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febrile seizures in Children at the Departmental Teaching Hospital of OuéméPlateau: Etiologies and Risk Factors for Death

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Open Journal of Pediatrics 2022年第2期12卷 364-375页

作者： Caroline Padonou Gilles Bognon Lutécia Zohoun Florence Alihonou Mauriella Edjrokinto Gratien Sagbo Pediatric Department Departmental Teaching Hospital of Ouémé Plateau Porto-Novo Benin Pediatric Department National Teaching Hospital-Hubert Koutoukou Maga Porto-Novo Benin

Background: febrile seizures are the most frequent neurological disorder in pediatrics. They have multiple etiologies and require urgent management. The aim of this survey was to study febrile seizures in children at the Departmental Teaching Hospital of Ouémé Plateau (DTH/OP). Method: This was a cross-sectional survey, conducted from January 1, 2020, to December 31, 2020, in the pediatric department of the DTH/OP. Children aged 1 month to 18 years, hospitalized for febrile seizures recognized at the anamnesis and/or during the physical examination were included in this study. Results: The frequency of seizures was 17.08% (510/2986). The male to female ratio was equal to 1.4. The mean age was 44.27 ± 40.75 months. The seizure was generalized tonic-clonic in 77.9% of cases and localized in 11.6% of cases. The main etiologies were severe malaria (75.5%), sepsis (21.6%), enteric infections (14.9%) and pneumonia (10.2%). Diazepam was the anticonvulsant treatment used in the first intention (79.7%). Most of the children were hospitalized for 3 to 7 days. The recovery rate was 82.3% and the fatality rate was equal to 17.7%. Eight children presented sequelae. There was a statistically significant link between the children’s clinical outcome and age (p febrile seizures were frequent in the pediatric emergency department of the DTH/OP. There is a need to intensify sensitization on malaria prevention measures in the community and improve case management at the hospital.

关键词： febrile seizures Severe Malaria Sepsis Child

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Effects of febrile seizures in mesial temporal lobe epilepsy with hippocampal sclerosis on gene expression using bioinformatical analysis

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Acta Epileptologica 2020年第1期2卷 174-184页

作者： Yinchao Li Chengzhe Wang Peiling Wang Xi Li Liemin Zhou The Seventh Affiliated Hospital Sun Yat-sen University Shenzhen 518107 China

Background:To investigate the effect of long-term febrile convulsions on gene expression in mesial temporal lobe epilepsy with hippocampal sclerosis(MTLE-HS)and explore the molecular mechanism of MTLE-HS.Methods:Microarray data of MTLE-HS were obtained from the Gene Expression Omnibus database.Differentially expressed genes(DEGs)between MTLE-HS with and without febrile seizure history were screened by the GEO2R software.Pathway enrichment and gene ontology of the DEGs were analyzed using the DAVID online database and FunRich software.Protein–protein interaction(PPI)networks among DEGs were constructed using the STRING database and analyzed by Cytoscape.Results:A total of 515 DEGs were identified in MTLE-HS samples with a febrile seizure history compared to MTLEHS samples without febrile seizure,including 25 down-regulated and 490 up-regulated genes.These DEGs were expressed mostly in plasma membrane and synaptic vesicles.The major molecular functions of those genes were voltage-gated ion channel activity,extracellular ligand-gated ion channel activity and calcium ion binding.The DEGs were mainly involved in biological pathways of cell communication signal transduction and transport.Five genes(SNAP25,SLC32A1,SYN1,GRIN1,and GRIA1)were significantly expressed in the MTLE-HS with prolonged febrile seizures.Conclusion:The pathogenesis of MTLE-HS involves multiple genes,and prolonged febrile seizures could cause differential expression of genes.Thus,investigations of those genes may provide a new perspective into the mechanism of MTLE-HS.

关键词： Bioinformatical analysis febrile seizures Epilepsy Hippocampal sclerosis

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febrile seizures lead to inheritance of memory defect mediated by hypermethylation of reelin gene in rats

Febrile seizures lead to inheritance of memory defect mediat...

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中国神经科学学会第十届全国学术会议

作者： Yun-Jian DAI Deng-Chang WU Bo FENG Yang-Sun TANG Zhong CHEN Institute of Neuroscience Department of PharmacologyCollege of Pharmaceutical SciencesZhejiang University

Objective febrile seizures(FSs) are the most common types of seizures in young children.Whether febrile seizures cause memory impairment that proceeds into adulthood is still in conflict.In addition,previous studies found that diseases induced by early-life environmental exposures influenced the aspects of behavior not only in affected individuals but also in their future offspring.Here we want to know whether the memory deficits after FSs could be transmitted to subsequent generation and if DNA methylation contributed to this transgenerational transmission.Methods Memory deficits were evaluated by Morris water maze,inhibitory avoidance task and contextual fear condition.Expression of DNA methyltransferases(DNMTs) and reelin were measured by RT-PCR and western blot.Rats of P9 were given DNMT inhibitor(zebularine) immediately after FSs and then daily for the following 5 days.Results(1) Acquired FSs lead to memory deficits in affected rats and their offspring.(2) DNMT1 mRNA was up-regulated in FSs rats and their offspring.(3) DNA hypennethylation after FSs lead to transcriptional silencing of the synaptic plasticity gene reelin.(4) DNMT inhibitor rescued the memory deficits in FSs rats and their offspring by preventing the hypennethylation of reelin gene.Conclusion FSs caused functional impairment in the hippocampus of adult rats and their offspring,and that DNA hypermethylation of reelin gene underling the cellular mechanism for the impaired memory function in these rats.

关键词： febrile seizures DNA methylation reelin Memory

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Microglial displacement of GABAergic synapses decreases cortical neuronal excitability during complex febrile seizures

Microglial displacement of GABAergic synapses decreases cort...

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中国神经科学学会第十二届全国学术会议

作者： Yu-Shan WAN Bo FENG Wei-Wei HU Zhong CHEN Department of Pharmacology Key Laboratory of Medical Neurobiology of The Ministry of Health of China School of Basic Medical Sciences College of Pharmaceutical Sciences Zhejiang University

Microglia can be activated by acute insults and chronic disease states. Recent studies have reported microglia-mediated synaptic displacement in the adult CNS while the contribution remains unclear. Fever-induced seizures（FS） are the most common form of infantile seizures, one-third of them are ‘complex’. The mechanisms of complex seizures remain unknown despite enormous studies have focused on it. In the present study, we observed that complex FS significantly activated microglia with robust morphology alteration. We then performed 3-D image reconstruction and observed that microglia significant ensheathed neurons and displaced axosomatic GABAergic synapses. Specific patch-clamp of microglia associated and non-associated neuron showed that microglia-mediated synaptic stripping displacement modified the frequency of spontaneous GABA-PSC, without affecting the GABA reversal potential. Moreover, treatment of lipopolysaccharide（LPS） and TRAM 34 changed the extent of synaptic stripping, latency to hyperthermia-induced seizures, suggesting that displacement of GABAergic terminals by activated microglia performs endogenous neuroprotective action. Collectively, these observations delineate a potential target to prevent occurrence of complex FS.

关键词： febrile seizures Microglia Synaptic displacement

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Effect of GABRG2 mutations on the GABAA receptor and other genes associated with generalized epilepsy with febrile seizures plus

Effect of GABRG2 mutations on the GABAA receptor and other g...

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第十五届中国医师协会神经外科医师年会

作者： Xinxiao Li Shengnan Guo Haigang Chang Feng Wang Tao Sun Ningxia Key Laboratory of Cerebrocranial Disease The Incubation Base of National Key LaboratoryNingxia Medical University Department of Neurosurgery General Hospital of Ningxia Medical University Department of Physiology Ningxia Medical University

Objective We constructed an GABRG2 gene knockout model using CRISPR/Cas9 genome editing technology to deprive the GABRG2 function in vitro.METHODS To design three different sgRNA sequence and synthesize the oligonucleotides corresponded to the sgRNA sequence to construct the CRISPR/Cas9 gene konck-out plasmids,PX459-GABRG2.The constructed plasmids were transfected into HT22 cells and the whole genomic DNA were extracted,short chain PCR sequencing analysis was performed to evaluate the activities of constructed plasmids.Then establish the stablae cell lines with PX459-GABRG2 plasmids,western blot assay was employed to check the effects of GABRG2 gene knock-out,those with best gene knock-out cell lines were used for the further experiments.Next we preformed genome-wide transcriptional profiling of GABRG2 cell lines.RESULTS The results of enzyme cutting,and DNA sequencing demonstrated that the GABRG2 sgRNA 1,2 and 3 wre successfully inserted into PX459 plasmid.The sgRNA sequences and the ORF were correct and consistent with the design.Based on the mutation and part DNA sequence missing when analyzed DNA sequencing,these results demonstrated that PX459-GABRG2 1,2 and 3 are active.Plasmids PX459-GABRG2 1,2 and 3 were transfected into HT22 cells and selected with puromycin to estblish the stable cell lines.The results of western blot demonstrated that GABRG2 gene was knock-out,GABRB2 and MMP13 expression level in the cells declined remarkably.CONCLUSIONS Sucessfully constructed GABRG2 gene knock-out plasmids,and all the activities of plasmids were evaluated.GABRG2 plays a key role in the regulatory effects of GABRB2 and MMP13 genceexperssion.A bief,rapid temperature rise can reduce GABRB2 receptors and MMP13,the mechanism of this regullation could be the reason of FS.

关键词： CRISPRSY/Cas9 GABRG2 febrile seizures HT22

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Transient augment of IL1β promotes seizure susceptibility via upregulating CB1 receptor in prolonged febrile seizures

Transient augment of IL1β promotes seizure susceptibility v...

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中国神经科学学会第十届全国学术会议

作者： Bin CHEN Bo FENG Yang-Shun TANG Deng-Chang WU Yun-Jian DAI Shi-Hong ZHANG Zhong CHEN Institute of Neuroscience Department of PharmacologyCollege of Pharmaceutical SciencesZhejiang University Department of Neurology First Affiliated HospitalZhejiang University School of Medicine

Objective The aim of this study was to discuss whether the transient augment of cytokine ILlp in hippocampus after prolonged febrile seizures promotes seizure susceptibility in later life and the mechanism about the effect of ILlp.Methods febrile seizures(FS) were induced by exposing rat or mouse pups(P8-10) to a hyperthermal chamber(44 + 2℃) to raise the body temperature with stereotyped behaviors and typical epileptic EEG.Interleukin 1receptor antagonist(IL-lra) was injected intracerebrally after FS.Besides,ILlβ was injected intracerebrally alone to normal pups(P8-10) or IL1R1 mice.Furthermore,CBl receptor antagonist SR141716A(i.p.) was injected after FS and ILlβ-treatment.When the pups became adults,they were treated with Maximal electroshock(MES) or kainic acid.The expression of ILlp and CBl receptor was measured by Western Blotting.RNA interference was used to knock down the expression of CB1R on mice.Results We found that:(1) IL-lra reversed the enhanced susceptibility of MES-induced seizures only when injected immediately and 12h after FS.(2) ILlp alone increased both the susceptibility of MES-induced seizures,whereas IL1R1 mice were resistant to seizures after prolonged FS or ILl p-injection.(3) Prolonged FS and ILlp upregulated expression of CBl receptor in long-term(at least to 50 days);and ILlra reversed this effect;(4) CBl receptor antagonist SR141716A and siRNA-CBlR prevented the enhanced susceptibility of MES-induced seizures,after prolonged FS or ILl p-injection.Conclusion Our study indicated that transient augment of ILlp in hippocampus after prolonged FS promotes seizure susceptibility in later life modulating endocannabinoid signaling.

关键词： febrile seizures IL1β IL-1ra CB1 receptor seizure susceptibility

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Partial epilepsy with antecedent febrile seizures plus characterized by antiepileptic drugs-induced seizure aggravation and loss of function of Nav1.1

Partial epilepsy with antecedent febrile seizures plus chara...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Wei-Ping LIAO~*,Yi-Wu SHI,Yue-Sheng LONG,Yang ZENG,Tao SU,Na HE,Bing-Mei LI,Xiao-Rong LIU, Yong-Hong YI Institute of Neuroscience and the Second Affiliated Hospital,Guangzhou Medical College,Guangzhou 510260,China

＜正＞Objective Generalized epilepsy with febrile seizures plus（GEFS+）and severe myoclonic epilepsy in infancy（SMEI）are associated with sodium channel a-subunit type-1 gene（SCNIA）mutations,although previous studies failed to correlate the functional defects（funotypes）with phenotypes.febrile seizures and partial epilepsy are the two common features of GEFS+ and SMEI.It is thus suspected that partial epilepsy with antecedent febrile seizures（PEFS+）may also be a phenotype of SCNIA abnormalities.Seizure aggravation induced by antiepileptic drugs（AEDs）,a feature of SMEI,is considered here as a clue to find SCNIA mutations in isolated PEFS+ patients. Methods Two isolated PEFS+ patients with AEDs-induced seizure aggravation were screened for mutations in SCNIA,SCN2A,SCN1B,and GABRG2 using denaturing high-performance liquid chromatography and direct sequencing.The biophysiological features of two newly defined mutants were studied in transfected tsA201 cells using whole-cell patch-clamp technique.To characterize PEFS+ biologically,the genotype-funotype-phenotype relationships in all previously reported SCNIA mutations were analyzed.Results One PEFS+ patient each had heterozygous de novo mutations of c.2837G＞A/p.R946H and c.5295 T＞A/p.F1765L in SCNIA,which cause the loss of function of the mutants.With the defining of PEFS+,classifying the funotype in detail,and considering the subtle differences in the amino acid substitution,a close genotype-funotype-phenotype relationship was found in epilepsies with SCNIA mutations at a submolecular level.GEFS+ is clinically mild,with also mild channel dysfunction and mutations outside the pore region.PEFS+ is clinically similar to GEFS+,but distinct from GEFS+ in its funotype and AEDs-induced seizure aggravation.PEFS+ is much milder than SMEI clinically,similar to SMEI biophysiologically with features of loss of function but less in degree,structurally different from SMEI by substitutions without changes in polarity. Conclusions PEFS+ may be a distinct phenotype of SCNIA mutations.Sodiu

关键词： SCN1A channelopathy partial epilepsy febrile seizures sodium channel

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Temporal lobe epilepsy associated with human herpes virus 6

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Acta Epileptologica 2021年第1期3卷 71-76页

作者： Jiaqi Wang Jinmei Li Department of Neurology West China HospitalSichuan UniversityChengdu 610041SichuanChina

Human herpes virus 6(HHV-6)is a ubiquitous and most common pathogen that affects humans.Human herpes virus 6B(HHV-6B)is a wide spread human herpesvirus that infects most people when they are children,establishes latent infections in the central nervous system(CNS),especially in the hippocampus and amygdala,and induces neurologic diseases.HHV-6 can establish a latent infection and be reactivated by various stimuli.Recently,viral genomic DNA of HHV-6B has been detected in surgically removed brain tissues of intractable epilepsy patients,suggesting the involvement of HHV-6B in the pathogenesis of epilepsy.Temporal lobe epilepsy(TLE)has been shown to be closely related with HHV-6B.TLE patients with HHV-6B in their brains suffer from reiterative attacks of febrile seizures and hippocampal sclerosis.However,the mechanisms underlying the contribution of this virus to the development of TLE remains unknown.The direct damage and immune activation caused by the virus are involved in the process of neuron damage,abnormal neural circuit formation and glial cell proliferation.In addition,some cytokines like interleukin-17A(IL-17A),nuclear factor-kappa B(NF-κb),transforming growth factor-β(TGF-β),mitogen-activated protein kinase(MAPK)and phospholipase A2 are up-regulated and involved in the pathological process of TLE.More studies are needed to clarify the mechanisms underlying the link between HHV-6B and epilepsy,and identify biomarkers to recognize different patient groups for anti-inflammatory or immunomodulatory therapies.

关键词： HHV-6 Epilepsy Mesial temporal lobe epilepsy Astrocytes febrile seizures

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The characteristics of the transmission of enhanced susceptibility after acquired febrile seizure in rats

The characteristics of the transmission of enhanced suscepti...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Bo FENG,Yun-Jian DAI,Deng-Chang WU,Shi-Hong ZHANG,Zhong CHEN~* Department of Pharmacology Key Laboratory of Medical Neurobiology of Ministry of Health of China Zhejiang Province Key Laboratory of Neurobiology College of Pharmaceutical Sciences,Zhejiang University, Hangzhou 310058,China

Objective Early exposure to enriched environment may deeply influence the developing synaptic plasticity and this effect can transmit to offspring.Prolonged febrile seizures(FSs) are associated with a risk of subsequent temporal lobe epilepsy.In this study,we tested whether this acquired enhancement of susceptibility can be transmitted to offspring,and what is the risk factor during this transmission.Methods Prolonged seizures were evoked by exposing rat pup(9) to a hyperthermic environment of(44±2)℃.Kainic acid,pentylenetetrazol(PTZ) and maximal electroshock(MES) were used to test the seizure susceptibility in rats that experienced FSs(FO) and the susceptibility of seizures in the following 2 generations(Fl,F2) was tested as well.FSs mothers were mated with non-FSs fathers and vice versa to reveal which parent contributed to the transmissional phenomenon.Results(ⅰ) Both MES and kainic acid induced higher scores of seizures in the Fl-FSs rats,while there is no significant difference in PTZ induced seizures compared with those of control rats,(ⅱ) There was no significant difference in scores of MES-induced epilepsy between the F2 control and FSs groups,(ⅲ) Offspring of FO rats that had experienced 10 FSs displayed higher scores to MES-induced seizures than that of offspring in control group and 4*2 FSs group;however, offspring of FO rats that had experienced 4*2 FSs did not display significant difference to MES-induced seizures, (iv) Scores of MES-induced seizures in Fl rats mated by FSs mother and non-FSs father are higher than that by FSs father and non-FSs mother.Conclusion These results indicate that(1) the transgenerational transmission showed severity-dependent and model-dependent characteristics;and(2) the transgenerational transmission was limited to Fl generation through the mother.Our finding may suggest non-Mendelian transgenerational inheritance play a role in the epileptogenesis.

关键词： febrile seizures kainic acid pentylenetetrazol maximal electroshock transmission

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The role of desensitization of G-protein-activated inward rectifier potassium(GIRK) channels in the development of febrile seizure

The role of desensitization of G-protein-activated inward re...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Ying-Ying WANG~1,Jiong QIN~(1,*),Ying HAN~1,Jie CAI~2,Guo-Gang XING~(2,*) 1 Department of Pediatrics,Peking University First Hospital,Beijing 100034,China 2 Neuroscience Research Institute and Department of Neurobiology,Peking University,Beijing 100191,China

febrile seizures(FS),or fever-induced seizures,are the most common form of seizures during childhood and have been associated with an increased risk of epilepsy later in life.It has been suggested that hyperthermia (temperature of≥38.4℃) during fever plays a crucial role in generation of FS.However,the mechanisms underlying the pathogenesis of hyperthermia-induced seizures are poorly understood.In previous studies,we and others have suggested that GABA receptors are likely to be associated with FS.In this study,by using whole-cell patch-clamp recording techniques,we demonstrated that hyperthermia(39-40℃) provoked a "febrile seizure-like event" expressed as spontaneous,recurrent,epileptiform discharges(SREDs) followed by a series of sustained depolarizations(SDs) in cultured rat cortical neurons(7-14 DIV).The SREDs were characterized by abruptly developing,paroxysmal depolarizing shifts(PDS) of membrane potential with high-frequency spike firing characteristic of electrographic seizures.Hyperthermia also induced persistent neuronal hyperexcitability as assessed by their intrinsic electrogenic characteristics,including decreased:baseline resting potential(RP),input resistance(R),amplitude,duration and afterhyperpolarization(AHP) of spontaneous action potentials and,decreased absolute value of the threshold potential (TP) and threshold current(I) for evoking the cell firing,shortened duration,decreased inter-spike intervals(ISI) as well as increased firing frequency of evoked action potentials.Baclofen(100μM),a specific GABA receptor agonist, significantly repressed the hyperthermia-induced neuronal hyperexcitability and epileptiform discharges in cultured cortical neurons,and these effects were prevented by treatment with the GABA receptor antagonist phaclofen. Moreover,hyperthermia elicited fast desensitization of G-protein activated inwardly rectifying K(GIRK) channels in cultured cortical neurons,whereas overexpression of GIRK1 and GIRK2 genes in cultured cortical cells could rescue the hyperthermia-induced neur

关键词： febrile seizures epileptiform discharges hyperthermia GABAB receptors GIRK channels cortical neurons

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