MRI abnormalities following febrile status epilepticus in children

Shinnar, Shlomo; Bello, Jacqueline A.; Chan, Stephen; Hesdorffer, Dale C.; Lewis, Darrell V.; MacFall, James R.; Pellock, John M.; Nordli, Douglas R.; Frank, Loren M.; Moshé, Solomon L.; Gomes, William A.; Shinnar, Ruth C.; Sun, Shumei S.

doi:10.1212/wnl.0b013e318266fcc5

Cited by 197 publications

(210 citation statements)

References 35 publications

Supporting

Mentioning

186

Contrasting

Unclassified

Order By: Relevance

“…This is in accordance with our study in adults with TLE where FLAIR hyperintensity in the parahippocampal gyrus was modulated by a history of febrile convulsions. Furthermore, the results from a prospective imaging study in children have shown visible T2 hyperintensity in the adjacent ipsi‐lesional temporal neocortex following febrile status epilepticus49 and suggests a particular vulnerability of the ipsilateral temporal pole to early insults. However, the causal relationship between febrile seizures and the subsequent development of mesial temporal lobe epilepsy is still unclear 50…”

Section: Discussionmentioning

confidence: 99%

Multimodal computational neocortical anatomy in pediatric hippocampal sclerosis

Adler

Blackwood

Northam

et al. 2018

Ann Clin Transl Neurol

View full text Add to dashboard Cite

ObjectiveIn contrast to adult cohorts, neocortical changes in epileptic children with hippocampal damage are not well characterized. Here, we mapped multimodal neocortical markers of epilepsy‐related structural compromise in a pediatric cohort of temporal lobe epilepsy and explored how they relate to clinical factors.MethodsWe measured cortical thickness, gray–white matter intensity contrast and intracortical FLAIR intensity in 22 patients with hippocampal sclerosis (HS) and 30 controls. Surface‐based linear models assessed between‐group differences in morphological and MR signal intensity markers. Structural integrity of the hippocampus was measured by quantifying atrophy and FLAIR patterns. Linear models were used to evaluate the relationships between hippocampal and neocortical MRI markers and clinical factors.ResultsIn the hippocampus, patients demonstrated ipsilateral atrophy and bilateral FLAIR hyperintensity. In the neocortex, patients showed FLAIR signal hyperintensities and gray–white matter boundary blurring in the ipsilesional mesial and lateral temporal neocortex. In contrast, cortical thinning was minimal and restricted to a small area of the ipsilesional temporal pole. Furthermore, patients with a history of febrile convulsions demonstrated more pronounced FLAIR hyperintensity in the ipsilesional temporal neocortex.InterpretationPediatric HS patients do not yet demonstrate the widespread cortical thinning present in adult cohorts, which may reflect consequences of a protracted disease process. However, pronounced temporal neocortical FLAIR hyperintensity and blurring of the gray–white matter boundary are already detectable, suggesting that alterations in MR signal intensities may reflect a different underlying pathophysiology that is detectable earlier in the disease and more pervasive in patients with a history of febrile convulsions.

show abstract

Section: Discussionmentioning

confidence: 99%

Multimodal computational neocortical anatomy in pediatric hippocampal sclerosis

Adler

Blackwood

Northam

et al. 2018

Ann Clin Transl Neurol

View full text Add to dashboard Cite

show abstract

“…Ancak afebril nöbet gelişimi açısından yüksek riske sahip; anormal nöromotor gelişim, fokal veya uzamış konvülziyon öykü-sü bulunan hastalarda taburculuğunda manyetik rezonans görüntüleme istenebilir. 48 Diazepam: Yüksek oranda yağda eriyen ve hızla beyine geçiş gösteren bir ilaçtır. GABA'erjik sinaptik inhibisyonun etkisini arttırarak beynin pek çok bölgesinde kritik nöronların ateşlen-mesini azaltır.…”

Section: Etyolojiunclassified

Approach to Febrile Convulsion

Elmas¹,

Tabanlı²

2016

Sakarya Med J

View full text Add to dashboard Cite

Febril konvülziyonlar, çocukluk çağı konvülziyonlarının en sık nedenidir. Öncesinde afebril nöbet hikayesi olmayan 3 ay-6 yaş arasındaki çocuklarda herhangi bir metabolik bozukluk veya merkezi sinir sistemi patolojisine bağlı olmaksızın 38˚C ve daha yüksek ateşin yol açtığı nöbetlerdir. İnsidansı % 2-4 civarındadır. Etyolojisinden çoğunlukla sistemik viral veya bakteriyel enfeksiyonlar sorumludur. Çocuğun yaşı, aile öyküsü, ateşin seviyesi ve yükselme hızı tekrarlama riskini arttırmaktadır. Febril nöbetlerin çoğunluğu kendiliğinden durur. Çoğu olguda benzodiazepin kullanımı gereksizdir. Aile açısından korkutucu bir tablo gibi gözükse de çoğunlukla selim bir olaydır ve gelecekte epilepsi gelişme riski düşüktür. Bu yazıda çocuk acil pratiğinde sık karşılaşılan febril konvülziyon ile ilgili literatür bilgileri gözden geçirilerek etyoloji, patogenez ve tedavi yaklaşımları ile ilgili yeni bilgiler derlenmiştir.

show abstract

“…In the FEBSTAT study, a longitudinal study to try and elucidate the pathogenic link between FS and late development of epilepsy, 11.5 % of children presenting with prolonged (>30 min) febrile status had increased or equivocal T 2 signal in the hippocampus and more widespread in the temporal lobe, compared with none among children with simple febrile seizures [85]. T2W hippocampal signal abnormality was associated with focal EEG slowing or attenuation suggestive of acute hippocampal injury [86].…”

Section: Signal Changesmentioning

confidence: 99%

“…In the FEBSTAT study, developmental abnormalities of the hippocampus (hippocampal malrotation being the most common) were seen in the group of children with prolonged FS, suggestive of a possible predisposition to the initial epileptogenic insult [85]. Seizure-generating hypothalamic hamartomas appear to always have a connection to one or both mammillary bodies [91].…”

Section: Volumetric and Morphological Analysismentioning

confidence: 99%

Neuroimaging the Epileptogenic Process

et al. 2014

View full text Add to dashboard Cite

Epilepsy is one of the most common chronic neurological conditions worldwide. Anti-epileptic drugs (AEDs) can suppress seizures, but do not affect the underlying epileptic state, and many epilepsy patients are unable to attain seizure control with AEDs. To cure or prevent epilepsy, disease-modifying interventions that inhibit or reverse the disease process of epileptogenesis must be developed. A major limitation in the development and implementation of such an intervention is the current poor understanding, and the lack of reliable biomarkers, of the epileptogenic process. Neuroimaging represents a non-invasive medical and research tool with the ability to identify early pathophysiological changes involved in epileptogenesis, monitor disease progression, and assess the effectiveness of possible therapies. Here we will provide an overview of studies conducted in animal models and in patients with epilepsy that have utilized various neuroimaging modalities to investigate epileptogenesis.

show abstract

MRI abnormalities following febrile status epilepticus in children

Abstract: This prospective study demonstrates that children with FSE are at risk for acute hippocampal injury and that a substantial number also have abnormalities in hippocampal development. Follow-up studies are in progress to determine the long-term outcomes in these children.

Cited by 197 publications

References 35 publications

Multimodal computational neocortical anatomy in pediatric hippocampal sclerosis

Multimodal computational neocortical anatomy in pediatric hippocampal sclerosis

Approach to Febrile Convulsion

Neuroimaging the Epileptogenic Process

Contact Info

Product

Resources

About