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We performed virological analysis of resected brain tissues from a patient with temporal lobe epilepsy associated with mesial temporal sclerosis after febrile status epilepticus caused by human herpesvirus 6 infection. The patient had febrile status epilepticus at 9 months of age associated with human herpesvirus 6 infection. Magnetic resonance imaging revealed reduced water diffusion in the right temporal lobe and hippocampus. Polymerase chain reaction analysis detected 1.6 × 105 copies/μg of human herpesvirus 6 DNA in whole blood, but none in the cerebrospinal fluid. The patient developed temporal lobe epilepsy associated with mesial temporal sclerosis at 67 months of age, necessitating surgical treatment. Anterior temporal lobectomy was performed at 171 months of age. Real‐time polymerase chain reaction analysis of resected brain tissues revealed no viral DNA. In our patient, human herpesvirus 6 infection triggered febrile status epilepticus, while direct evidence to prove contribution of HHV‐6 to the development of MTS was not obtained. [ABSTRACT FROM AUTHOR]

Objective: We examined the clinical manifestations of acute encephalopathy (AE) and identify risk factors for AE in children with tuberous sclerosis complex (TSC).Methods: The clinical data of 11 children with clinically diagnosed TSC associated with AE and 109 children with clinically diagnosed TSC alone aged 4 years or older were collected from 13 hospitals.Results: Of the 11 children with AE, 5 had histories of febrile seizures (FS), and all had histories of febrile status epilepticus (FSE). AE developed within 24 h after fever onset in all children with seizures lasting 30 min or longer. All children developed coma after seizure cessation. Head magnetic resonance imaging (MRI) revealed widespread abnormalities in the cerebral cortex, subcortical white matter, corpus callosum, basal ganglia, and thalamus. One child died; seven had severe neurological sequelae; and the other three, mild sequelae. Logistic regression analysis revealed that a history of FSE was correlated with the development of AE.Significance: AE in children with TSC was characterized by sudden onset after fever, followed by coma, widespread brain edema evident on MRI, and poor outcomes. A history of FSE was a risk factor for the development of AE. [ABSTRACT FROM AUTHOR]

Background: An outbreak of acute flaccid myelitis was chronologically correlated with an outbreak of severe respiratory illness in Japan in 2015. We hypothesized that increases in children hospitalized with severe respiratory illnesses might also be associated with increase in acute flaccid myelitis in autumn 2018. Methods: We explored the temporal correlations between respiratory illness outbreaks and acute flaccid myelitis during autumn season between 2016 and 2018 using questionnaire surveys. One questionnaire explored the monthly numbers of children with acute flaccid myelitis, Guillain–Barré syndrome, and other acute flaccid paralyses. The other questionnaire explored the monthly numbers of children hospitalized with respiratory illnesses associated with wheezing. A correlation between the monthly numbers of children with acute flaccid myelitis and those with respiratory illness was analyzed using the Pearson correlation test. Results: Although the number of patients hospitalized with respiratory illness did not correlate with the number of those admitted with myelitis, increases in children aged 7–12 and 13–19 years requiring intensive care unit admission correlated temporally with an outbreak of acute flaccid myelitis. Conclusions: An increase in intensive care unit admissions to treat respiratory disease occurred in association with a cluster of acute flaccid myelitis. An increase in the number of intensive care unit admissions due to respiratory illness may be a clue to expect the occurrence of acute flaccid myelitis. [ABSTRACT FROM AUTHOR]

This study examined relationships between valproate (VPA) and platelet count and immature platelet fraction (IPF). We compared the platelet count and IPF among three groups of children: those treated with VPA, those treated with other antiepileptic drugs (AEDs), and a reference group. IPF was measured using flow cytometry, and absolute immature platelet count (A-IPC) was calculated. The platelet count was significantly lower in the VPA group than in other AED and reference groups. In all groups, IPF was negatively correlated with platelet count. IPF was significantly higher in the VPA group than in the reference group, whereas A-IPC was similar among all groups. After stratification of the platelet count, IPF and A-IPC of the three groups did not differ significantly in any strata. No relationship was observed between serum VPA level and platelet count, IPF, or A-IPC. Our study suggests that VPA is associated with a decreased platelet count, although thrombocytopoiesis is not affected, even in children with a reduced platelet count. The suppression of platelet production in the bone marrow is unlikely to be the cause of thrombocytopenia in patients treated with VPA. [ABSTRACT FROM AUTHOR]