Febrile Status Epilepticus

2019 ◽  
Vol 08 (03) ◽  
pp. 079-082
Author(s):  
Isaac Molinero ◽  
Shlomo Shinnar

AbstractFebrile status epilepticus (FSE) is defined as a febrile seizure lasting 30 minutes or more and is considered the extreme end of the complex febrile seizure spectrum. It remains unclear why some children are predisposed to the development of FSE compared with others. FSE is considered as medical emergency and as such, early treatment is crucial. The consequences of FSE have been a topic of interest for many years, specially its association with temporal lobe epilepsy and hippocampal sclerosis. In this article, we review the epidemiology, risk factors, pathophysiology, treatment, and prognosis including findings from the “Consequences of Prolonged Febrile Seizures in Childhood” (FEBSTAT) study.

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Yinchao Li ◽  
Chengzhe Wang ◽  
Peiling Wang ◽  
Xi Li ◽  
Liemin Zhou

Abstract 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 MTLE-HS 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.


2014 ◽  
Vol 11 (2) ◽  
pp. 242-250 ◽  
Author(s):  
Katelin P. Patterson ◽  
Tallie Z. Baram ◽  
Shlomo Shinnar

Epilepsia ◽  
2020 ◽  
Vol 61 (4) ◽  
pp. 787-797
Author(s):  
Smriti Patodia ◽  
Beatrice Paradiso ◽  
Maria Garcia ◽  
Matthew Ellis ◽  
Beate Diehl ◽  
...  

2010 ◽  
Vol 176 (1) ◽  
pp. 330-342 ◽  
Author(s):  
Mark Dunleavy ◽  
Sachiko Shinoda ◽  
Clara Schindler ◽  
Claire Ewart ◽  
Ross Dolan ◽  
...  

2021 ◽  
Vol 15 (3-4) ◽  
pp. 10-18
Author(s):  
V. E. Kitaeva ◽  
A. S. Kotov

Background. The status epilepticus of focal impaired-awareness seizures (SE FIAS) is a series of focal seizures with loss or change of consciousness, between which there is no complete recovery of consciousness. This status epilepticus occurs in patients with temporal (especially with hippocampal sclerosis) and frontal epilepsy. It is important to differentiate SE FIAS with the absence status epilepticus, with psychiatric disorder, with postictal confusion. As a rule, this status epilepticus is self-terminate, without special treatment.Objective: to study the features of epidemiology, etiology, diagnosis, therapy and prognosis in patients with SE FIAS.Materials and methods. The study included 1350 consecutive patients diagnosed with epilepsy.Results and discussion. A history of SE FIAS was found in 20 patients (14 women and 6 men), it occurred in the age range from 5 to 66 years. 13 patients (65 %) had mesial temporal lobe epilepsy, 5 patients (25 %) had frontal lobe epilepsy, and 2 patients (10 %) had lateral temporal lobe epilepsy. Only in 80 % of patients treatment was adequate before the development of SE FIAS, in 20 % of patients it was inadequate and subsequently caused the development of status epilepticus. In 40 % of patients the occurrence of SE FIAS is associated with their own non-compliance; in 30 % of patients the development of status epilepticus had iatrogenic causes. Measures to prevent the development of status epilepticus were ineffective only in patients with pharmacoresistant symptomatic epilepsy and in non-compliant patients.Conclusions. SE FIAS occurs in 1 % of patients with epilepsy. Among patients, women with temporal or frontal epilepsy dominate; status epilepticus occurs at any age and is often triggered by changes in therapy due to doctors’ recommendations or patient non-compliance. Usually the status is self-terminating. To prevent its recurrence, adequate antiepileptic therapy is necessary. The prognosis in patients with SE FIAS is favorable; however, the general prognosis remains serious due to the severity of the course of epilepsy.


2016 ◽  
Vol 20 (4) ◽  
pp. 652-656 ◽  
Author(s):  
Robertino Dilena ◽  
Gabriella Nebbia ◽  
Lorenzo Fiorica ◽  
Marcello Farallo ◽  
Irene Degrassi ◽  
...  

2009 ◽  
Vol 97 (3) ◽  
pp. 146-153 ◽  
Author(s):  
V. Salanova ◽  
O. Markand ◽  
R. Worth ◽  
R. Smith ◽  
H. Wellman ◽  
...  

2007 ◽  
Vol 7 (4) ◽  
pp. 100-101
Author(s):  
Bassel W. Abou-Khalil

Temporal Lobe Epilepsy and GEFS+ Phenotypes Associated with SCN1B Mutations. Scheffer IE, Harkin LA, Grinton BE, Dibbens LM, Turner SJ, Zielinski MA, Xu R, Jackson G, Adams J, Connellan M, Petrou S, Wellard RM, Briellmann RS, Wallace RH, Mulley JC, Berkovic SF. Brain 2007;130(Pt 1):100–109. SCN1B, the gene encoding the sodium channel β1 subunit, was the first gene identified for generalized epilepsy with febrile seizures plus (GEFS+). Only three families have been published with SCN1B mutations. Here, we present four new families with SCN1B mutations and characterize the associated phenotypes. Analysis of SCN1B was performed on 402 individuals with various epilepsy syndromes. Four probands with missense mutations were identified. Detailed electroclinical phenotyping was performed on all available affected family members including quantitative MR imaging in those with temporal lobe epilepsy (TLE). Two new families with the original C121W SCN1B mutation were identified; novel mutations R85C and R85H were each found in one family. The following phenotypes occurred in the six families with SCN1B missense mutations: 22 febrile seizures, 20 febrile seizures plus, five TLE, three other GEFS+ phenotypes, two unclassified and ten unaffected individuals. All individuals with confirmed TLE had the C121W mutation; two underwent temporal lobectomy (one with hippocampal sclerosis and one without) and both are seizure free. We confirm the role of SCN1B in GEFS+ and show that the GEFS+ spectrum may include TLE alone. TLE with an SCN1B mutation is not a contraindication to epilepsy surgery.


1995 ◽  
Vol 12 (3) ◽  
pp. 201-206 ◽  
Author(s):  
A.Simon Harvey ◽  
J.Damien Grattan-Smith ◽  
Patricia M. Desmond ◽  
C.W. Chow ◽  
Samuel F. Berkovic

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