Neurological Performance Research Articles

Activation of Nurr1 with Amodiaquine Protected Neuron and Alleviated Neuroinflammation after Subarachnoid Hemorrhage in Rats

Background. Nurr1, a member of the nuclear receptor 4A family (NR4A), played a role in neuron protection, anti‐inflammation, and antioxidative stress in multidiseases. We explored the role of Nurr1 on subarachnoid hemorrhage (SAH) progression and investigated the feasibility of its agonist (amodiaquine, AQ) as a treatment for SAH. Methods. SAH rat models were constructed by the endovascular perforation technique. AQ was administered intraperitoneally at 2 hours after SAH induction. SAH grade, mortality, weight loss, neurological performance tests, brain water content, western blot, immunofluorescence, Nissl staining, and qPCR were assessed post‐SAH. In vitro, hemin was introduced into HT22 cells to develop a model of SAH. Results. Stimulation of Nurr1 with AQ improved the outcomes and attenuated brain edema. Nurr1 was mainly expressed in neuron, and administration of AQ alleviated neuron injury in vivo and enhanced the neuron viability and inhibited neuron apoptosis and necrosis in vitro. Besides, AQ reduced the amount of IL‐1β+Iba‐1+ cells and inhibited the mRNA level of proinflammatory cytokines (IL‐1β and TNF‐α) and the M1‐like phenotype markers (CD68 and CD86). AQ inhibited the expression of MMP9 in HT22 cells. Furthermore, AQ reduced the expression of nuclear NF‐κB and Nurr1 while increased cytoplasmic Nurr1 in vivo and in vitro. Conclusion. Pharmacological activation of Nurr1 with AQ alleviated the neuron injury and neuroinflammation. The mechanism of antineuroinflammation may be associated with the Nurr1/NF‐κB/MMP9 pathway in the neuron. The data supported that AQ might be a promising treatment strategy for SAH.

Activation of nucleotide-binding oligomerization domain-containing protein 1 by diaminopimelic acid contributes to cerebral ischemia-induced cognitive impairment

Cerebral ischemia-reperfusion (I/R)-induced brain tissue injury is a major obstacle for acute stroke management. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is reported to play a critical role in the regulation of myocardial or hepatic I/R injury. However, its role in cerebral I/R remains elusive. The mouse model of middle cerebral artery occlusion (MCAO) was applied in the study. The cerebral I/R mice were received either PBS or diaminopimelic acid (DAP)-pretreatment. All sham, MCAO, and MCAO + DAP mice were subject to the neurological behavior tests. The proinflammatory cytokines and autophagy-related proteins were determined by ELISA, RT-qPCR, and Western blot analysis, respectively. We found that NOD1 was substantially upregulated in the hippocampus of MCAO mice. DAP treatment significantly enhanced proinflammatory cytokine production and autophagy-related protein expression, leading to enlarged cerebral infarction size and poor neurological performance in MCAO + DAP mice compared to MCAO mice. We concluded that activation of NOD1 promotes cerebral I/R injury suggesting that NOD1 may serve as a promising target for alleviating the adverse effects of cerebral I/R.

Clinical and radiological outcome after minimally invasive surgical approach for type II unstable odontoid fractures

IntroductionAnterior odontoid screw fixation is a valid surgical option for unstable odontoid fractures, as type II Anderson D’Alonzo fractures. Grauer further divided type II fractures in subtypes according to the fracture line, providing recommendations for implementation of screw fixation techniques. ObjectivePrimary endpoint of our study is to evaluate the postoperative results of minimally invasive odontoid screw insertion in terms of outcome, fusion rate and stability of cranio-cervical junction. Secondary endpoint was to investigate the influence of age or fractures’ features on outcome and fusion rate. Materials and methodsWe report the clinical and radiological features of 32 patients harbouring unstable type II fractures operated by a minimally invasive odontoid screw insertion technique. All patients underwent a high resolution multiplanar CT in order to assess fracture features according to Grauer's classification; the integrity of ligaments was investigated by MRI. In addition, a preoperative neurological performance (modified Rankin Scale, mRS) was evaluated for patients either directly or interviewing their families. Follow-up at one, three and six months and 1 year have been performed (averaging 13.5 months) by cervical CT (fusion rate and stability) and mRS update. In order to investigate the influence of age on postoperative neurological performance, two groups (≤50 yrs, 9 pts/>50 yrs, 23 pts) were separately considered and analysed. Overall, we observed no surgery related complications. We also analysed the fusion rate and its correlation with patient age and Grauer's subtype of fracture. ResultsAt last available clinical follow-up, the preoperative performance was preserved (mRS 0/1: 24, 75%; mRS 2–4: 9, 15%) although with slight reduction of intact patients (mRS 0: 22 vs. 19; 71.8 vs. 59.3%). Younger patients (≤50 yrs) fared significantly better than older ones, achieving a good clinical outcome (mRS 0/1) in 100% vs. 69.5% (9/9 vs. 16/23 pts). Statistical analysis showed a fair correlation between age and outcome. Other factors such as sex and Grauer's type did not influence significantly the clinical outcome. Nine patients did not complete a full radiological follow-up and were therefore excluded from analysis of radiological outcome. Among the remaining 23 patients, only 25% of those who were followed three months or less showed fusion; conversely, all patients who have been examined from 6 to 48 months fused. Among the non-union patients, two underwent a second surgery by posterior approach. ConclusionsIn our recent experience, the minimally invasive AOSF proved safe and effective in treating odontoid peg fractures. Selection based on Grauer's type is mandatory to achieve best results. While in the elderly, an anterior approach is well accepted as the first choice treatment, we recommend that this option should be offered as a suitable alternative to Halo or orthosis also in younger patients since it provides prompt, excellent clinical outcome and high fusion rate especially in this age group.

Breviscapine Alleviates Cognitive Impairments Induced by Transient Cerebral Ischemia/Reperfusion through Its Anti-Inflammatory and Anti-Oxidant Properties in a Rat Model.

Cerebral ischemia/reperfusion (I/R)-induced injury is a common phenomenon of stroke, and the effective treatment for I/R-induced brain tissue damage is limited. Breviscapine has been widely used in China as herbal medicine to treat cardiovascular diseases for hundreds of years and has been demonstrated to possess potent cardiovascular pharmacological effects. This study aims to investigate the neuroprotective effect of breviscapine on cerebral I/R-induced injury. The rat model of middle cerebral artery occlusion (MCAO) was applied in our study. The cerebral I/R rats received multiple injections of breviscapine. All rats were subject to neurological behavior tests by open field test and Morris water maze test. The pro-inflammatory cytokines and oxidative stress marker levels were determined by ELISA and colorimetric analysis, respectively. We demonstrated that administration of breviscapine dose-dependently ameliorated cerebral I/R-induced injury and improved the neurological performance of cerebral I/R rats. Further studies illustrated that breviscapine treatment effectively attenuated inflammatory cytokine expression, reduced oxidative stress, and pro-apoptosis protein expression and inhibited the activation of NF-κB signaling and microglia in the I/R injury tissues. Breviscapine may serve as a single drug or a promising adjuvant that can be used in conjunction with other medicine for the treatment of cerebral I/R-induced injury.

Effects of Melatonin on Neurological Function and Maintenance of Physical and Motor Fitness in Collegiate Student-Athletes Following Sleep Deprivation

Background: Melatonin is one of the Supplements used to treat sleep problems such as insomnia and jet lag. Objectives: Since sleep deprivation may affect athletic performance, the aim of this study was to investigate the effect of melatonin on neurological function and maintenance of physical and motor fitness in collegiate student-athletes following sleep deprivation. Methods: Ten collegiate student-athletes participated in randomized, double‐blind crossover trial with placebo control. Subjects were divided into six experimental groups: without sleep deprivation (WSD), 4 hours sleep deprivation (4HSD) and 24 hours sleep deprivation (24HSD) with melatonin (MEL) or placebo (PLA). WSD were allowed to sleep eight hours per night. Six milligrams of melatonin was administered 30 min before the training protocols. Training protocols included the Wingate Anaerobic test, Good Balance test, Vienna reaction time with the Stroop test. Data were analyzed using repeated measures ANOVA. Significant difference was set at P ≤ 0.05. Results: Six mg/day of MEL 30 min before training had no significant effect on anaerobic power, balance and reaction time in collegiate student-athletes WSD (P > 0.05). Although, 4HSD and 24HSD negatively affected balance function, MEL reduced its negative effects. Furthermore, 24HSD decrease neurological and physical performance in collegiate student-athletes and MEL improved anaerobic power and reaction time in collegiate student-athletes (P < 0.05). Conclusions: Pre-training MEL supplementation would alleviate neurological, physical and motor performance impairment in collegiate student-athletes following sleep deprivation. MEL appears to be more effective in athletes with longer sleep deprivation.

Lasting metabolic effect of a high-fructose diet on global cerebral ischemia

ABSTRACT Introduction: Obesity is a public health problem that is associated with cerebrovascular diseases, such as ischemic stroke. The coexistence of obesity with cerebral ischemia has been suggested to be considerably detrimental to the neurological system. Objective: Hence, in this study, we evaluated the long-term effects of a 20% high fructose diet (HFD) and global cerebral ischemia on neurological, cognitive and emotional performance in three-month-old male Wistar rats. Results: Our results demonstrated that fructose intake led to increases in body weight and blood glucose, as well as reduced insulin sensitivity. The co-morbidity of fructose intake and cerebral ischemia resulted to hyperlipidemia, as well as increases in liver and adipocyte damage, which worsened neurological performance and resulted in alterations in learning and emotional skills at two weeks post-ischemia. No significant biochemical changes in autophagy and plasticity markers at the late stage of ischemia were observed. Conclusion: These results suggested that obesity causes a lasting effect on metabolic disorders that can contribute to increased neurological impairment after cerebral ischemia.

Changes in structural and functional connectivity during two years of fingolimod therapy for multiple sclerosis

BackgroundFingolimod, an oral drug, has been reported to reduce relapse rate in multiple sclerosis (MS). However disease progression may still occur in spite of control of inflammation. Functional imbalances within and between cerebral networks associated with disruption of structural and functional network integrity, have been reported in MS. An effective therapy is expected to stabilize such functional network integrity. ObjectiveThe purpose of this study was to investigate changes in structural and resting-state functional connectivity of motor and cognitive networks, and associated changes in neurologic scores in MS, during 2 years of fingolimod therapy. MethodsTwenty five subjects with MS were recruited for this study. Subjects were scanned with diffusion tensor imaging (DTI) and resting-state functional connectivity MRI (fcMRI) scan protocol at 3 T with 6-month interval over a period of 2 years. Neurologic performance scores of motor and cognitive performances were also obtained. ResultsDTI measures worsened during the 1st year and then stabilized; any trend of stabilization of fcMRI was delayed until the 2nd year. While motor performance did not change, cognitive performance showed improvement. Several baseline DTI measures correlated with relevant neurologic scores. ConclusionInitial worsening of motor and cognitive network was reported after 1 year of treatment, but seems DTI and fcMRI measures seem to stabilize after around one year fingolimod therapy.

A new transpedicular lag screw fixation for treatment of unstable Hangman\u2019s fracture: a minimum 2-year follow-up study

BackgroundA new C2 transpedicular lag screw designed by our team has been used in human cadaver spines for biomechanical testing, and the results showed that the biomechanical properties of the new C2 transpedicular lag screw were better than ordinary screws. The objective of this study is to analyze the clinical efficacy and safety of the new C2 transpedicular lag screw fixation for the treatment of unstable Hangman’s fracture.MethodsFrom March 2013 to June 2017, 25 patients who had unstable Hangman’s fractures were operated on with a new C2 transpedicular lag screw fixation. The patients included 18 males and 7 females whose ages ranged from 31 to 62 years (average 45.4 ± 9.3 years). The cause of the injury was a traffic accident in 17 patients and a fall from height in 8 patients. Other associated lesions included rupture of the spleen (1 patient) and rib fractures (2 patients). According to the Levine-Edwards classification, 17 patients were type II and 8 patients were type IIA, and according to the Frankel Neurological Performance scale, 8 cases and 17 cases were graded as spinal cord injury D and E, respectively. Twenty-three cases received bilateral screw fixation, and 2 cases had unilateral screw fixation because another pedicle was chipped. The whole procedure was accomplished with monitoring by “C”-arm fluoroscopy.ResultsThe mean follow-up time was 36 ± 12 months and ranged from 24 to 60 months. No obvious symptomatic or radiologic postoperative complications were found during the follow-up period. Six cases were restored from D to E while 2 cases remained D according to the American Spinal Injury Association (ASIA) grade. Pre- and postoperative visual analogue scale (VAS) and Neck Disability Index (NDI) were statistically different (P < 0.001). Osseous union was achieved in all cases, and the range of cervical motion recovered to the normal level up to the last follow-up.ConclusionsThe primary clinical and radiographic efficacies of a new C2 transpedicular lag screw fixation for the treatment of unstable Hangman’s fracture were satisfactory. This approach could be considered a simple, effective, reliable, and economic surgical method for managing unstable Hangman’s fractures.

Synaptic Plasticity After Focal Cerebral Ischemia Was Attenuated by Gap26 but Enhanced by GAP-134.

Objective: Synaptic plasticity is critical for neurorehabilitation after focal cerebral ischemia. Connexin 43 (Cx43), the main component of the gap junction, has been shown to be pivotal for synaptic plasticity. The objective of this study was to investigate the role of the Cx43 inhibitor (Gap26) and gap junction modifier (GAP-134) in neurorehabilitation and to study their contribution to synaptic plasticity after focal ischemia.Methods: Time course expression of both total and phosphorylated Cx43 (p-Cx43) were detected by western blotting at 3, 7, and 14 d after focal ischemia. Gap26 and GAP-134 were administered starting from 3 d post focal ischemia. Neurological performances were evaluated by balance beam walking test and Y-maze test at 1, 3, and 7 d. Golgi staining and transmission electron microscope (TEM) detection were conducted at 7 d for observing dendritic spine numbers and synaptic ultrastructure, respectively. Immunofluorescent staining was used at 7 d for detection of synaptic plasticity markers, including synaptophysin (SYN) and growth-associated protein-43 (GAP-43).Results: Expression levels of both total Cx43 and p-Cx43 were increased after focal cerebral ischemia, peaking at 7 d. Compared with the MCAO group, Gap26 worsened the neurological behavior and decreased the dendritic spine number while GAP-134 improved the neurobehavior and increased the number of dendritic spines. Moreover, Gap26 further destroyed the synaptic structure, concomitant with downregulated SYN and GAP-43, whereas GAP-134 alleviated synaptic destruction and upregulated SYN and GAP-43.Conclusion: These findings suggested that Cx43 or the gap junction was involved in synaptic plasticity, thereby promoting neural recovery after ischemic stroke. Treatments enhancing gap junctions may be potential promising therapeutic measures for neurorehabilitation after ischemic stroke.

Comparison of Dopamine and Norepinephrine Use for the Treatment of Hypotension in Out-Of-Hospital Cardiac Arrest Patients with Return of Spontaneous Circulation.

In patients experiencing out-of-hospital cardiac arrest (OHCA), hypotension is common after return of spontaneous circulation (ROSC). Both dopamine and norepinephrine are recommended as inotropic therapeutic agents. This study aimed to determine the impact of the use of these two medications on hypotension. This is a multicenter retrospective cohort study. OHCA patients with ROSC were divided into three groups according to the post resuscitation inotropic agent used for treatment in the emergency department, namely, dopamine, norepinephrine, and dopamine and norepinephrine combined therapy. Thirty-day survival and favorable neurologic performance were analyzed among the three study groups. The 30-day survival and favorable neurologic performance rates in the three study groups were 12.5%, 13.0%, and 6.8% as well as 4.9%, 4.3%, and 1.2%, respectively. On controlling the potential confounding factors by logistic regression, there was no difference between dopamine and norepinephrine treatment in survival and neurologic performance (adjusted odds ratio (aOR): 1.0, 95% confidence interval (CI) 0.48-2.06; aOR: 0.8, 95% CI: 0.28-2.53). The dopamine and norepinephrine combined treatment group had worse outcome (aOR: 0.6, 95% CI: 0.35-1.18; aOR: 0.2, 95% CI: 0.05-0.89). In conclusion, there was no significant difference in post-ROSC hypotension treatment between dopamine and norepinephrine in 30-day survival and favorable neurologic performance rates.

Neurological outcome after resection of spinal schwannoma

IntroductionSpinal schwannoma (SS) is the most frequently diagnosed benign spinal tumor, constituting approximately 25 % of all intradural tumors. Aim of our study was to identify factors that potentially affect immediate postoperative neurological outcome, and the rate of functional recovery within 12 months. MethodsScreening of our institutional database yielded 90 consecutive patients (mean age 57.1 years, 39 women [43.3 %]) with newly diagnosed SS between March 1997 and October 2018. We pre- and postoperatively reviewed patient charts, surgical reports, radiographic data, use of IOM, duration of symptoms, histopathology, co-morbidities, radiographic extension, surgical strategy, neurological performance (Japanese Orthopedic Association Score [JOA score] and Frankel Grade Classification). ResultsMean duration of preoperative symptoms was 3.6 ± 1.6 months. Most common symptoms were local pain (n = 77, 85.6 %). Macroscopic complete resection was achieved in 84 patients (93.3 %). During follow-up, complete recovery from local pain was documented for 41 patients (59.7 %), from radiating pain for 41 (69.5 %; p < 0.001).Postoperatively, 25 (27.7 %) patients developed a new neurological deficit (motor deficits n = 3 and sensory deficits n = 23; one patient developed both); after 12 months, however, motor deficits had abated in all patients, and 16 (69.5 %) patients had completely recovered from sensory deficits.Use of intraoperative monitoring (IOM) was a significant predictor for good functional outcome (p < 0.001). ConclusionResection of SS accompanied by IOM whenever feasible should be advocated. We achieved a high number of complete resections with a low rate of morbidity. New postoperative motor or sensory deficits had a very high rate of complete recovery within 12 months.

Urinary polycyclic aromatic hydrocarbon metabolites, peripheral blood mitochondrial DNA copy number, and neurobehavioral function in coke oven workers

BackgroundPolycyclic aromatic hydrocarbons (PAHs) are the risk factors for workers’ neurological performance, which were widely exist in the occupational environment. ObjectiveWe aimed to investigate the dose-response relationship between various PAH metabolites and workers’ neurobehavioral changes and to explore whether mitochondrial DNA copy number (mtDNAcn) can be used as a potential biomarker to reflect changes in neurobehavioral behavior. MethodA total of 697 workers were recruited from a coke oven plant. The concentrations of eleven PAHs metabolites were determined by HPLC-MS/MS. Peripheral blood mtDNAcn was measured using QPCR. Neurobehavioral function was measured by NCTB questionnaire. The dose-response relationships were evaluated using restricted cubic spline models. Mediation analysis was also carried out. ResultsWe found dose-response relationships between urinary 2-hydroxynaphthalene (2-OH Nap), sum of PAH metabolites (Ʃ –OH PAHs) and total digit span (DSP), backward digit span (DSPB), forward digit span (DSPF) and mtDNAcn. Each one-unit increase in ln-transformed of 2-OH Nap or Ʃ –OH PAHs was associated with a 2.64 or 3.22 decrease in DSP, a 1.20 or 1.58 decrease in DSPF, a 1.44 or 1.62 decrease in DSPB and a 0.13 or 0.12 decrease in mtDNAcn. However, we did not find a significant mediation effect of mtDNAcn between PAHs metabolites and DSP, DSPF, or DSPB. ConclusionOur data indicated that workers urinary 2-hydroxynaphthalene and sum of PAH metabolites levels were inversely associated with mtDNAcn and neurobehavior, especially their auditory memory. However, there was no significant mediation effect of mtDNAcn between urinary PAHs metabolites and neurobehavior.

Melatonin Alleviates Neuronal Damage After Intracerebral Hemorrhage in Hyperglycemic Rats.

BackgroundThis study sought to investigate a novel effect of melatonin in reducing brain injury in an in vivo hyperglycemic intracerebral hemorrhage (ICH) model and further explore the mechanisms of protection.MethodsHyperglycemia ICH was induced in Sprague-Dawley rats by streptozocin injection followed by autologous blood injection into the striatum. A combined approach including RNA-specific depletion, electron microscopy, magnetic resonance, Western blots, and immunohistological staining was applied to quantify the brain injuries after ICH.ResultsHyperglycemia resulted in enlarged hematoma volume, deteriorated brain edema, and aggravated neuronal mitochondria damage 3 days after ICH. Post-treatment with melatonin 2 hours after ICH dose-dependently improved neurological behavioral performance lasting out to 14 days after ICH. This improved neurological function was associated with enhanced structural and functional integrity of mitochondria. Mechanistic studies revealed that melatonin alleviated mitochondria damage in neurons via activating the PPARδ/PGC-1α pathway. Promisingly, melatonin treatment delayed until 6 hours after ICH still reduced brain edema and improved neurological functions. Melatonin supplementation reduces neuronal damage after hyperglycemic ICH by alleviating mitochondria damage in a PPARδ/PGC-1α-dependent manner.ConclusionMelatonin may represent a therapeutic strategy with a wide therapeutic window to reduce brain damage and improve long-term recovery after ICH.

Analysis of Delirium From the Dynamic Symptoms Model

Delirium is a manifestation of brain injury or acute and generalized dysfunction of the upper cerebral cortical processes. In this way, it is important to analyze delirium more broadly as a symptom to understand and intervene taking into account that it is manifesting the presence of brain lesions whose consequences are deleterious to the neurological performance of patients. This article is intended to present a comprehensive approach of delirium analyzed from a symptom perspective and from theoretical and conceptual structure, such as the Dynamic Symptoms Model, specific to the nursing practice. A literature review related to delirium and components of Dynamic Symptoms Model was carried out. We searched the MEDLINE, ScienceDirect, SciELO, and Scopus databases using the terms Delirium, Intensive Care Units, Nursing, and Risk Factor. The existing literature provides evidence of the antecedents, experience, interventions, interactions, and consequences of delirium, which are components of the Model. Thus, the analysis from the Dynamic Symptoms Model perspective bears relevance and contributes to the understanding and approach of delirium.

The Influence of Career Choice on Neurological Academic Performance Among Critical Care Students In Abuja, Nigeria

In Nigeria, Critical care is yet to subspecialize; the neurology curriculum is a core subject. The evidence of career choice motivation and neurological academic performance has not been well elucidated, as such, demonstrating a valid premise that critical care students choice resulted in better academic performance will be very useful. The value can be seen in improved students' guidance, better curriculum development and improved healthcare setting goals. This study was set up to ascertain the relationship between career choice motivators and learning outcomes among critical care nursing students with emphasis on neurological curriculum. A cross sectional quantitative descriptive study and analysis techniques were explored using three academic sessions of critical care nursing students of the School of Post Basic Critical Care Nursing of University of Abuja, Nigeria. Responses to the question “why did you choose critical care nursing” were collated and then themes developed. Their score in neurology was used to assess academic performance. Statistical analysis conducted using IBM-SPSS version 23. Ninety students responded with males constituting 24 (26.7) and females, 66 (73.3). There was statistical difference between 'passion for critically ill', 'having no reason' and academic performance, (χ2=8.707, p=0.003), and (χ2=13.306, p &lt;0.001) respectively. Passion was found to be responsible for career choice and motivating influence on neurocritical academic performance.

Intranasal Insulin Treatment Attenuates Metabolic Distress and Early Brain Injury After Subarachnoid Hemorrhage in Mice

Intranasal administration of insulin to the brain bypasses the blood brain barrier (BBB) and can increase cerebral glucose uptake and prevent energy failure. Intranasal insulin treatment has shown neuroprotective effects in multiple central nervous system (CNS) lesions, but the effects of intranasal insulin on the metabolic and pathological process of subarachnoid hemorrhage (SAH) are not clear. This study is designed to explore the effects of intranasal insulin treatment on metabolic distress and early brain injury (EBI) after experimental SAH. SAH model was built by endovascular filament perforation method in adult male C57BL/6J mice, and then, insulin was administrated via intranasal route at 0, 24, and 48h post-SAH. EBI was assessed according to the neurological performance, BBB damage, brain edema, neuroinflammatory reaction, and neuronal apoptosis at each time point. To evaluate metabolic conditions, microdialysis was used to continuously monitor the real-time levels of glucose, pyruvate, and lactate in interstitial fluid (ISF) in living animals. The mRNA and protein expression of glucose transporter-1 and 3 (GLUT-1 and -3) were also tested by RT-PCR and Western blot in brain after SAH. Compared to vehicle, intranasal insulin treatment promoted the relative mRNA and protein levels of GLUT-1 in SAH brain (0.98 ± 0.020 vs 0.33 ± 0.016 at 24h, 0.91 ± 0.25 vs 0.21 ± 0.013 at 48h and 0.94 ± 0.025 vs 0.28 ± 0.015 at 72h in mRNA/0.96 ± 0.023 vs 0.36 ± 0.015 at 24h, 0.91 ± 0.022 vs 0.22 ± 0.011 at 48h and 0.95 ± 0.024 vs 0.27 ± 0.014 at 72h in protein, n = 8/Group, p < 0.001). Similar results were also observed in GLUT-3. Intranasal insulin reduced the lactate/pyruvate ratio (LPR) and increased ISF glucose level. It also improved neurological dysfunction, BBB damage, and brain edema and attenuated the levels of pro-inflammatory cytokines as well as neuronal apoptosis after SAH. The intranasal insulin treatment protects brain from EBI possibly via improving metabolic distress after SAH.

Opium consumption exerts protective effect against cerebral ischemia through reducing inflammation and enhancing antioxidant defense in male rats

ObjectiveBrain ischemia is an arterial vascular disorder, the second cause of death in the world. In this study, the effect of oral consumption of opium on the inflammation status, oxidative stress, infarction volume and neurological function after stroke in male rats were investigated. Materials and methodsA total of 48 male Wistar rats were randomly assigned into three groups: 1- Sham group: these rats underwent sham surgery. 2- Stroke group: rats of this group underwent 2 h transient focal cerebral ischemia. 3- Opium group: opium administration began eight days before the ischemia, and then rats were underwent 2 h of transient focal cerebral ischemia. After that, the rats were evaluated for neurological impairment 24 h after stroke. The cerebral edema and infarct volume were evaluated by Image j software, and the concentration of total antioxidant capacity (TAC), Malondialdehyde (MDA), TNF-α, and C-reactive protein (CRP) of the brain tissue were measured as an indicator of inflammation and oxidative stress. ResultsTAC concentration in the opium group was significantly higher than of stroke group. Also, the TNF-α, CRP and MDA concentrations in the opium group were significantly lower than stroke group. The degree of cerebral edema and infarct volume in the opium group was significantly lower than stroke group. Moreover, the opium group had better neurological performance than the stroke group. ConclusionBased on the results of this study, the use of opium by enhancing the antioxidant capacity and decreasing inflammation after cerebral ischemia can reduce the extent of damage.

Functional outcome after surgical treatment of spinal meningioma

ObjectiveSpace-occupying spinal meningiomas (SM), commonly diagnosed due to gradual neurological deterioration, are treated surgically by decompression and tumor resection. In this series of patients with surgically treated SM, we determined individual predictors of functional outcome in the context of intraoperative neuromonitoring (IOM). MethodsThis retrospective study included 45 patients (39 women, 6 men; mean age 63 years). We reviewed pre- and postoperative charts, surgical reports, radiographic data for demographics, use of IOM, duration of symptoms, histopathology, co-morbidities, radiographic extension, surgical strategy, neurological performance (Japanese Orthopedic Association Score [JOA score]. Median follow-up was 34 months (12–190 months). ResultsMost frequent surgical approaches were laminectomy (71.1%, n = 32) and hemi-laminectomy (28.9%, n = 13). Predominant SM site was the thoracic spine (55.6%, n = 25). Most common symptoms were sensory deficits (77.8%, n = 35), gait disorders (55.6%, n = 25), motor deficits (42.2%, n = 19), and radiating pain (37.8%, n = 17). Simpson grade 1 resection was achieved in 6 patients, most common type of resection was Simpson grade 2 in 36 patients. During follow-up, 80.0% of patients had fully recovered sensory deficits (p < 0.001), 76.0% of patients with preoperative gait disorders had been asymptomatic (p < 0.001), and motor deficits in 12/19 (63.1%). Pain had decreased significantly from admission to follow-up (p = 0.001). IOM was used in 20 (44.4%) patients. Postoperatively, 6(13.3%) patients had developed a new neurological deficit, 4 of them operated without IOM. ConclusionResection of SM with IOM showed good recovery, excellent functional results with low surgical morbidity.

Resveratrol reduces cerebral edema through inhibition of de novo SUR1 expression induced after focal ischemia

Cerebral edema is a clinical problem that frequently follows ischemic infarcts. Sulfonylurea receptor 1 (SUR1) is an inducible protein that can form a heteromultimeric complex with aquaporin 4 (AQP4) that mediate the ion/water transport involved in brain tissue swelling. Transcription of the Abcc8 gene coding for SUR1 depends on the activity of transcriptional factor SP1, which is modulated by the cellular redox environment. Since oxidative stress is implicated in the induced neuronal damage in ischemia and edema formation, the present study aimed to evaluate if the antioxidant resveratrol (RSV) prevents the damage by reducing the de novo expression of SUR1 in the ischemic brain. Male Wistar rats were subjected to 2 h of middle cerebral artery occlusion followed by different times of reperfusion. RSV (1.9 mg/kg; i.v.) was administered at the onset of reperfusion. Brain damage and edema formation were recognized by neurological evaluation, time of survival, TTC (2,3,5-Triphenyltetrazolium chloride) staining, Evans blue extravasation, and water content. RSV mechanism of action was studied by SP1 binding activity measured through the Electrophoretic Mobility Shift Assay, and Abcc8 and Aqp4 gene expression evaluated by qPCR, immunofluorescence, and Western blot. We found that RSV reduced the infarct area and cerebral edema, prevented blood-brain barrier damage, improved neurological performance, and increased survival. Additionally, our findings suggest that the antioxidant activity of RSV targeted SP transcription factors and inhibited SUR1 and AQP4 expression. Thus, RSV by decreasing SUR1 expression could contribute to reducing edema formation, constituting a therapeutic alternative for edema reduction in stroke.

The Sequential Organ Failure Assessment (SOFA) score predicts mortality and neurological outcome in patients with post-cardiac arrest syndrome

BackgroundPatients experiencing out-of-hospital cardiac arrest (OHCA) and subsequent post-cardiac arrest syndrome are often compromised by multi-organ failure. The Sequential Organ Failure Assessment (SOFA) score has been used to predict clinical outcome of patients requiring intensive care for multi-organ failure. Thus, the assessment of SOFA score is recommended as a criterion for sepsis. Although post-cardiac arrest patients frequently develop sepsis-like status in ICU, there are limited reports evaluating the SOFA score in post-cardiac arrest patients. We investigated the predictive value of the SOFA score in survival and neurological outcomes in patients with post-cardiac arrest syndrome. MethodsA total of 231 cardiovascular arrest patients achieving return of spontaneous circulation (ROSC) were finally extracted from the institutional consecutive database comprised of 1218 OHCA patients transferred to the institution between January 2015 and July 2018. The SOFA score was calculated on admission and after 48h. Predictors of survival and neurological outcome defined as having cerebral-performance-category (CPC) 1 or 2 at 30 days were determined. ResultsSOFA score was lower in survived patients (5.0 vs 10.0, p<0.001) and those with favorable neurological outcome (5.0 vs 8.0, p<0.001) as compared with the counterparts. The SOFA score on admission was an independent predictor of survival (OR 0.68, 95% confidence interval [CI] 0.59–0.78; p<0.001) and favorable neurological performance (OR 0.79; 95% CI 0.69–0.90; p<0.001) at 30 days. Furthermore, a change in SOFA score (48–0h) was predictive of favorable 30-day neurological outcome (OR 0.71, 95% CI 0.60–0.85; p<0.001). ConclusionsEvaluation of the SOFA score in the ICU is useful to predict survival and neurological outcome in post-cardiac arrest patients.