-free sedation group (adjusted odds ratio (aOR)=1.903, 95% CI=1.018-3.560, p=0.044). In addition, subgroup analysis of the matched cohort showed a relationship between preoperative neurological symptoms and postoperative neurological deficits in the BZD-based sedation group (aOR=3.756, 95% CI=1.390-10.147, p=0.009). Our findings support the notion that the increased incidence of postoperative neurological deficits with BZD sedation may in part be related to the unmasking of preoperative neurological deficits. Further studies are required to confirm this phenomenon. [ABSTRACT FROM AUTHOR]

Objective: Patients presenting with neurological deficit secondary to metastatic epidural spinal cord compression (MESCC) are often treated with surgery in combination with high-dose corticosteroids. Despite steroids being commonly used, the evidence regarding the effect of corticosteroids on patient outcomes is limited. The objective of this study was to describe the effect of corticosteroid use on preoperative neurological function in patients with MESCC. Methods: Patients who underwent surgery between August 2013 and February 2017 for the treatment of spinal metastases and received steroids to prevent neurologic deficits were included. Data regarding demographics, diagnosis, treatment, neurological function, adverse events, health-related quality of life, and survival were extracted from an international multicenter prospective cohort. Results: A total of 30 patients treated surgically and receiving steroids at baseline were identified. Patients had a mean age of 58.2 years (standard deviation, 11.2 years) at time of surgery. Preoperatively, 50% of the patients experienced deterioration of neurological function, while in 30% neurological function was stable and 20% improved in neurological function. Lengthier steroid use did not correlate with improved or stabilized neurological function. Postoperative adverse events were observed in 18 patients (60%). Patients that stabilized or improved neurologically after steroid use showed a trend towards improved survival at 3- and 24-month postsurgery. Conclusion: This study described the effect of steroids on preoperative neurological function in patients with MESCC. Stabilization or improvement of preoperative neurological function occurred in 50% of the patients. [ABSTRACT FROM AUTHOR]

Background: Traumatic brain injury (TBI) is a kind of acquired brain injury, which is caused by external mechanical forces. Moreover, the neuroprotective role of sevoflurane (Sevo) has been identified in TBI. Therefore, this research was conducted to figure out the mechanism of Sevo in TBI via FGF2.Methods: The key factors of neuroprotective effects of Sevo in TBI rats were predicted by bioinformatics analysis. A TBI model was induced on rats that then inhaled Sevo for 1 h and grouped via lentivirus injection. Modified Neurological Severity Score was adopted to evaluate neuronal damage in rats, followed by motor function and brain water content measurement. FGF2, EZH2, and HES1 expression in brain tissues was evaluated by immunofluorescence staining, and expression of related genes and autophagy factors by RT-qPCR and Western blot analysis. Methylation-specific PCR was performed to assess HES1 promoter methylation level, and ChIP assay to detect the enrichment of EZH2 in the HES1 promoter. Neuronal damage was assessed by cell immunofluorescence staining, and neuronal apoptosis by Nissl staining, TUNEL staining, and flow cytometry.Results: Sevo diminished brain edema, improved neurological scores, and decreased neuronal apoptosis and autophagy in TBI rats. Sevo preconditioning could upregulate FGF2 that elevated EZH2 expression, and EZH2 bound to the HES1 promoter to downregulate HES1 in TBI rats. Also, FGF2 or EZH2 overexpression or HES silencing decreased brain edema, neurological deficits, and neuronal autophagy and apoptosis in Sevo-treated TBI rats.Conclusions: Our results provided a novel insight to the neuroprotective mechanism of Sevo in TBI rats by downregulating HES1 via FGF2/EZH2 axis activation. [ABSTRACT FROM AUTHOR]

Previous research has indicated a prevalent co-occurrence of chronic lower back pain (CLBP) and Posttraumatic Stress Disorder (PTSD). Though the dual diagnosis of these disorders is prevalent, a cyclical nature of symptomology also exists. With trauma symptoms igniting chronic pain symptoms and bouts of pain engaging trauma symptoms, there continues to be a lack of understanding as to the neurological underpinnings of this phenomena. Further, there has been little exploration into the treatment of said co-occurring disorders. An investigation by Lankster and Williams (2018) recommended the use of Acceptance and Commitment Therapy for individuals triply diagnosed with PTSD, CLBP, and alexithymia. However, the previous study excluded the neurological effects of these disorders, as well as their behavioral and physiological manifestations, which are considered in the current study to develop an intervention with increased efficacy. The purpose of this systematic review was to investigate the neurological effects of these conditions, the manner in which they overlapped, and the cognitive and behavioral manifestation of dual neurological deficits. A structured psychological treatment, which includes various aspects of neurological, cognitive, behavioral, and somatic interventions with concurrent pharmacological treatment, is developed to holistically address deficits based on combined neurological effects. [ABSTRACT FROM AUTHOR]