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Les unités pour malades difficiles (UMD) sont des institutions psychiatriques françaises prenant en charge des patients « présentant pour autrui un danger tel qu'ils nécessitent des protocoles thérapeutiques intensifs adaptés et des mesures de sûreté particulières ». Dans ces unités, la prévalence des intrications neuropsychiatriques apparaît élevée. Pour évaluer, voire valider cette impression, il a été réalisé une revue systématique des dossiers des patients de l'UMD de Plouguernével le 1er mars 2024, au nombre de 34. Il est montré que : la moitié des patients souffrent de psychose sévère, un tiers de ces patients présentent un déficit intellectuel. Dix patients comptent dans leurs antécédents des atteintes neurologiques acquises, plus ou moins graves. De plus, 75 % d'entre eux sont polytoxicomanes. Les causes des atteintes neurologiques de ces patients sont multiples : congénitales, périnatales, traumatiques, toxiques, dues à de graves maltraitances... Ces causes sont ici analysées. Cette analyse permet de réfléchir à des actions de prévention à mettre en place, ainsi qu'à une possible réorganisation des prises en charge de ces patients aux profils si hétéroclites. Psychiatric high security care units are French psychiatric institutions caring for patients "presenting such a danger to others that they require adapted intensive therapeutic protocols and special safety measures". In these units the prevalence of neuropsychiatric complications appears high. To evaluate or even validate this impression, a systematic review of the 34 patients of the unit of Plouguernével was carried out on March 1, 2024. It is shown: that half of the patients suffer from severe psychosis, that a third of these patients have an intellectual deficit. Ten patients have acquired neurological symptoms in their history, more or less serious. In addition, 75 % of them are polydrug addicts. The causes of the neurological damages in these patients are multiple: congenital, perinatal, traumatic, toxic, due to serious abuse, etc. These causes are analyzed here. This analysis allows us to consider preventive actions to be implemented, as well as a possible reorganization of the care of these patients with such heterogeneous profiles. [ABSTRACT FROM AUTHOR]

Hemoglobinopathies are commonly occurring genetic disorders worldwide. The aim of this study is to determine the biochemical predictors of cerebrovascular complications in pediatric patients with sickle cell anemia. We investigated the relationship between levels of neurological damage markers, such as Serum S100 calcium-binding protein B (S100B), Glial Fibrillary Acidic Protein (GFAP), and Neuron-Specific Enolase (NSE), and radiological findings in these patients. A total of 72 SCD patients and 30 healthy children were included in the study. Clinical and laboratory findings were recorded. Time-averaged maximum mean velocity (TAMMV) values were obtained from transcranial Doppler ultrasonography imaging (TCDI) of the middle cerebral artery. Serum levels of S100B, GFAP, and NSE were measured using the ELISA method both in the SCD group and the control group. Among the patients, 51 had sickle cell anemia (HbSS), 21 had HbSβ0 thalassemia, with 32 (44.4%) being female and 40 (55.6%) male. Their mean age was 12.68 ± 4.56 (ranging from 3 to 24) years old. S100B, GFAP, and NSE serum levels were significantly higher in the SCD group compared to the control group. It was observed that serum levels of S100B, NSE, and GFAP were higher in the group with TAMMV ≥ 170 cm/s. As known, in patients with SCD, the disruption of the blood-brain barrier begins with the occurrence of vaso-occlusive events. Hence, the risk of cerebrovascular events increases. Our study's indication that serum levels of S100B, GFAP, and NSE could be used in predicting or detecting cerebrovascular events in the early stages is noteworthy. [ABSTRACT FROM AUTHOR]

Over the past two decades, the use of tumor necrosis factor alpha (TNF-α) inhibitors has significantly improved the treatment of patients with immune-mediated inflammatory diseases. Firstly, introduced for rheumatoid arthritis, these inhibitors are currently approved and used for a variety of conditions, including ankylosing spondylitis, Crohn's disease, juvenile idiopathic arthritis, psoriasis, psoriatic arthritis, ulcerative colitis, and chronic uveitis. Despite their immense therapeutic efficacy, TNF-α inhibitors have been associated with neurological adverse effects that bring new clinical challenges. The present review collects data from multiple studies to evaluate the incidence and the relationship between TNF-α inhibitors and neurological side effects and to explore the potential underlying mechanisms of this association. Moreover, it highlights the importance of patient selection, particularly in the case of individuals with a history of demyelinating diseases, raises awareness for clinicians, and calls for ongoing research that will improve TNF-α targeting strategies and offer safer and more effective therapeutic options. [ABSTRACT FROM AUTHOR]

Resumen: Objetivo: Descripción y análisis de la relación entre las fracturas de húmero proximal y la lesión traumática del nervio axilar circunflejo. Material y método: Estudio prospectivo, observacional, de una serie de casos consecutivos de fracturas de extremo proximal de húmero. Se realizó valoración radiográfica, clasificando las fracturas según el sistema AO (Arbeitsgemeinshaft für Osteosynsthesefragen, Asociación de Grupo de Trabajo para el Estudio de la Fijación Interna de las Fracturas), y electromiografía (EMG) para la evaluación de la lesión del nervio axilar. Resultados: De 105 casos consecutivos de fracturas de húmero proximal, 31 pacientes cumplían los criterios de inclusión. Muestra: 86% mujeres y 14% hombres con edad media de 71,8 años (30-96 años). De los pacientes incluidos en el estudio, 58% presentó una EMG normal o leve axonotmesis, 23% presentó neuropatía del nervio axilar sin denervación muscular y 19%, lesión con denervación del nervio axilar. Los pacientes que sufrieron fracturas complejas de húmero proximal (AO11B y AO11C) tuvieron más riesgo de presentar lesiones tipo neuropatía axilar con denervación muscular en la EMG, siendo esta relación estadísticamente significativa (p < 0,001). Conclusiones: Los pacientes que sufren fracturas complejas de húmero proximal (AO11B y AO11C) tienen más riesgo de presentar lesiones tipo neuropatía axilar con denervación muscular en la EMG (p < 0,001). Abstract: Objective: Description and analysis of the relation between the proximal humerus fracture patterns and the traumatic injury of the axillary nerve. Material and method: Prospective, observational study of a consecutive case series that analyzed proximal humerus fractures. Radiographic evaluation was performed, and AO (Arbeitsgemeinshaft für Osteosynsthesefragen) system was used to classify the fractures. Electromyography was used to diagnose the axillary nerve injury. Results: Thirty-one patients on 105 who had a proximal humerus fracture met inclusion criteria. Eighty-six percent of the patients included were women and 14% men. The mean age was 71.8 years (30–96 years). Of the patients included in the study, 58% had normal or mild axonotmesis EMG, 23% had axillary nerve neuropathy without muscle denervation and 19% had injury with axillary nerve denervation. Patients who suffered complex fractures of the proximal humerus (AO11B and AO11C) had a higher risk of presenting axillary neuropathy type lesions with muscle denervation in the EMG, this relationship being statistically significant (p

Ischemic stroke is a common neurological disease. Currently, there are no Food and Drug Administration-approved drugs that can maximize the improvement in ischemic stroke-induced nerve damage. Hence, treating ischemic stroke remains a clinical challenge. Ferroptosis has been increasingly studied in recent years, and it is closely related to the pathophysiological process of ischemic stroke. Iron overload, reactive oxygen species accumulation, lipid peroxidation, and glutamate accumulation associated with ferroptosis are all present in ischemic stroke. This article focuses on describing the relationship between ferroptosis and ischemic stroke and summarizes the relevant substances that ameliorate ischemic stroke-induced neurological damage by inhibiting ferroptosis. Finally, the problems in the treatment of ischemic stroke targeting ferroptosis are discussed, hoping to provide a new direction for its treatment. [ABSTRACT FROM AUTHOR]

Background Objectives Materials and methods Results Discussion: Conclusion: Since the outbreak of coronavirus disease 2019, it has had a serious impact on people's physical and mental health. However, in our clinical work, we have found that the erectile function of coronavirus disease 2019 patients with neurological decline was often seriously affected.To further explore the relationship between erectile dysfunction and neurological dysfunction caused by coronavirus disease 2019.We conducted a survey from August 2022 to February 2023 at the First Affiliated Hospital of Anhui Medical University and the Third People's Hospital of Linyi City. A total of 251 subjects with a history of coronavirus disease 2019 infection were included. Symptoms and changes in erectile function after the coronavirus disease 2019 infection were collected and assessed using the International Index of Erectile Function‐5 scale and several targeted questions.In this study, we found that in patients infected with novel coronavirus, the proportion of erectile dysfunction was higher in those with neurological manifestations such as olfactory and taste impairment or psychological symptoms such as anxiety.We found that neurological decline and psychological factors were independent and significant risk factors for erectile dysfunction caused by coronavirus disease 2019.Patients with neurological damage or psychiatric symptoms are more likely to have erectile dysfunction, suggesting that the 2019 novel coronavirus may affect erectile function by damaging nerves. This provides a new insight into the mechanism of erectile dysfunction [ABSTRACT FROM AUTHOR]

ObjectiveTo analyze the clinical characteristics, treatment, and prognosis of children infected with SARS-CoV-2 following the adjustment of COVID-19 prevention and control policies in China in December 2022.MethodsA retrospective study was conducted on 9 cases of severe neurological dysfunction caused by SARS-CoV-2 infection in children admitted to Foshan First People's Hospital from December 17 to 31, 2022.ResultsAmong the 9 cases, 7 (71.43%) were under 3 years old, and 2 (22.2%) were over 3 years old with underlying diseases. All patients presented with fever and neurological symptoms such as consciousness disturbance and/or convulsions, and their conditions deteriorated rapidly within 24 h after the onset of fever, without respiratory symptoms. Levels of IL-6, LDH, and d-dimer were significantly elevated. Five cases died within 48 h of admission, one case died after 7 days of treatment due to secondary bacterial infection, and three cases survived for more than 48 h after the initial rescue. All patients developed rapid shock, and five cases experienced multi-organ failure within a short period. In terms of treatment, glucocorticoids were used in 5 cases, intravenous immunoglobulin (IVIG) in 3 cases, and blood purification and tocilizumab in 2 cases.ConclusionSARS-CoV-2 infection in children can lead to severe neurological damage. High fever, convulsions, and inflammatory factors serve as early warning indicators. Glucocorticoids, immunoglobulins, blood purification, and tocilizumab may have some therapeutic effects, but further research is needed to confirm the efficacy.

Abstract Alzheimer's disease (AD) is a progressively debilitating neurodegenerative condition primarily affecting the elderly. Emerging research suggests that microRNAs (miRNAs) play a role in the development of AD. This study investigates the impact of miR‐107‐5p on neurological damage, oxidative stress, and immune responses in AD. We utilized APP/PS1 mice as AD mouse models and C57BL/6 J mice as controls. AD mice received treatment with agomir miR‐107‐5p (to overexpress miR‐107‐5p) or BAY11‐7082 (an NF‐κB pathway inhibitor). We evaluated learning and memory abilities through the Morris water maze test. Histopathological changes, hippocampal neuron distribution, and apoptosis were assessed using hematoxylin–eosin, Nissl, and TUNEL staining. Reactive oxygen species (ROS) levels, amyloid‐Aβ (Aβ1‐40/42) contents, and inflammatory factors (TNF‐α, IL‐6, IL‐1β) in hippocampal tissues were measured using ROS kits and enzyme‐linked immunosorbent assay (ELISA). Microglial activation in hippocampal tissues was observed under a fluorescence microscope. miR‐107‐5p's binding to TLR4 was predicted via the TargetScan database and confirmed through a dual‐luciferase assay. miR‐107‐5p expression, along with TLR4, APOE, and TREM2 in hippocampal tissue homogenate, and NF‐κB p65 protein expression in the nucleus and cytoplasm were assessed via RT‐qPCR and Western blot. Overexpression of miR‐107‐5p ameliorated hippocampal neurological damage, oxidative stress, and immune responses. This was evidenced by improved enhanced learning/memory abilities, reduced Aβ1‐40 and Aβ1‐42 levels, diminished neuronal injuries, decreased ROS and TNF‐α, IL‐6, and IL‐1β levels, increased APOE and TREM2 levels, and suppressed microglial activation. miR‐107‐5p directly targeted and inhibited TLR4 expression, leading to reduced nuclear translocation of NF‐κB p65 in the NF‐κB pathway. Inhibition of the NF‐κB pathway similarly improved neurological damage, oxidative stress, and immune response in AD mice. miR‐107‐5p exerts its beneficial effects by suppressing the TLR4/NF‐κB pathway, ultimately ameliorating neurological damage, oxidative stress, and immune responses in AD mice.

This article examines the impact of early treatment on the extent of neurological damage in stroke patients. The study found that the initial treatment administered at home by family members did not have a direct correlation with the neurological damage experienced by stroke patients. However, the initial treatment did affect the stiffness reported by the respondents. The article emphasizes the importance of prompt and accurate treatment for stroke patients, as delayed treatment can have fatal consequences. The research design used in the study was quantitative, employing a cross-sectional approach, and data was collected through questionnaires. The article provides details about the characteristics of the patients and their family members, as well as the types of stroke observed in the study. It discusses the prevalence of non-hemorrhagic stroke, which accounts for 83% of all strokes. The article includes tables that illustrate the management of stroke patients at home and the timing of medical treatment. These tables also present information on the signs of neurological damage experienced by stroke patients, such as numbness, visual disturbances, confusion, dizziness, and balance disorders. The article concludes that early treatment of stroke is only associated with stiffness and does not have a significant impact on other neurological damage. It also discusses risk factors for stroke and provides recommendations for stroke prevention. [Extracted from the article]

Alzheimer's disease (AD) is a progressively debilitating neurodegenerative condition primarily affecting the elderly. Emerging research suggests that microRNAs (miRNAs) play a role in the development of AD. This study investigates the impact of miR‐107‐5p on neurological damage, oxidative stress, and immune responses in AD. We utilized APP/PS1 mice as AD mouse models and C57BL/6 J mice as controls. AD mice received treatment with agomir miR‐107‐5p (to overexpress miR‐107‐5p) or BAY11‐7082 (an NF‐κB pathway inhibitor). We evaluated learning and memory abilities through the Morris water maze test. Histopathological changes, hippocampal neuron distribution, and apoptosis were assessed using hematoxylin–eosin, Nissl, and TUNEL staining. Reactive oxygen species (ROS) levels, amyloid‐Aβ (Aβ1‐40/42) contents, and inflammatory factors (TNF‐α, IL‐6, IL‐1β) in hippocampal tissues were measured using ROS kits and enzyme‐linked immunosorbent assay (ELISA). Microglial activation in hippocampal tissues was observed under a fluorescence microscope. miR‐107‐5p's binding to TLR4 was predicted via the TargetScan database and confirmed through a dual‐luciferase assay. miR‐107‐5p expression, along with TLR4, APOE, and TREM2 in hippocampal tissue homogenate, and NF‐κB p65 protein expression in the nucleus and cytoplasm were assessed via RT‐qPCR and Western blot. Overexpression of miR‐107‐5p ameliorated hippocampal neurological damage, oxidative stress, and immune responses. This was evidenced by improved enhanced learning/memory abilities, reduced Aβ1‐40 and Aβ1‐42 levels, diminished neuronal injuries, decreased ROS and TNF‐α, IL‐6, and IL‐1β levels, increased APOE and TREM2 levels, and suppressed microglial activation. miR‐107‐5p directly targeted and inhibited TLR4 expression, leading to reduced nuclear translocation of NF‐κB p65 in the NF‐κB pathway. Inhibition of the NF‐κB pathway similarly improved neurological damage, oxidative stress, and immune response in AD mice. miR‐107‐5p exerts its beneficial effects by suppressing the TLR4/NF‐κB pathway, ultimately ameliorating neurological damage, oxidative stress, and immune responses in AD mice. [ABSTRACT FROM AUTHOR]

Background: The incidence of neurological complications associated with nitrous oxide (N2O) abuse, including N2O-induced myelopathy and neuropathy, has risen in the past decade. N2O-induced neuropathy often presents as a subacute axonal pathology; however, demyelinating patterns mimicking Guillain–Barré syndrome have also been observed. This study explores the metabolic pathophysiology of N2O-induced neuropathy, focusing on the alteration in metabolism to provide a deeper understanding of the biochemical pathways influencing the diverse electrophysiological patterns observed. Methods: We conducted a combined metabolic and electrophysiological exploration of 35 patients who underwent electromyographic exams at our referral center over a three-year period for sensorimotor symptoms linked to recreational N2O use. We collected demographic, clinical, radiological, electrophysiological, and biological data. Patients were categorized into axonal or demyelinating groups based on their electrophysiological patterns, and metabolic parameters were compared. Results: Our cohort predominantly exhibited a length-dependent sensorimotor axonal symmetrical neuropathy affecting the lower limbs. Among the patients, 40% met the demyelinating criteria, with four patients exhibiting conduction blocks. The demyelinating group had a significantly higher peripheral neuropathy disability (PND) score at diagnosis. Elevated homocysteine and methylmalonic acid (MMA) levels were noted in all patients, but these were lower in the demyelinating group. Conclusions: This study highlights the diverse electrophysiological manifestations of N2O-induced neuropathy and underscores the potential role of metabolic parameters as biomarkers to understand its pathophysiology. Lower hyperhomocysteinemia and MMA levels were observed in demyelinating patterns. In this study, we did not observe further improvement, but it is well-known that demyelinating features have a better prognosis related to the further remyelination. These findings contribute to a better understanding of N2O-related neuropathic damage and could guide future therapeutic interventions based on biochemical–neurophysiological stratifications. [ABSTRACT FROM AUTHOR]

Copyright of China Tropical Medicine is the property of China Tropical Medicine Editorial Office 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.)

Abstract Purpose Serum neurofilament light chain (sNfL) can reflect nerve damage. Whether migraine can cause neurological damage remain unclear. This study assesses sNfL levels in migraine patients and explores whether there is nerve damage in migraine. Methods A case–control study was conducted in Xiamen, China. A total of 138 migraine patients and 70 healthy controls were recruited. sNfL (pg/mL) was measured on the single-molecule array platform. Univariate, Pearson correlation and linear regression analysis were used to assess the relationship between migraine and sNfL levels, with further subgroup analysis by migraine characteristics. Results Overall, 85.10% of the 208 subjects were female, with a median age of 36 years. sNfL levels were higher in the migraine group than in the control group (4.85 (3.49, 6.62) vs. 4.11 (3.22, 5.59)), but the difference was not significant (P = 0.133). The two groups showed an almost consistent trend in which sNfL levels increased significantly with age. Subgroup analysis showed a significant increase in sNfL levels in patients with a migraine course ≥ 10 years (β = 0.693 (0.168, 1.220), P = 0.010). Regression analysis results show that age and migraine course are independent risk factors for elevated sNfL levels, and there is an interaction between the two factors. Patients aged

Over the past two decades, the use of tumor necrosis factor alpha (TNF-α) inhibitors has significantly improved the treatment of patients with immune-mediated inflammatory diseases. Firstly, introduced for rheumatoid arthritis, these inhibitors are currently approved and used for a variety of conditions, including ankylosing spondylitis, Crohn’s disease, juvenile idiopathic arthritis, psoriasis, psoriatic arthritis, ulcerative colitis, and chronic uveitis. Despite their immense therapeutic efficacy, TNF-α inhibitors have been associated with neurological adverse effects that bring new clinical challenges. The present review collects data from multiple studies to evaluate the incidence and the relationship between TNF-α inhibitors and neurological side effects and to explore the potential underlying mechanisms of this association. Moreover, it highlights the importance of patient selection, particularly in the case of individuals with a history of demyelinating diseases, raises awareness for clinicians, and calls for ongoing research that will improve TNF-α targeting strategies and offer safer and more effective therapeutic options.

Recreational nitrous oxide use has grown in popularity among young people and has become a serious public health problem. Chronic use of nitrous oxide can lead to a functional vitamin B12 deficiency and neuropsychiatric complications. This study aimed to investigate the characteristics of neuropsychiatric complications associated with nitrous oxide use and to enhance clinicians' awareness of this public health problem. We retrospectively reviewed 16 patients with neuropsychiatric disorders related to nitrous oxide use who were treated in our hospital from June 2021 to October 2022. Their demographics, clinical features, investigations, treatments and outcomes were analyzed. There were ten males and six females between the ages of 17 and 25 with a mean age of 20.5 ± 2.6 years. Thirteen patients sought medical help from the neurology clinic. Two patients presented to the psychiatric department and one patient presented to the emergency department with acute cognitive impairment. All 16 patients presented with neurological symptoms, such as paresthesia in four limbs or the lower limbs, unsteady gait and weakness. Twelve patients developed psychiatric symptoms, such as hallucinations, agitation, depression, emotional indifference and personality changes. Twelve patients had vitamin B12 deficiency. All 16 patients had hyperhomocysteinemia. Fourteen patients showed abnormal high signal on T2-weighted imaging and an inverted "V" sign in axial view, mainly involving the cervical cord. Neuropsychiatric symptoms improved with vitamin B12 treatment and cessation of nitrous oxide use in all cases. Young adults are predominately involved in recreational use of nitrous oxide, which can cause neuropsychiatric complications. The clinical response to vitamin B12 supplementation and cessation of nitrous oxide use is generally good. Clinicians should recognize nitrous oxide use as a public health problem and a cause of a wide range of neuropsychiatric symptoms, particularly in younger patients. [ABSTRACT FROM AUTHOR]

Introduction. Congenital disorders of glycosylation (CDG) represent a group of inborn errors of metabolism with multisystem damage determined by the disruption of the glycosylation process. The primary system affected in 80% of cases is the central nervous system, which encompasses a variety of clinical symptoms from mild muscular hypotonia to severe psychomotor retardation, treatment-resistant seizures, and cortical/cerebellar MRI brain changes. Aim. The aim of the review is the summary the variability of clinical manifestations in CDG and the pathologies that mimic them. Materials and methods: The bibliographic sources studied were taken from the online databases MedLine, Cochrane library, Wiley Online Library and National Library of Medicine, NCBI, using keywords: CDG, IEFT, glycosylation, multisystemic damage. More than 350 scientific articles were identified, obtaining relevant literature data for the differential diagnosis of these group of pathologies. Results. The variety of clinical manifestations often mimics other pathologies, which results in the underdiagnosis of CDG. Many metabolic disorders include similar signs and symptoms, and comparisons can be helpful for a thorough and accurate differential diagnosis. Urea cycle disorders, inborn errors of bile metabolism, fatty acid oxidation disorders, organic acidosis, peroxisome biogenesis disorders, and sphingolipidoses are recommended to be included in the differential diagnosis algorithm of glycosylation disorders. At the same time, patients who present clinical signs under the guise of Infantile cerebral palsy, need to be tested for CDG through the screening method of Isoelectric focusing of transferrin (IEFT). Prader-Willi, Smith-Lemli-Opitz, Weaver, and Robinow syndromes, but also some congenital coagulation disorders, Ataxia-telangiectasia, and other hereditary ataxias, show a clinical picture similar to congenital glycosylation disorders. Conclusion. The IEFT represents a tool with an imposing applicative value in the diagnosis of CDG, that comes to the aid of clinicians, for the differential diagnosis of neurological genetic pathologies. [ABSTRACT FROM AUTHOR]

Several biofluid-based biomarkers for traumatic brain injury show promise for use in diagnosis and outcome prediction. In contrast, few studies have investigated biomarkers for non-traumatic brain injury. We focused on ubiquitin C-terminal hydrolase-L1 (UCH-L1), which has been proposed as a screening tool for traumatic brain injury, and investigated whether the plasma UCH-L1 level could also be a useful biomarker in patients with non-traumatic brain injury. We measured UCH-L1 in 25 patients who had experienced neurological complications after allogeneic hematopoietic cell transplantation (HCT) and 22 control patients without any complications or graft-versus-host disease. Although UCH-L1 levels before HCT did not differ significantly (P = 0.053), levels after HCT were higher in patients with neurological complications compared with the control group (P < 0.001). At a UCH-L1 cutoff value of 0.072 ng/ml, sensitivity was 68.0% and specificity was 100%. The statistical power of UCH-L1 for neurological complications seemed to be higher than that of CT and comparable to that of MRI. Thus, increased levels of UCH-L1 might reflect the presence of neurological damage even in patients with non-traumatic brain injury. Further large cohort investigations are warranted. [ABSTRACT FROM AUTHOR]

Maple syrup urine disease (MSUD) is an inherited metabolic disorder caused by a deficiency in branched-chain alpha-ketoacid dehydrogenase complex (BCKAC). The treatment is a standard therapy based on a protein-restricted diet with low branched-chain amino acids (BCAA) content to reduce plasma levels and, consequently, the effects of accumulating their metabolites, mainly in the central nervous system. Although the benefits of dietary therapy for MSUD are undeniable, natural protein restriction may increase the risk of nutritional deficiencies, resulting in a low total antioxidant status that can predispose and contribute to oxidative stress. As MSUD is related to redox and energy imbalance, melatonin can be an important adjuvant treatment. Melatonin directly scavenges the hydroxy radical, peroxyl radical, nitrite anion, and singlet oxygen and indirectly induces antioxidant enzyme production. Therefore, this study assesses the role of melatonin treatment on oxidative stress in brain tissue and behavior parameters of zebrafish (Danio rerio) exposed to two concentrations of leucine-induced MSUD: leucine 2 mM and 5mM; and treated with 100 nM of melatonin. Oxidative stress was assessed through oxidative damage (TBARS, DCF, and sulfhydryl content) and antioxidant enzyme activity (SOD and CAT). Melatonin treatment improved redox imbalance with reduced TBARS levels, increased SOD activity, and normalized CAT activity to baseline. Behavior was analyzed with novel object recognition test. Animals exposed to leucine improved object recognition due to melatonin treatment. With the above, we can suggest that melatonin supplementation can protect neurologic oxidative stress, protecting leucine-induced behavior alterations such as memory impairment. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), a novel coronavirus, causes coronavirus disease 2019 (COVID‐19) which led to neurological damage and increased mortality worldwide in its second and third waves. It is associated with systemic inflammation, myocardial infarction, neurological illness including ischemic strokes (e.g., cardiac and cerebral ischemia), and even death through multi‐organ failure. At the early stage, the virus infects the lung epithelial cells and is slowly transmitted to the other organs including the gastrointestinal tract, blood vessels, kidneys, heart, and brain. The neurological effect of the virus is mainly due to hypoxia‐driven reactive oxygen species (ROS) and generated cytokine storm. Internalization of SARS‐CoV‐2 triggers ROS production and modulation of the immunological cascade which ultimately initiates the hypercoagulable state and vascular thrombosis. Suppression of immunological machinery and inhibition of ROS play an important role in neurological disturbances. So, COVID‐19 associated damage to the central nervous system, patients need special care to prevent multi‐organ failure at later stages of disease progression. Here in this review, we are selectively discussing these issues and possible antioxidant‐based prevention therapies for COVID‐19‐associated neurological damage that leads to multi‐organ failure. [ABSTRACT FROM AUTHOR]

Background: The incidence of neurological complications associated with nitrous oxide (N2O) abuse, including N2O-induced myelopathy and neuropathy, has risen in the past decade. N2O-induced neuropathy often presents as a subacute axonal pathology; however, demyelinating patterns mimicking Guillain–Barré syndrome have also been observed. This study explores the metabolic pathophysiology of N2O-induced neuropathy, focusing on the alteration in metabolism to provide a deeper understanding of the biochemical pathways influencing the diverse electrophysiological patterns observed. Methods: We conducted a combined metabolic and electrophysiological exploration of 35 patients who underwent electromyographic exams at our referral center over a three-year period for sensorimotor symptoms linked to recreational N2O use. We collected demographic, clinical, radiological, electrophysiological, and biological data. Patients were categorized into axonal or demyelinating groups based on their electrophysiological patterns, and metabolic parameters were compared. Results: Our cohort predominantly exhibited a length-dependent sensorimotor axonal symmetrical neuropathy affecting the lower limbs. Among the patients, 40% met the demyelinating criteria, with four patients exhibiting conduction blocks. The demyelinating group had a significantly higher peripheral neuropathy disability (PND) score at diagnosis. Elevated homocysteine and methylmalonic acid (MMA) levels were noted in all patients, but these were lower in the demyelinating group. Conclusions: This study highlights the diverse electrophysiological manifestations of N2O-induced neuropathy and underscores the potential role of metabolic parameters as biomarkers to understand its pathophysiology. Lower hyperhomocysteinemia and MMA levels were observed in demyelinating patterns. In this study, we did not observe further improvement, but it is well-known that demyelinating features have a better prognosis related to the further remyelination. These findings contribute to a better understanding of N2O-related neuropathic damage and could guide future therapeutic interventions based on biochemical–neurophysiological stratifications.

Symbiotic microbes impact the function and development of the central nervous system (CNS); however, little is known about the contribution of the microbiota during viral-induced neurologic damage. We identify that commensals aid in host defense following infection with a neurotropic virus through enhancing microglia function. Germfree mice or animals that receive antibiotics are unable to control viral replication within the brain leading to increased paralysis. Microglia derived from germfree or antibiotic-treated animals cannot stimulate viral-specific immunity and microglia depletion leads to worsened demyelination. Oral administration of toll-like receptor (TLR) ligands to virally infected germfree mice limits neurologic damage. Homeostatic activation of microglia is dependent on intrinsic signaling through TLR4, as disruption of TLR4 within microglia, but not the entire CNS (excluding microglia), leads to increased viral-induced clinical disease. This work demonstrates that gut immune-stimulatory products can influence microglia function to prevent CNS damage following viral infection.

Abstract Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), a novel coronavirus, causes coronavirus disease 2019 (COVID‐19) which led to neurological damage and increased mortality worldwide in its second and third waves. It is associated with systemic inflammation, myocardial infarction, neurological illness including ischemic strokes (e.g., cardiac and cerebral ischemia), and even death through multi‐organ failure. At the early stage, the virus infects the lung epithelial cells and is slowly transmitted to the other organs including the gastrointestinal tract, blood vessels, kidneys, heart, and brain. The neurological effect of the virus is mainly due to hypoxia‐driven reactive oxygen species (ROS) and generated cytokine storm. Internalization of SARS‐CoV‐2 triggers ROS production and modulation of the immunological cascade which ultimately initiates the hypercoagulable state and vascular thrombosis. Suppression of immunological machinery and inhibition of ROS play an important role in neurological disturbances. So, COVID‐19 associated damage to the central nervous system, patients need special care to prevent multi‐organ failure at later stages of disease progression. Here in this review, we are selectively discussing these issues and possible antioxidant‐based prevention therapies for COVID‐19‐associated neurological damage that leads to multi‐organ failure.

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Organic solvents are a class of volatile, lipophilic substances that can easily enter the human body through skin and mucous membrane contact as well as air inhalation, and can lead to toxic encephalopathy (TE), especially after entering the lipid-rich nervous system. The present case reports a patient with acute organic solvent toxic encephalopathy (AOSTE), which may have been caused by occasional ink leakage from Xuzhou (Jiangsu, China). By summarizing the history the patient to exposure to organic solvents, clinical manifestations, radiology findings and relevant laboratory tests, we hypothesize that a history of ink exposure, brain magnetic resonance imaging findings and hippuric acid testing were indispensable factors in the diagnosis of AOSTE. After neurological treatment, the patient experienced notable improvement in symptoms. The present study reports on its clinical features, imaging features, treatment and follow-up, and review relevant literature to summarize its clinical experience, hoping to improve our understanding of AOSTE. [ABSTRACT FROM AUTHOR]

Saffron, a traditional Chinese medicine, is derived from Crocus sativus L. stigmas and has been reported to possess neuroprotective properties and potentially contribute to the inhibition of apoptosis and inflammation. Safranal, a potent monothyral aldehyde, is a main component of saffron that has been reported to have antiepileptic activity. However, the specific mechanism by which safranal suppresses epileptic seizures via its antiapoptotic and anti-inflammatory properties is unclear. To evaluate the effect of safranal on seizure severity, inflammation, and postictal neuronal apoptosis in a mouse model of pentetrazole (PTZ)-induced seizures and explore the underlying mechanism involved. The seizure stage and latency of stage 2 and 4 were quantified to assess the efficacy of safranal in mitigating PTZ-induced epileptic seizures in mice. Electroencephalography (EEG) was employed to monitor epileptiform afterdischarges in each experimental group. The cognitive abilities and motor functions of the mice were evaluated using the novel object recognition test and the open field test, respectively. Neurons were quantified using hematoxylin and eosin staining. Additionally, bioinformatics tools were utilized to predict the interactions between safranal and specific target proteins. Glycogen synthase kinase-3β (GSK-3β), mitochondrial apoptosis-related proteins, and inflammatory factor levels were analyzed through western blotting. Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) concentrations in brain tissue were assessed by ELISA. Safranal decreased the average seizure stage and increased the lantency of stage 2 and 4 seizures in PTZ-induced epileptic mice. Additionally, safranal exhibited neuroprotective effects on hippocampal CA1 and CA3 neurons and reduced hyperactivity caused by postictal hyperexcitability. Bioinformatics analysis revealed that safranal can bind to five specific proteins, including GSK-3β. By promoting Ser9 phosphorylation and inhibiting GSK-3β activity, safranal effectively suppressed the NF-κB signaling pathway. Moreover, the findings indicate that safranal treatment can decrease TNF-α and IL-1β levels in the cerebral tissues of epileptic mice and downregulate mitochondrial apoptosis-related proteins, including Bcl-2, Bax, Bak, Caspase 9, and Caspase 3. Safranal can suppress the NF-κB signaling pathway and mitochondrial-dependent apoptosis through GSK-3β inactivation, suggesting that it is a promising therapeutic agent for epilepsy treatment. [Display omitted] • Safranl alleviates PTZ-induced epileptic seizures. • Safranal induces post-ictal GSK-3β inactivation. • GSK-3β inactivation inhibits mitochondrial-dependent apoptosis. • GSK-3β inactivation counteract post-ictal inflammation. [ABSTRACT FROM AUTHOR]

Cerebral malaria (CM) caused by Plasmodium falciparum is a fatal neurological complication of malaria, resulting in coma and death, and even survivors may suffer long-term neurological sequelae. In sub-Saharan Africa, CM occurs mainly in children under five years of age. Although intravenous artesunate is considered the preferred treatment for CM, the clinical efficacy is still far from satisfactory. The neurological damage induced by CM is irreversible and lethal, and it is therefore of great significance to unravel the exact etiology of CM, which may be beneficial for the effective management of this severe disease. Here, we review the clinical characteristics, pathogenesis, diagnosis, and clinical therapy of CM, with the aim of providing insights into the development of novel tools for improved CM treatments. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the effects of sodium valproate combined with lamotrigine on cognitive function, immune function and neurological damage of children with epilepsy. METHODS: Retrospective analysis was performed on clinical data of 140 children with epilepsy admitted into the hospital from Jul. 2017 to Jul. 2021, all children were extracted to be divided into the control group (n = 70) and the observation group (n = 70) according to the intervention method. The control group was treated with sodium valproate, while the observation group received lamotrigine on the basis of the control group. Both groups were treated with continuous treatment for 3 months. Before and after treatment, cognitive function [mini-mental state examination (MMSE) score], anxiety [ self-rating anxiety scale (SAS) score], depression [ self-rating depression scale ( SDS) score], immune function [ immunoglobulin G (IgG), immunoglobulin M (IgM)], degree of neurological impairment [clinical neurological impairment rating scale (CSS) score], quality of life [ score of short form for health survey ( SF-36)], and adverse drug reactions in two groups were detected and compared. RESULTS: After treatment, the MMSE scores of two groups were higher than those before treatment, and the SAS and SDS scores were lower than those before treatment; the MMSE scores of the observation group was higher than that of the control group, and the SAS and SDS scores were lower than those of the control group, with statistically significant differences (P<0. 05). After treatment, the levels of IgG and IgM in two groups were lower than those before treatment, and the levels of IgG and IgM in the observation group were lower than those in the control group, with statistically significant differences (P<0. 05). After treatment, the CSS scores of two groups were lower than those before treatment, and the CSS scores of the observation group were lower than those of the control group, with statistically significant differences (P < 0. 05). After treatment, the SF-36 scores of two groups were higher than those before treatment, and the SF-36 scores of the observation group were higher than those of the control group, with statistically significant differences ( P < 0. 05). There was no significant difference in the total incidence of adverse drug reactions between two groups (P>0. 05). CONCLUSIONS: Sodium valproate combined with lamotrigine can effectively improve the cognitive function, anxiety and depression in children with epilepsy, reduce the neurological deficit score, control the recent infection and improve the quality of life in children, and does not increase the obvious adverse drug reactions. [ABSTRACT FROM AUTHOR]

Aim: Methotrexate (MTX), a folic acid antagonist, is widely used in the treatment of many malignancies. However, various serious side effects caused by MTX limit its clinical use. Neurotoxicity is one of the most important side effects seen during MTX treatment. Oxidative damage is explained as one of the side-effect mechanisms caused by MTX. In addition to the many health benefits of fish oil (FO), its antioxidant properties have also been shown in various studies. In this study, it was aimed to investigate the potential beneficial effects of FO against oxidative brain damage caused by MTX. Materials and Methods: Twenty-eight rats were randomly divided into 4 groups (n = 7). The first group is the control group. The second group was determined as the FO group and 1000 mg / kg / day FO was given by gavage to the rats in this group for two weeks. The third group was determined as MTX group and a single dose of 20 mg / kg MTX was injected intraperitoneally to the rats in this group on the third day. The fourth group was determined as MTX + FO group, and the rats in the group were given MTX and FO in similar doses together. Results: The administration of MTX caused significant increase in TBARS levels compared to the control group, and significant decrease in SOD, GPx and CAT activities. However, the administration of FO with MTX caused statistically significant decrease in TBARS level and a significant increase in SOD and GPx activities compared to MTX group. On the other hand, there was no difference between the groups in terms of GSH levels. In addition, administration of MTX did not cause a histopathologically significant lesion in the brain tissue. Conclusion: Our results support that the use of FO may benefit against neurological oxidative damage caused by MTX. [ABSTRACT FROM AUTHOR]

Based on a variant strain, we constructed a gE/gI/TK-deleted pseudorabies virus (PRV). A total of 18 female mice were randomized to a vaccination group to receive PRV XJ delgE/gI/TK, a vehicle group to receive Dulbecco's modified Eagle's medium, and a mock group to confirm the protection of PRV delgE/gI/TK on the central nervous system in mice. Subsequently, the vaccination and vehicle groups were infected with PRV XJ. The mice in the vehicle group showed more severe neurological symptoms and higher viral loads than those in the vaccination group. The exudation of Evans blue and the expression of tight junction protein showed no difference in all groups. HE staining showed vacuolar neuronal degeneration in the vehicle group brain, but no tissue lesions were observed in the vaccination group. TNF-α, IL-6, and synuclein were upregulated in the brain of mice in the vehicle group, while those were inhibited among mice in the vaccination group. IFN-β, IFN-γ, ISG15, Mx1, and OAS1 showed no difference in the brain between the vaccination and vehicle groups. In addition, TNF-α and IL-6 were inhibited, and antiviral factors were increased in the intestine of the mice in the vaccination group compared to those in the vehicle group. Our study showed that PRV XJ delgE/gI/TK inhibited neurological damage and the inflammation of the intestine and brain induced by PRV and activated the innate immunity of the intestine. [ABSTRACT FROM AUTHOR]

Lead poisoning caused by lead pollution seriously affects people's health. Lactic acid bacteria has been shown to be useful for biological scavenging of lead. In this experiment, Sprague-Dawley (SD) rats were treated with 200 mg/L of lead acetate solution daily to induce chronic lead poisoning, and oral Limosilactobacillus fermentum (L. fermentum) SCHY34 to study its mitigation effects and mechanisms on rat neurotoxicity. The L. fermentum SCHY34 showed competent results on in vitro survival rate and the lead ion adsorption rate. Animal experiments showed that L. fermentum SCHY34 maintained the morphology of rat liver, kidney, and hippocampi, reduced the accumulation of lead in the blood, liver, kidney, and brain tissue. Further, L. fermentum SCHY34 alleviated the lead-induced decline in spatial memory and response capacity of SD rats, and also regulated the secretion of neurotransmitters and related enzyme activities in the brain tissue of rats, such as glutamate (Glu), monoamine oxidase (MAO), acetylcholinesterase (AchE), cyclic adenosine monophosphate (cAMP), and adenylate cyclase (AC). In addition, the expression of genes related to cognitive capacity, antioxidation, and anti-apoptotic in rat brain tissues were increased L. fermentum SCHY34 treatment, such as brain-derived neurotrophic factor (BDNF), c-fos, c-jun, superoxide dismutase (SOD)1/2, Nuclear factor erythroid 2-related factor 2 (Nrf2), and B-cell lymphoma 2 (Bcl-2), and so on. L. fermentum SCHY34 showed a great biological scavenging and potential effect on alleviating the toxicity of lead ions.

Based on a variant strain, we constructed a gE/gI/TK-deleted pseudorabies virus (PRV). A total of 18 female mice were randomized to a vaccination group to receive PRV XJ delgE/gI/TK, a vehicle group to receive Dulbecco’s modified Eagle’s medium, and a mock group to confirm the protection of PRV delgE/gI/TK on the central nervous system in mice. Subsequently, the vaccination and vehicle groups were infected with PRV XJ. The mice in the vehicle group showed more severe neurological symptoms and higher viral loads than those in the vaccination group. The exudation of Evans blue and the expression of tight junction protein showed no difference in all groups. HE staining showed vacuolar neuronal degeneration in the vehicle group brain, but no tissue lesions were observed in the vaccination group. TNF-α, IL-6, and synuclein were upregulated in the brain of mice in the vehicle group, while those were inhibited among mice in the vaccination group. IFN-β, IFN-γ, ISG15, Mx1, and OAS1 showed no difference in the brain between the vaccination and vehicle groups. In addition, TNF-α and IL-6 were inhibited, and antiviral factors were increased in the intestine of the mice in the vaccination group compared to those in the vehicle group. Our study showed that PRV XJ delgE/gI/TK inhibited neurological damage and the inflammation of the intestine and brain induced by PRV and activated the innate immunity of the intestine.

Objectives: Fetal growth restriction (FGR) is associated with chronic fetal hypoxia, poor perinatal outcome and increased perinatal mortality. There are no reliable methods to detect cell damage in the central nervous system (CNS) in these patients. The findings of increased an acidic calcium-binding protein (S100B) concentration in biological fluids of infants after brain injury have supported the use of S100B as a biochemical marker of CNS damage. The purpose of the study was to assess blood S100B concentrations in small for gestational age (SGA) and appropriate for gestational age (AGA) newborns and to evaluate the usefulness of S100B for early detection of hypoxia. Material and methods: The investigation was carried out between November 2011 and April 2014. Serum S100B protein level was assessed in cord blood collected from newborns after birth. Medical records of mothers of neonates studied were reviewed for pregnancy induced hypertension (PIH), preeclampsia, maternal smoking during pregnancy and abnormalities in umbilical artery (UA) Doppler ultrasound examination. Results: The study was carried out in 88 SGA neonates and 80 AGA neonates. The median value of S100B protein concentration in the SGA study group was significantly higher than in AGA controls (p < 0.001). Cord blood serum S100B concentration in SGA neonates with prenatal normal UA Doppler ultrasound findings (n = 32) did not differ from that SGA neonates with abnormal prenatal UA Doppler findings (n = 25) (p = 0.74), but was significantly higher than in AGA newborns (p < 0.001). Conclusions: Elevated S100B protein levels in cord blood collected from SGA newborns may be helpful in detecting infants at higher risk of postnatal neurologic disturbances at an early stage. [ABSTRACT FROM AUTHOR]

Drinking alcohol is an established and normalised practice in our society, even though it can physically harm us. High-risk alcohol drinking patterns can increase the chance of negative consequences for the drinkers or their environment. The liver is by far the organ most affected by alcohol abuse; however, alcohol use disorder is a systemic disease which affects a wide range of organs and psychological processes. Other systems that can be affected by continued alcohol consumption include the immune, neurological, and cardiovascular systems. In addition, alcohol can lead to epigenetic alterations that may be transmitted from one generation to the next. [ABSTRACT FROM AUTHOR]

Objective: To analyze the clinical characteristics, treatment, and prognosis of children infected with SARS-CoV-2 following the adjustment of COVID-19 prevention and control policies in China in December 2022., Methods: A retrospective study was conducted on 9 cases of severe neurological dysfunction caused by SARS-CoV-2 infection in children admitted to Foshan First People's Hospital from December 17 to 31, 2022., Results: Among the 9 cases, 7 (71.43%) were under 3 years old, and 2 (22.2%) were over 3 years old with underlying diseases. All patients presented with fever and neurological symptoms such as consciousness disturbance and/or convulsions, and their conditions deteriorated rapidly within 24 h after the onset of fever, without respiratory symptoms. Levels of IL-6, LDH, and d-dimer were significantly elevated. Five cases died within 48 h of admission, one case died after 7 days of treatment due to secondary bacterial infection, and three cases survived for more than 48 h after the initial rescue. All patients developed rapid shock, and five cases experienced multi-organ failure within a short period. In terms of treatment, glucocorticoids were used in 5 cases, intravenous immunoglobulin (IVIG) in 3 cases, and blood purification and tocilizumab in 2 cases., Conclusion: SARS-CoV-2 infection in children can lead to severe neurological damage. High fever, convulsions, and inflammatory factors serve as early warning indicators. Glucocorticoids, immunoglobulins, blood purification, and tocilizumab may have some therapeutic effects, but further research is needed to confirm the efficacy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Chen, Liang and Jiang.)

The aim of this exploration is to analyze the elements related to infections as well as neurological damage complications after transcatheter arterial chemoembolization (TACE) by computer information health analysis using deep learning. In this exploration, there were 80 primary liver cancer patients who were selected as the study subjects. After each patient was treated with TACE, analysis is made on their postoperative complication incidence as well as the complication differences among different groups. Moreover, comparison is carried out among the levels of alpha-fetoprotein, grades of liver function, iodized oil dosage, arteriovenous fistula, tumor blood supply, as well as tumor morphology in operation. The patient's information was input into the deep learning system to analyze the patient's disease status. There were statistical differences at P < 0.05. The research results suggested that ectopic embolization of iodized oil, myelosuppression, liver function impairment, gastrointestinal symptoms, fever, as well as infection could lead to neurological damage. The incidence that they caused was 1.25%, 22.5%, 77.5%, 86.25%, 90%, and 58.75%, respectively. There was no obvious relationship between alpha-fetoprotein and the postoperative complications mentioned above; moreover, tumor morphology as well as tumor blood supply could affect the postoperative infection, fever, gastrointestinal symptoms, as well as liver function damages obviously. In addition, the classification of liver function could greatly influence the symptoms of postoperative gastrointestinal, myelosuppression, as well as damages of liver function. Therefore, the analysis of TACE postoperative neurological damage complications as well as correlated factors revealed that it was necessary to take appropriate nursing treatment measures, which can not only enhance the TACE surgery's success rate, but also prolong the survival of patients. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID-19) is a devastating viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The incidence and mortality of COVID-19 patients have been increasing at an alarming rate. The mortality is much higher in older individuals, especially the ones suffering from respiratory distress, cardiac abnormalities, renal diseases, diabetes, and hypertension. Existing evidence demonstrated that SARS-CoV-2 makes its entry into human cells through angiotensin-converting enzyme 2 (ACE-2) followed by the uptake of virions through cathepsin L or transmembrane protease serine 2 (TMPRSS2). SARS-CoV-2-mediated abnormalities in particular cardiovascular and neurological ones and the damaged coagulation systems require extensive research to develop better therapeutic modalities. As SARS-CoV-2 uses its S-protein to enter into the host cells of several organs, the S-protein of the virus is considered as the ideal target to develop a potential vaccine. In this review, we have attempted to highlight the landmark discoveries that lead to the development of various vaccines that are currently under different stages of clinical progression. Besides, a brief account of various drug candidates that are being tested to mitigate the burden of COVID-19 was also covered. Further, in a dedicated section, the impact of SARS-CoV-2 infection on neuronal inflammation and neuronal disorders was discussed. In summary, it is expected that the content covered in this article help to understand the pathophysiology of COVID-19 and the impact on neuronal complications induced by SARS-CoV-2 infection while providing an update on the vaccine development. [ABSTRACT FROM AUTHOR]

BackgroundCerebrospinal fluid (CSF) and neuroimaging abnormalities demonstrate neuronal injury during chronic AIDS, but data on these biomarkers during primary human immunodeficiency virus (HIV) infection is limited.MethodsWe compared CSF concentrations of neurofilament light chain, t-tau, p-tau, amyloid precursor proteins, and amyloid-beta 42 in 92 subjects with primary HIV infection and 25 controls. We examined relationships with disease progression and neuroinflammation, neuropsychological testing, and proton-magnetic resonance spectroscopy (MRS)-based metabolites.ResultsNeurofilament light chain was elevated in primary HIV infection compared with controls (P = .0004) and correlated with CSF neopterin (r = 0.38; P = .0005), interferon gamma-induced protein 10 (r = 0.39; P = .002), white blood cells (r = 0.32; P = .004), protein (r = 0.59; P < .0001), and CSF/plasma albumin ratio (r = 0.60; P < .0001). Neurofilament light chain correlated with decreased N-acteylaspartate/creatine and glutamate/creatine in the anterior cingulate (r = -0.35, P = .02; r = -0.40, P = .009, respectively), frontal white matter (r = -0.43, P = .003; r = -0.30, P = .048, respectively), and parietal gray matter (r = -0.43, P = .003; r = -0.47, P = .001, respectively). Beta-amyloid was elevated in the primary infection group (P = .0005) and correlated with time infected (r = 0.34; P = .003). Neither marker correlated with neuropsychological abnormalities. T-tau and soluble amyloid precursor proteins did not differ between groups.ConclusionsElevated neurofilament light chain and its correlation with MRS-based metabolites suggest early neuronal injury in a subset of participants with primary HIV infection through mechanisms involving central nervous system inflammation.

Objective: Description and analysis of the relation between the proximal humerus fracture patterns and the traumatic injury of the axillary nerve., Material and Method: Prospective, observational study of a consecutive case series that analysed proximal humerus fractures. Radiographic evaluation was performed, and AO (Arbeitsgemeinshaft für Osteosynsthesefragen) system was used to classify the fractures. Electromyography was used to diagnose the axillary nerve injury., Results: Thirty-one patients on 105 who had a proximal humerus fracture met inclusion criteria. Eighty-six percent of the patients included were women and 14% men. The mean age was 71.8 years (30-96 years). Of the patients included in the study, 58% had normal or mild axonotmesis EMG, 23% had axillary nerve neuropathy without muscle denervation and 19% had injury with axillary nerve denervation. Patients who suffered complex fractures of the proximal humerus (AO11B and AO11C) had a higher risk of presenting axillary neuropathy type lesions with muscle denervation in the EMG, this relationship being statistically significant (p<0.001)., Conclusion: Patients who have more risk on presenting axillary nerve neuropathy with muscle denervation in electromyography are those who present complex proximal humerus fractures AO11B and AO11C (p<0.001)., (Copyright © 2023 SECOT. Publicado por Elsevier España, S.L.U. All rights reserved.)

Objective: Description and analysis of the relation between the proximal humerus fracture patterns and the traumatic injury of the axillary nerve., Material and Method: Prospective, observational study of a consecutive case series that analyzed proximal humerus fractures. Radiographic evaluation was performed, and AO (Arbeitsgemeinshaft für Osteosynsthesefragen) system was used to classify the fractures. Electromyography was used to diagnose the axillary nerve injury., Results: Thirty-one patients on 105 who had a proximal humerus fracture met inclusion criteria. Eighty-six percent of the patients included were women and 14% men. The mean age was 71.8 years (30-96 years). Of the patients included in the study, 58% had normal or mild axonotmesis EMG, 23% had axillary nerve neuropathy without muscle denervation and 19% had injury with axillary nerve denervation. Patients who suffered complex fractures of the proximal humerus (AO11B and AO11C) had a higher risk of presenting axillary neuropathy type lesions with muscle denervation in the EMG, this relationship being statistically significant (p<0.001)., Conclusion: Patients who have more risk on presenting axillary nerve neuropathy with muscle denervation in electromyography are those who present complex proximal humerus fractures AO11B and AO11C (p<0.001)., (Copyright © 2023 SECOT. Publicado por Elsevier España, S.L.U. All rights reserved.)

The recent pandemic outbreak of coronavirus is pathogenic and a highly transmittable viral infection caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2). In this time of ongoing pandemic, many emerging reports suggested that the SARS-CoV-2 has inimical effects on neurological functions, and even causes serious neurological damage. The neurological symptoms associated with COVID-19 include headache, dizziness, depression, anosmia, encephalitis, stroke, epileptic seizures, and Guillain-Barre syndrome along with many others. The involvement of the CNS may be related with poor prognosis and disease worsening. Here, we review the evidence of nervous system involvement and currently known neurological manifestations in COVID-19 infections caused by SARS-CoV-2. We prioritize the 332 human targets of SARS-CoV-2 according to their association with brain-related disease and identified 73 candidate genes. We prioritize these 73 genes according to their spatio-temporal expression in the different regions of brain and also through evolutionary intolerance analysis. The prioritized genes could be considered potential indicators of COVID-19-associated neurological symptoms and thus act as a possible therapeutic target for the prevention and treatment of CNS manifestations associated with COVID-19 patients. [ABSTRACT FROM AUTHOR]

Methanol poisoning although a rare entity, but has life threatening outcomes due to its highly toxic effects on body. It may be ingested accidentally or may be with suicidal intentions as well as habitual. Methanol intoxication leads to metabolic acidosis, neurological damage resulting in extrapyramidal symptoms, blindness and coma. According to our knowledge the MRI findings of methanol poisoning have been described in only few literatures. Therefore we present a case of one such patient who presented to emergency department with altered level of consciousness, drowsiness and vomiting. His MRI Brain revealed typical features of methanol poisoning. [ABSTRACT FROM AUTHOR]

Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is an emergent infectious disease that has caused millions of deaths throughout the world. COVID-19 infection’s main symptoms are fever, cough, fatigue, and neurological manifestations such as headache, myalgias, anosmia, ageusia, impaired consciousness, seizures, and even neuromuscular junctions’ disorders. In addition, it is known that this disease causes a series of systemic complications such as adverse respiratory distress syndrome, cardiac injury, acute kidney injury, and liver dysfunction. Due to the neurological symptoms associated with COVID-19, damage in the central nervous system has been suggested as well as the neuroinvasive potential of SARS-CoV-2. It is known that CoV infections are associated with an inflammation process related to the imbalance of the antioxidant system; cellular changes caused by oxidative stress contribute to brain tissue damage. Although anti-COVID-19 vaccines are under development, there is no specific treatment for COVID-19 and its clinical manifestations and complications; only supportive treatments with immunomodulators, anti-vascular endothelial growth factors, modulating drugs, statins, or nutritional supplements have been used. In the present work, we analyzed the potential of antioxidants as adjuvants for the treatment of COVID-19 and specifically their possible role in preventing or decreasing the neurological manifestations and neurological complications present in the disease.

Symbiotic microbes impact the function and development of the central nervous system (CNS); however, little is known about the contribution of the microbiota during viral-induced neurologic damage. We identify that commensals aid in host defense following infection with a neurotropic virus through enhancing microglia function. Germfree mice or animals that receive antibiotics are unable to control viral replication within the brain leading to increased paralysis. Microglia derived from germfree or antibiotic-treated animals cannot stimulate viral-specific immunity and microglia depletion leads to worsened demyelination. Oral administration of toll-like receptor (TLR) ligands to virally infected germfree mice limits neurologic damage. Homeostatic activation of microglia is dependent on intrinsic signaling through TLR4, as disruption of TLR4 within microglia, but not the entire CNS (excluding microglia), leads to increased viral-induced clinical disease. This work demonstrates that gut immune-stimulatory products can influence microglia function to prevent CNS damage following viral infection.

Abstract INTRODUCTION: Exposure to human immunodeficiency virus (HIV)-1 during pregnancy is a major risk factor for neurodevelopmental delay and deleterious effects in children. However, limited information about these conditions exists in poor geographical areas in Brazil. Prevention of vertical transmission of HIV-1 is dealt differently in different regions of the country and in poorer areas it is more difficult to evaluate the impact of the prevention methods. The outcomes of the exposure to HIV-1 and the impact of vertical HIV-1 transmission on neuropsychomotor development was evaluated for the first time in children born to HIV-infected mothers in the North region of Brazil, where the majority of the population has poor access to health services. METHODS: Sixty children born to HIV-1-infected mothers (case group) and 58 born to non-infected mothers (control group) were followed for the first 12 months of life in a prospective case-control study. Neuropsychomotor development was assessed using the Denver II test. RESULTS: Suspected neuropsychomotor developmental delays were more frequent in the case group (33.3%), namely in language (38.9%) and gross motor skills (27.8%). These delays were reversed in most children after 12 months of life due to therapeutic intervention. The delays were not reversed in three children, all of whom belonged to the case group. Only one of these was infected with HIV-1, and this child had the poorest neuropsychomotor outcomes. CONCLUSIONS: Maternal HIV-1 infection negatively affected the neuropsychomotor development in children, although other factors may have played a role.

Non-alcoholic fatty liver disease (NAFLD) is associated with high cardiovascular morbidity and mortality which usually is considered to be related to cardiac involvement, while scarce attention is addressed to brain damage. Viceversa NAFLD is associated with asymptomatic brain lesions, alterations in cerebral perfusion and activity, cognitive impairment and brain aging and with increased risk and severity of both ischemic and haemorrhagic stroke. Besides known metabolic risk factors, NAFLD is characterized by a pro inflammatory state, which contributes to atherosclerosis and microglia activation, endothelial dysfunction, pro-coagulant state and platelets activation, which in turn promote both micro and macrovascular damage eventually responsible for clinical and subclinical cerebrovascular alterations. A better knowledge of the association between NAFLD and brain alterations could lead to an improved management of risk factors underpinning both liver and cerebral disease, possibly preventing the progression of asymptomatic brain lesions to clinical cerebrovascular accidents. [ABSTRACT FROM AUTHOR]