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Purpose: Since late 2019, coronavirus disease 2019 (COVID-19) has rapidly spread worldwide. Some children with COVID-19 present with seizures; in particular, studies have reported an increase in seizure episodes during the Omicron wave of the pandemic. This study was performed to describe the clinical characteristics of seizures among children hospitalized with COVID-19 before and during the Omicron wave. Methods: A retrospective cross-sectional study was conducted on all pediatric admissions for COVID-19 at Hospital Tunku Azizah from June 2021 to May 2022. Results: During this period, 1,586 children were admitted with COVID-19, of whom 111 (7.0%) experienced seizures. Patients with seizures were more likely to have a history of seizure (odds ratio [OR], 71.4; 95% confidence interval [CI], 23.7 to 215.2; P<0.001) and prior antiseizure medication use (OR, 55.1; 95% CI, 6.1 to 497.4; P<0.001). Most seizures (55.0%) occurred on the first day of illness, with 86.5% lasting less than 5 minutes. None of the children required intubation or admission to the pediatric intensive care unit, and all were discharged without complications. Between June 2021 and January 2022, the seizure rate varied from 1.3% to 3.4%; however, it increased to 18% in April 2022, coinciding with the period of Omicron variant predominance in Malaysia. Children admitted during the Omicron wave had significantly higher odds of experiencing seizures (OR, 7.89; 95% CI, 2.07 to 13.07; P<0.001) than children hospitalized prior to this wave. Conclusion: In conclusion, the study revealed a marked increase in seizures associated with pediatric COVID-19 cases during the Omicron wave. [ABSTRACT FROM AUTHOR]

Purpose Since late 2019, coronavirus disease 2019 (COVID-19) has rapidly spread worldwide. Some children with COVID-19 present with seizures; in particular, studies have reported an increase in seizure episodes during the Omicron wave of the pandemic. This study was performed to describe the clinical characteristics of seizures among children hospitalized with COVID-19 before and during the Omicron wave. Methods A retrospective cross-sectional study was conducted on all pediatric admissions for COVID-19 at Hospital Tunku Azizah from June 2021 to May 2022. Results During this period, 1,586 children were admitted with COVID-19, of whom 111 (7.0%) experienced seizures. Patients with seizures were more likely to have a history of seizure (odds ratio [OR], 71.4; 95% confidence interval [CI], 23.7 to 215.2; P

Purpose We aimed to analyze the clinical characteristics, recurrence, neurological outcomes, and the impact of coronavirus disease 2019 pandemic in children who visited 2 emergency departments (EDs) with febrile seizure (FS). Methods We retrospectively reviewed medical records of 3,172 episodes, involving 2,510 children aged 6-60 months whose diagnoses were FSs at the EDs in 2 hospitals from 2013 through 2022. Through the review, we analyzed clinical characteristics and associated factors for the recurrence of FS. As a sub-analysis, the variables were compared between before (2017-2019) and during (2020-2022) the pandemic. Results A total of 3,172 FS-related visits to the EDs were found in 2,510 children. Of these, 890 children (35.5%) underwent recurrences of FS. The recurrence of FS was associated with boys (63.3% vs. 57.8%; P = 0.007), seizures lasting longer than 5 minutes (16.6% vs. 12.7%; P = 0.007), family history of FS (23.7% vs. 16.2%; P < 0.001), complex FS (13.3% vs. 8.0%; P < 0.001), and epilepsy diagnosed thereafter (9.1% vs. 3.0%; P < 0.001). During the pandemic, we noted a decrease in the number of FS-related visits to the EDs (from 1,274 to 383), an increase in the percentage of complex FS (9.3% vs. 13.8%; P = 0.012), and a decrease in the percentage of recurrent FS (49.4% vs. 33.4%; P < 0.001), compared to before the pandemic. Conclusion Our study identified factors associated with recurrence of FS, and confirmed the increase in complex FS with the decrease in the recurrence during the coronavirus disease 2019 pandemic. These findings could be helpful when caring for children with FS in EDs.

Objective To summarize the clinical features and treatment of genetic epilepsy with febrile seizures plus (GEFS+) caused by SCN1A gene mutations, to improve the understanding of SCN1A gene mutations, and to provide a basis for the clinical diagnosis and treatment of this disease. Methods Clinical data were collected from a child with GEFS+ and her family members who attended Department of Neurology in our hospital, and the third-generation gene sequencing technique was used to perform genetic analysis and validation of peripheral blood DNA of the child and her parents and aunt. Results A girl, aged 7 years, was admitted to the hospital due to "paroxysmal seizures lasting for more than 4 years", with loss of consciousness during seizures and more seizures during pyrexia. The seizures increased after the use of oxcarbazepine and were controlled after the admi-nistration of sodium valproate. Her father had a history of seizures, while her aunt had no clinical symptoms. Third-generation gene sequencing showed the same heterozygous mutation, c.4787G>A(p.R1596H), in the SCN1A gene in the child and her father and aunt. Conclusion The onset of GEFS+ is associated with SCN1A gene mutations, but there is heterogeneity in clinical manifestations among patients in one family, and sodium channel blockers as anti-epileptic drugs will aggravate epileptic seizures in GEFS+.

Listeria monocytogenes is a rare cause of bacterial meningitis, particularly beyond the neonatal period. This article describes a 16-month-old girl who presented with a new-onset febrile status epilepticus, and subsequently developed altered mentality and lethargy. L. monocytogenes was detected on a point-of-care, multiplex polymerase chain reaction using the cerebrospinal fluid. On day 3, she developed a rapidly progressive hydrocephalus. Her consciousness improved after placement of an external ventricular drain. After 3-week antibiotic therapy, she was successfully discharged without residual complications.

Background Although febrile seizure (FS) is generally considered benign and self-limiting, there are differences regarding the risk factors, the prognosis, and the development of epilepsy.

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Introduction. Seizures associated with mild acute gastroenteritis are very common in early childhood. The aim of this study is to provide basic information about seizures associated with acute gastroenteritis in order to distinguish these two entities and contribute to proper diagnosis and treatment. Material and Methods. Data were collected retrospectively from the medical records of consecutive children admitted to the Pediatric Clinic due to seizures associated with mild acute gastroenteritis in the period from October 2021 to April 2022. Patients were divided into two groups: febrile and afebrile. We compared the demographic and clinical characteristics of these two groups, as well as the microbiological, neurophysiological and neuroradiological characteristics. Results. Of the children with acute gastroenteritis and seizures, 11 were afebrile and 20 were febrile, with male predominance. The most frequently identified enteropathogen was rotavirus. Most patients presented with generalized seizures. The comparison of febrile and afebrile patients showed that cluster seizures were more common in the afebrile group (p < 0.05). Seven patients had a seizure that lasted longer than 5 minutes and all of them were from the febrile group (p < 0.01). All patients presented with normal neuroimaging findings. Conclusion. In clinical settings, making a distinction between febrile and afebrile gastroenteritis-related seizures as separate entities can be very difficult. It is still unclear what effect fever has on the onset of gastroenteritis- associated seizures, and whether febrile and afebrile seizures have a distinctly different pathophysiological mechanism, which is why further research is needed. [ABSTRACT FROM AUTHOR]

Purpose We aimed to identify the factors associated with the repeated febrile seizures (RFS), defined as recurrent seizures during the same febrile illness. Methods We reviewed the medical records of children with febrile seizure who visited 4 academic emergency departments from October 2016 through September 2018. Differences were identified in variables regarding clinical and laboratory characteristics between the children with and without RFS. The RFS was the primary outcome. Logistic regression was conducted to identify factors associated with the occurrence of RFS. Results Among 1,551 children, 922 were included in the study, of whom, 198 (21.5%) underwent RFS. Of the children with RFS, 188 (94.9%) underwent the recurrences within the initial 24 hours. Logistic regression showed focal seizure (adjusted odds ratio, 6.67; 95% confidence interval, 2.37-18.82), venous pH < 7.31 (5.89; 3.13-11.08), and postictal drowsiness > 30 minutes (1.90; 1.30-2.78) as the factors for RFS. Conclusion In children with febrile seizure, focal seizure, acidosis, and prolonged postictal state may be independent risk factors for RFS. These findings may be informed to healthcare professionals and parents caring for children with febrile seizure.

Febrile infection-related epilepsy syndrome (FIRES) is a rare, catastrophic epileptic syndrome that strikes previously healthy children. Its pathogenesis is unknown, it has few treatments, and it is typically refractory. In FIRES, refractory status epilepticus or a cluster of seizures starts a few days after the onset of an acute febrile illness, and it may continue as drug-resistant epilepsy, with neuropsychological impairments occurring without latency. Clinical knowledge and guidelines on FIRES are limited because it is sporadic and extremely rare. To date, the absence of specific biomarkers poses a significant diagnostic challenge; nevertheless, early diagnosis is very important for optimal management. Despite treatment with multiple immunotherapies and anti-seizure medications, the majority of patients with FIRES are left with significant cognitive disabilities and refractory epilepsy. This review aims to highlight the most recent insights into the clinical features, terminology, epidemiology, pathogenesis, diagnostic challenges, and therapeutic options associated with FIRES.

Purpose Recognition of cardiogenic syncope caused by acute myocarditis masquerading as febrile seizures (FS) in children can be difficult in the emergency department (ED) before a cardiac work-up. We aimed to identify clinical and laboratory characteristics of children with seizure-like activity and fever caused by myocarditis that would enable their condition to be distinguished from benign FS. Methods We identified seven children who visited the ED for paroxysmal seizure-like activity with fever and were diagnosed with acute myocarditis between 2012 and 2015, as well as 204 children who were diagnosed with benign FS during the same period. A detailed retrospective review of the medical charts of both groups was conducted. Results Age at onset of seizure-like activity was much higher in the myocarditis group than in the FS group (4.4±1.9 years vs. 2.4±1.1 years, P=0.033). Body temperature at seizure-like activity onset was significantly lower in the myocarditis group than in the FS group (37.9°C±0.2°C vs. 38.7°C±0.6°C, P

Background: Febrile seizures (FS) are the most common seizure disorder in children and a common neurologic complication in children with coronavirus disease 2019 (COVID-19). This study aimed to identify differences in clinical characteristics and disease burden between FS with and without COVID-19., Materials and Methods: We conducted a retrospective analysis of medical data at our hospital from December 2019 to July 2023, focusing on hospitalized patients under the age of 14 diagnosed with FS who underwent COVID-19 polymerase chain reaction (PCR) testing. Descriptive statistics and analysis of variance were employed to compare the COVID-19 and non-COVID-19 groups in terms of clinical characteristics and disease burden., Results: A total of 514 patients were included, with 106 testing positive for COVID-19 and 408 testing negative. Patients with COVID-19 were older (34.87 ± 6.16 vs. 28.61 ± 11.35 months, P < 0.001) and had a higher proportion of males (79.2% vs. 62.3%, P = 0.001). The COVID-19 group had longer seizure durations (4.57 ± 4.38 vs. 3.22 ± 2.91 min, P = 0.006) and more complex FS (25.5% vs. 15.9%, P = 0.022). Laboratory tests showed lower lymphocyte counts in the COVID-19 group (1.87 ± 1.48 vs. 2.75 ± 1.51 × 103/µL, P < 0.001) and higher creatine kinase levels (158.49 ± 82.89 vs. 110.89 ± 56.11 U/L, P < 0.001). No significant differences were found in hospital costs, length of hospitalization, and intensive care unit admissions., Conclusion: Clinicians should be knowledgeable about the distinct clinical characteristics of FS in children with COVID-19. Despite distinct features, the prognosis remains favorable and does not require excessive intervention. Ongoing monitoring and research are needed to fully understand the impact of COVID-19 on FS and optimize management strategies., (© 2024. The Author(s).)

Purpose Cytokines demonstrate active roles in the occurrence of febrile seizures (FS). However, whether a genetic predisposition to inflammation is implicated in FS, febrile seizure plus (FS+) or genetic epilepsy with febrile seizure plus (GEFS+) are still unclear. Therefore we perform this study to find the association of promotor variants in pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) genes and anti-inflammatory cytokine interleukin 10 (IL-10) genes either with FS, FS+, and GEFS+ in Korean children. Methods Fifty-seven children with FS, 32 FS+, and 12 GEFS+ patients were compared with 108 controls. The allelic and genotypic distributions were compared for TNF-α-238 (rs361525), -308 (rs1800629), -857 (rs1799724), -863 (rs1800630), and IL-10-592 (rs1800872), -819 (rs1800871), -1082 (rs1800896), and -1352 (rs1800893). Results Allelic and genotypic frequencies of TNF-α and IL-10 promotor variants showed no significant differences between FS, FS+, and GEFS+ versus controls. However, AA genotypes at TNF-α-863 were present only in controls. TNF-α-863 (rs1800630) promoter variants showed an association with FS, FS+, and GEFS+ in a recessive mode of inheritance pattern (P

The GNOM (GN) Guanine nucleotide Exchange Factor for ARF small GTPases (ARF-GEF) is among the best studied trafficking regulators in plants, playing crucial and unique developmental roles in patterning and polarity. The current models place GN at the Golgi apparatus (GA), where it mediates secretion/recycling, and at the plasma membrane (PM) presumably contributing to clathrin-mediated endocytosis (CME). The mechanistic basis of the developmental function of GN, distinct from the other ARF-GEFs including its closest homologue GNOM-LIKE1 (GNL1), remains elusive. Insights from this study largely extend the current notions of GN function. We show that GN, but not GNL1, localizes to the cell periphery at long-lived structures distinct from clathrin-coated pits, while CME and secretion proceed normally in gn knockouts. The functional GN mutant variant GN fewerroots , absent from the GA, suggests that the cell periphery is the major site of GN action responsible for its developmental function. Following inhibition by Brefeldin A, GN, but not GNL1, relocates to the PM likely on exocytic vesicles, suggesting selective molecular associations en route to the cell periphery. A study of GN-GNL1 chimeric ARF-GEFs indicates that all GN domains contribute to the specific GN function in a partially redundant manner. Together, this study offers significant steps toward the elucidation of the mechanism underlying unique cellular and development functions of GNOM., Competing Interests: MA, IM, JF No competing interests declared, (© 2024, Adamowski et al.)

Background and Objectives: More than 2,900 US children aged younger than 4 years die from unknown causes each year, accounting for more than 219,000 life years lost annually. They are mostly sleep-related and unwitnessed with unremarkable autopsies, limiting our understanding of death mechanisms. We sought to understand potential mechanisms of death by evaluating videos of sudden deaths in toddlers., Methods: In our registry of 301 sudden unexplained child deaths, a series of 7 consecutively enrolled cases with home video recordings of the child's last sleep period were independently assessed by 8 physicians for video quality, movement, and sound., Results: Four boys and 3 girls (13-27 months at death) with terminal videos shared similar demographic features to the 293 other registry cases without video recordings. Five video recordings were continuous and 2 were triggered by sound or motion. Two lacked audio. All continuous recordings included a terminal convulsive event lasting 8-50 seconds; 4 children survived for >2.5 minutes postconvulsion. Among discontinuous videos, time lapses limited review; 1 suggested a convulsive event. Six were prone with face down, and 1 had autopsy evidence of airway obstruction. Primary cardiac arrhythmias were not supported; all 7 children had normal cardiac pathology and whole-exome sequencing identified no known cardiac disease variants., Discussion: Audio-visual recordings in 7 toddlers with unexplained sudden deaths strongly implicate that deaths were related to convulsive seizures, suggesting that many unexplained sleep-related deaths may result from seizures.

Mutations of the SCN1A gene, which encodes the voltage-dependent Na + channel's α subunit, are associated with diverse epileptic syndromes ranging in severity, even intra-family, from febrile seizures to epileptic encephalopathy. The underlying cause of this variability is unknown, suggesting the involvement of additional factors. The aim of our study was to describe the properties of mutated channels and investigate genetic causes for clinical syndromes' variability in the family of five SCN1A gene p.Arg1596Cys mutation carriers. The analysis of additional genetic factors influencing SCN1A -associated phenotypes was conducted through exome sequencing (WES). To assess the impact of mutations, we used patch clamp analysis of mutated channels expressed in HEK cells and in vivo neural excitability studies (NESs). In cells expressing the mutant channel, sodium currents were reduced. NESs indicated increased excitability of peripheral motor neurons in mutation carriers. WES showed the absence of non-SCA1 pathogenic variants that could be causative of disease in the family. Variants of uncertain significance in three genes, as potential modifiers of the most severe phenotype, were identified. The p.Arg1596Cys substitution inhibits channel function, affecting steady-state inactivation kinetics. Its clinical manifestations involve not only epileptic symptoms but also increased excitability of peripheral motor fibers. The role of Nav1.1 in excitatory neurons cannot be ruled out as a significant factor of the clinical phenotype.

Objective: This study aimed to assess the prevalence and characteristics of epilepsy in dystrophinopathies within a cohort of 142 patients at a tertiary neuromuscular center in Istanbul, Turkey., Methods: We recorded the age at seizure onset, seizure type, family history, history of febrile seizures, treatment, and EEG results. Epilepsy was classified according to the latest International League Against Epilepsy (ILAE) classification., Results: Of the 142 DMD patients, 8 experienced epileptic seizures (5.6 %). The median age of the patients was 11 years (8.0-15.2). The median age for the first DMD symptoms was 24 months (16.5-37.5). All seizures were consistent with generalized tonic-clonic seizures. Three patients are currently on anti-seizure medication., Significance: The prevalence of epilepsy in our study (5.6 %) exceeds that of the general pediatric population (0.5-1 %). However, the frequency of febrile seizures in children with dystrophinopathy is similar to that of the general population., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: High mobility group box-1 (HMGB1) is an endogenous danger signal that mediates activation of the innate immune response including NLR pyrin domain containing 3 (NLRP3) inflammasome activation and proinflammatory cytokine release. Although HMGB1 and NLRP3 have been implicated in the pathophysiology of seizures, the correlation between HMGB1 and NLRP3 expression has not been determined in children with febrile seizures (FS). To explore the relationship between extra-cellular HMGB1 and NLRP3 in children with FS, we analyzed serum HMGB1, NLRP3, caspase-1, and proinflammatory cytokines in patients with FS., Methods: Thirty children with FS and thirty age-matched febrile controls were included in this study. Blood was obtained from the children with FS within 1 h of the time of the seizure; subsequently, the serum contents of HMGB1, NLRP3, caspase-1, interleukin (IL)-1β, interleukin (IL)-6, and tumour necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay. The Mann‒Whitney U test was used to compare serum cytokine levels between FS patients and controls. Spearman's rank correlation coefficient was calculated to detect significant correlations between cytokine levels., Results: Serum levels of HMGB1, NLRP3, caspase-1, IL-1β, IL-6, and TNF-α were significantly higher in FS patients than in febrile controls (p < 0.05). Serum levels of HMGB1 were significantly correlated with levels of NLRP3 and caspase-1 (both, p < 0.05). Serum levels of caspase-1 were significantly correlated with levels of IL-1β (p < 0.05). Serum levels of IL-1β were significantly correlated with levels of IL-6 and TNF-α (p < 0.05)., Conclusions: HMGB1 is up-regulated in the peripheral serum of FS patients, which may be responsible, at least in part, for the increased expression of NLRP3 and Caspase-1. Increased expression of caspase-1 was significantly associated with elevated serum levels of IL-1β. Given that activated Caspase-1 directly regulates the expression of mature IL-1β and positively correlates with activation of the NLRP3 inflammasome, our data suggest that increased levels of peripheral HMGB1 possibly mediate IL-1β secretion through the activation of the NLRP3 inflammasome in children with FS. Thus, both HMGB1 and NLRP3 might be potential targets for preventing or limiting FS., (© 2024. The Author(s).)

Background: Neurological complications with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) omicron variant have been reported in adults; however, there are little data in the pediatric population. We aimed to report on the prevalence and clinical characteristics of children with neurological symptoms during the SARS-CoV-2 omicron wave., Methods: This was a single-center, retrospective cohort review of children (<18 years old) hospitalized for SARS-CoV-2 infection from December 2, 2021, to June 30, 2022., Results: During the study period, 455 children (mean age 4.8 years, range 0.67 to 18, male 58.9%) were hospitalized with SARS-CoV-2 infection. A total of 108 (23.7%) children experienced neurological symptoms; most common were seizures (62.0%), headaches (32.4%) and giddiness (14.8%). Seizures included febrile seizures (64.1%), acute symptomatic seizures (17.9%), and breakthrough seizures in known epileptics (17.9%). Children with neurological manifestations were older (7.3 vs 4.0 years, P < 0.00001), more likely to have underlying epilepsy (9.3% vs 1.2%, P = 0.0002) or neurodevelopmental disorders (17.6% vs 1.7%, P < 0.00001), and presented earlier in their illness (2.1 vs 2.8 days, P < 0.00001), compared with those without neurological manifestations. Neurological symptoms fully resolved in all but one patient at discharge. There were no mortalities and no difference in duration of hospitalization (3.1 vs 3.7 days, P = 0.5) between the groups., Conclusions: One in four hospitalized children with SARS-CoV-2 infection when omicron variant was dominant experienced mild neurological symptoms. Overall risk factors for neurological symptoms associated with SARS-CoV-2 included older age, pre-existing febrile seizures/epilepsy and neurodevelopmental disorders., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Aim: Electroencephalogram (EEG) is specific, but not sensitive, for the diagnosis of epilepsy. This study aimed to correlate the clinico-electrographic and radiological features of seizure disorders in children attending a tertiary care centre in northern India., Methods: Children aged between one to 18 years with seizure episodes were included. Clinical details, including historical as well as physical findings, were evaluated along with EEG and neuroimaging (Magnetic resonance imaging). Details were noted on pre-designed proforma. Variables were analysed by using appropriate statistical methods., Results: A total of 110 children with seizures were enrolled in the study. Male to female ratio was 1.6: 1, and the mean age of the study children was 8 years. The majority of the children were symptomatic for more than one year. The most common seizure type was Generalised Tonic Clonic Seizure (GTCS), and Hypoxic-ischemic Encephalopathy (HIE) sequelae was the most commonly attributed etiology, followed by neurocysticercosis. EEG and neuroimaging findings were found to correlate well with seizure semiology from history. The incidence of febrile seizures was 10% in this study, with nearly three-fourths of them being simple febrile seizures., Conclusion: Microcephaly and developmental delay were the most distinctive clinical correlates in children with seizures. There was a fair agreement between the types of seizures described in history and depicted on EEG with Cohen's kappa of 0.4. Also, there was a significant association between the type of seizures on EEG and the duration of symptoms., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Purpose: To study seizure manifestations and outcomes in children with cortical versus white matter injury, differences potentially explaining variability of epilepsy in children with cerebral palsy., Methods: In this population-based retrospective cohort study, MRIs of children with cerebral palsy due to ischemia or haemorrhage were classified according to presence or absence of cortical injury. MRI findings were then correlated with history of neonatal seizures, seizures during childhood, epilepsy syndromes, and seizure outcomes., Results: Of 256 children studied, neonatal seizures occurred in 57 and seizures during childhood occurred in 93. Children with neonatal seizures were more likely to develop seizures during childhood, mostly those with cortical injury. Cortical injury was more strongly associated with (1) developing seizures during childhood, (2) more severe epilepsy syndromes (infantile spasms syndrome, focal epilepsy, Lennox-Gastaut syndrome), and (3) less likelihood of reaching > 2 years without seizures at last follow-up, compared to children without cortical injury. Children without cortical injury, mainly those with white matter injury, were less likely to develop neonatal seizures and seizures during childhood, and when they did, epilepsy syndromes were more commonly febrile seizures and self-limited focal epilepsies of childhood, with most achieving > 2 years without seizures at last follow-up. The presence of cortical injury also influenced seizure occurrence, severity, and outcome within the different predominant injury patterns of the MRI Classification System in cerebral palsy, most notably white matter injury., Conclusions: Epileptogenesis is understood with cortical injury but not well with white matter injury, the latter potentially related to altered postnatal white matter development or myelination leading to apoptosis, abnormal synaptogenesis or altered thalamic connectivity of cortical neurons. These findings, and the potential mechanisms discussed, likely explain the variability of epilepsy in children with cerebral palsy and epilepsy following early-life brain injury in general., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Adenovirus is a major pathogen causing febrile illness among children. It may also cause acute encephalitis/encephalopathy. This study aimed to elucidate the clinical features of adenovirus-associated encephalitis/encephalopathy (AdVE) among children in Japan., Methods: A nationwide survey of children with AdVE was conducted. An initial survey was distributed among pediatricians to obtain information about children with AdVE treated between January 2014 and March 2019. A second survey was used to obtain the clinical information of children with AdVE from hospitals that responded to the initial survey and those identified from a literature search of the reported cases. We collected demographic data and information about symptoms of infection, neurological symptoms, laboratory parameters, treatment, and outcomes. Outcomes were determined using the Pediatric Cerebral Performance Category Score., Results: Clinical information was available for 23 children with a median age of 39 months. Two had preexisting neurological disorders and six had a history of febrile seizures. The outcome was good in 15 patients and poor in eight patients. Serum lactate dehydrogenase, glucose, and ammonia levels were higher among children with a poor outcome compared to those with a good outcome. Clinically mild encephalitis/encephalopathy with a reversible splenial lesion was the most common type (n = 8), followed by acute encephalopathy with biphasic seizures and late reduced diffusion (n = 7)., Conclusion: A prior history of febrile seizures was frequent in children with AdVE. Several different subtypes of acute encephalopathy were seen in children with AdVE, and the outcome was poor in those with acute encephalopathy with biphasic seizures and late reduced diffusion and hemorrhagic shock and encephalopathy syndrome. Elevated lactate dehydrogenase, glucose, and ammonia levels on admission were found to correlate with a poor outcome., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.)

Purpose: Recognition of cardiogenic syncope caused by acute myocarditis masquerading as febrile seizures (FS) in children can be difficult in the emergency department (ED) before a cardiac work-up. We aimed to identify clinical and laboratory characteristics of children with seizure-like activity and fever caused by myocarditis that would enable their condition to be distinguished from benign FS. Methods: We identified seven children who visited the ED for paroxysmal seizure-like activity with fever and were diagnosed with acute myocarditis between 2012 and 2015, as well as 204 children who were diagnosed with benign FS during the same period. A detailed retrospective review of the medical charts of both groups was conducted. Results: Age at onset of seizure-like activity was much higher in the myocarditis group than in the FS group (4.4±1.9 years vs. 2.4±1.1 years, P=0.033). Body temperature at seizure-like activity onset was significantly lower in the myocarditis group than in the FS group (37.9°C±0.2°C vs. 38.7°C±0.6°C, P<0.001). Prodromal symptoms were significantly different, with nausea/vomiting (85.7% vs. 1.5%, P<0.001), abdominal pain (42.9% vs. 0.0%, P=0.021), and lethargic mentality (57.10% vs. 0.0%, P=0.015) being more frequent in the myocarditis group. The initial laboratory findings significantly differed between the two groups, with higher levels of liver enzymes, lactate dehydrogenase, creatinine, uric acid, creatine kinase, and potassium in the myocarditis group. Conclusion: Prodromal symptoms and initial laboratory results were significantly different between the myocarditis and FS groups. A good clinical history and laboratory findings can be helpful for differentiating cardiogenic syncope from benign FS. [ABSTRACT FROM AUTHOR]