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Studies using experimental animal models have demonstrated IL-1[beta] expression in microglia and astrocytes after seizures and that IL-1[beta] itself can enhance neuronal excitability. 4 Based on these findings, a hypothesis has been proposed that the vicious cycle consisting of seizure activity and inflammation contribute to the further progression of inflammation-mediated status epilepticus. 1 However, this paradigm has not been definitively demonstrated in human status epilepticus. [...]the present study unveiled a previously unrecognised relationship between a group of proinflammatory cytokines/chemokines and refractory status epilepticus in a human disease.

This report aimed to analyze the potential effects of cytokines and neutrophils-to-lymphocytes ratio (NLR) on the occurrence of febrile seizures (FS) in children during the epidemic of novel coronavirus and influenza virus. Between July 2022 and April 2023, clinical data of 422 children with FS hospitalized in the Pediatrics, Shaoxing People’s Hospital and the First Affiliated Hospital of Shaoxing University, during the epidemic and non-epidemic periods of novel coronavirus and influenza virus were analyzed. By comparing the various clinical characteristics of children with FS at different periods, comparison of variations in peripheral blood cell count, neutrophils, lymphocytes, hypersensitive C-creation protein, NLR, and inflammatory cytokines. Among 422 cases, 130 cases were classified as complex FS (CFS), while 292 cases of simple FS (SFS) were identified. During the time of the viral epidemic, 315 FS cases were observed, among which the incidence of CFS was 33.65%. In the non-viral epidemic period, there were 105 cases of FS. The incidence of CFS accounted for 22.86%. In addition, the levels of IL-4, IL-10, and tumor necrosis factor α (TNF-α) in children in the viral epidemic period were significantly higher than those in the non-epidemic period ( P  < 0.05). ROC curve analysis revealed that during the epidemic period, NLR (AUC = 0.724), IL-4 (AUC = 0.826), and IL-10 (AUC = 0.688) exhibited high predictive value for CFS children, and the indexes were statistically significant ( P  < 0.05). This study suggests that IL-4, IL-10, and NLR may play an important role in the pathogenesis of children with FS, especially those with CFS.

This trial assessed the efficacy of the vaccine RTS,S/AS01 E as compared with chemoprevention in preventing malaria. The protective efficacy of RTS,S/AS01 E was noninferior to that of chemoprevention, and the combination of RTS,S/AS01 E and chemoprevention was more effective than either intervention alone.

Complex febrile seizures (CFS), a subset of paediatric febrile seizures (FS), have been studied for their prognosis, epileptogenic potential and neurocognitive outcome. We evaluated their functional connectivity differences with simple febrile seizures (SFS) in children with recent-onset FS. Resting-state fMRI (rs-fMRI) datasets of 24 children with recently diagnosed FS (SFS-n = 11; CFS-n = 13) were analysed. Functional connectivity (FC) was estimated using time series correlation of seed region–to-whole-brain-voxels and network topology was assessed using graph theory measures. Regional connectivity differences were correlated with clinical characteristics (FDR corrected p  < 0.05). CFS patients demonstrated increased FC of the bilateral middle temporal pole (MTP), and bilateral thalami when compared to SFS. Network topology study revealed increased clustering coefficient and decreased participation coefficient in basal ganglia and thalamus suggesting an inefficient-unbalanced network topology in patients with CFS. The number of seizure recurrences negatively correlated with the integration of Left Thalamus (r = − 0.58) and FC of Left MTP to 'Right Supplementary Motor and left Precentral' gyrus (r = − 0.53). The FC of Right MTP to Left Amygdala, Putamen, Parahippocampal, and Orbital Frontal Cortex (r = 0.61) and FC of Left Thalamus to left Putamen, Pallidum, Caudate, Thalamus Hippocampus and Insula (r 0.55) showed a positive correlation to the duration of the longest seizure. The findings of the current study report altered connectivity in children with CFS proportional to the seizure recurrence and duration. Regardless of the causal/consequential nature, such observations demonstrate the imprint of these disease-defining variables of febrile seizures on the developing brain.

Febrile seizures (FS) are a common childhood neurological condition triggered by fever in children without prior neurological disorders. While generally benign, some individuals, particularly those with complex FS or genetic predispositions, may develop epilepsy or other neurological comorbidities. The mechanisms underlying this transition remain unclear. Mutations in SCN1A , encoding the Na V 1.1 sodium channel α-subunit, have been linked to several epilepsy syndromes associated with FS. This study examines phenotypic variability in individuals carrying the same SCN1A c.434T > C mutation, using induced pluripotent stem cell (iPSC)-derived neurons from two siblings with FS. Despite sharing the mutation, only the older sibling developed temporal lobe epilepsy (TLE). Transcriptomic analysis revealed downregulation of GABAergic pathway genes in both siblings’ neurons, aligning with SCN1A -associated epilepsy. However, neurons from the sibling with TLE exhibited additional abnormalities, including altered AMPA receptor subunit composition, changes in GABA A receptor subunits and chloride cotransporters expression, and reduced brain-derived neurotrophic factor (BDNF) levels, indicative of developmental immaturity. Voltage-clamp recordings confirmed impaired GABAergic and AMPA receptor-mediated synaptic activity. These findings suggest that combined GABAergic dysfunction, aberrant AMPA receptor composition, and reduced BDNF signaling contribute to the more severe phenotype and increased epilepsy susceptibility.

A febrile seizure is a seizure occurring in a child six months to five years of age that is accompanied by a fever (100.4°F or greater) without central nervous system infection. Febrile seizures are classified as simple or complex. A complex seizure lasts 15 minutes or more, is associated with focal neurologic findings, or recurs within 24 hours. The cause of febrile seizures is likely multifactorial. Viral illnesses, certain vaccinations, and genetic predisposition are common risk factors that may affect a vulnerable, developing nervous system under the stress of a fever. Children who have a simple febrile seizure and are well-appearing do not require routine diagnostic testing (laboratory tests, neuroimaging, or electroencephalography), except as indicated to discern the cause of the fever. For children with complex seizures, the neurologic examination should guide further evaluation. For seizures lasting more than five minutes, a benzodiazepine should be administered. Febrile seizures are not associated with increased long-term mortality or negative effects on future academic progress, intellect, or behavior. Children with febrile seizures are more likely to have recurrent febrile seizures. However, given the benign nature of febrile seizures, the routine use of antiepileptics is not indicated because of adverse effects of these medications. The use of antipyretics does not decrease the risk of febrile seizures, although rectal acetaminophen reduced the risk of short-term recurrence following a febrile seizure. Parents should be educated on the excellent prognosis of children with febrile seizures and provided with practical guidance on home management of seizures.

Febrile seizures (FS) is the most common type of convulsion in infants and preschool children. This study aimed to investigate the associations between gut microbiota abundance, plasma metabolites, circulating cytokines, and FS. Summary statistics of 211 gut microbiota traits, 1,400 plasma metabolite traits, 91 circulating cytokine traits, and FS were obtained from publicly available genome-wide association studies. Two-sample Mendelian randomization (MR) analysis and causality was inferred using Inverse variance-weighted (IVW), Weighted median, MR-Egger, simple mode-based estimate and weighted mode-based estimate 5 methods. Several sensitivity analyses were also used to ensure the robustness of the results. Furthermore, mediation analysis was used to determine the pathway from gut microbiota to FS mediated by plasma metabolites and circulating cytokines. MR revealed the associations of 1 gut microbiota (phylum Verrucomicrobia), 4 circulating cytokines and 50 plasma metabolites on FS. Based on the known pathogenic metabolites, we observed that the tryptophan, androgen, and sphingolipids pathways are associated with FS. Mediation analysis revealed 1 strongly documented plasma metabolite (Ascorbic acid 2-sulfate) as a mediator linking “gut microbiota to plasma metabolite to FS”. Sensitivity analysis was represented no heterogeneity or pleiotropy in this study.Our study provides some causal evidence concerning the effects of the gut microbiota, circulating cytokines, and plasma metabolites on FS, which needs to be verified in randomized controlled trials. These biomarkers provide new insights into the underlying mechanisms of FS and contribute to its prevention, diagnosis, and treatment.

Febrile seizures (FS), events associated with a fever in the absence of an intracranial infection, hypoglycaemia, or an acute electrolyte imbalance, occur in children between six months and six years of age. FS are the most common type of convulsions in children. FS can be extremely frightening for parents, even if they are generally harmless for children, making it important to address parental anxiety in the most sensitive manner. The aim of this review was to focus on the management of FS in the pediatric age. An analysis of the literature showed that most children with FS have an excellent prognosis, and few develop long-term health problems. The diagnosis of FS is clinical, and it is important to exclude intracranial infections, in particular after a complex FS. Management consists of symptom control and treating the cause of the fever. Parents and caregivers are often distressed and frightened after a FS occurs and need to be appropriately informed and guided on the management of their child’s fever by healthcare professionals. Due to the inappropriate use of diagnostic tests and treatments, it is extremely important to improve the knowledge of pediatricians and neurologists on FS management and to standardize the diagnostic and therapeutic work-up.

Background Febrile seizures (FS) represent the most common type of seizures in children; however, their exact pathogenesis remains incompletely understood. Currently, there is a lack of specific biomarkers for predicting FS occurrence, and existing prophylactic drug strategies remain controversial. Using untargeted metabolomics, this study investigates metabolic differences between children with FS and those with fever but without seizures (non-febrile seizures, NFS), aiming to elucidate the metabolic profile of FS and identify potential biomarkers, thereby providing new insights for clinical prediction and treatment. Methods Plasma samples were collected from 31 children with FS and 31 children with NFS. Untargeted metabolomic profiling was performed using high-performance liquid chromatography coupled with high-resolution mass spectrometry (HPLC-HRMS). Peak extraction and metabolite identification were conducted with the XCMS software. Differential metabolites were screened using both univariate and multivariate statistical analyses, followed by metabolic pathway enrichment analysis. A random forest algorithm was applied to construct a predictive model, and significantly altered metabolites were selected as candidate biological predictors. Results Children with FS exhibited significant metabolic disturbances across multiple pathways, including necroptosis, glycerophospholipid metabolism, linoleic acid metabolism, sphingolipid signaling, phagocytosis, ferroptosis, and sphingolipid metabolism. The random forest model identified 10 significantly altered metabolites as potential predictors: SM(d18:1/24:1), LysoPC(22:0/0:0), SM(d18:0/18:0), Cer(d18:1/16:0), LysoPC(24:0/0:0), 12,13-DHOME, diethanolamine, pantothenic acid, arachidonic acid, and 3-carbamoyl-2-phenylpropionaldehyde. The model demonstrated a predictive accuracy of 83% and achieved an area under the curve (AUC) of 0.98. Conclusion Patients with FS exhibited a distinct metabolic profile characterized by activated necroptosis, dysregulated lipid metabolism, and inflammatory imbalance. Metabolites such as arachidonic acid, lysophosphatidylcholines, and sphingolipids may serve as potential biomarkers and therapeutic targets. This study provides new metabolomic evidence for early prediction and targeted intervention of FS.

Febrile seizures during childhood are linked to the development of chronic epilepsy. Now, Ryuta Koyama and colleagues show that febrile seizures are associated with enhanced GABAergic excitation and ectopic granule cell migration in the hippocampus. Temporal lobe epilepsy (TLE) is accompanied by an abnormal location of granule cells in the dentate gyrus. Using a rat model of complex febrile seizures, which are thought to be a precipitating insult of TLE later in life, we report that aberrant migration of neonatal-generated granule cells results in granule cell ectopia that persists into adulthood. Febrile seizures induced an upregulation of GABA A receptors (GABA A -Rs) in neonatally generated granule cells, and hyperactivation of excitatory GABA A -Rs caused a reversal in the direction of granule cell migration. This abnormal migration was prevented by RNAi-mediated knockdown of the Na + K + 2Cl − co-transporter (NKCC1), which regulates the excitatory action of GABA. NKCC1 inhibition with bumetanide after febrile seizures rescued the granule cell ectopia, susceptibility to limbic seizures and development of epilepsy. Thus, this work identifies a previously unknown pathogenic role of excitatory GABA A -R signaling and highlights NKCC1 as a potential therapeutic target for preventing granule cell ectopia and the development of epilepsy after febrile seizures.