Hippocampal sclerosis after febrile status epilepticus

The FEBSTAT study

Darrell V. Lewis, Shlomo Shinnar, Dale C. Hesdorffer, Emilia Bagiella, Jacqueline A. Bello, Stephen Chan, Yuan Xu, James MacFall, William A. Gomes, Solomon L. Moshe, Gary W. Mathern, John M. Pellock, Douglas R. Nordli, L. Matthew Frank, James Provenzale, Ruth C. Shinnar, Leon G. Epstein, David Masur, Claire Litherland, Shumei Sun

Research output: Contribution to journalArticle

102 Citations (Scopus)

Abstract

Objective Whether febrile status epilepticus (FSE) produces hippocampal sclerosis (HS) and temporal lobe epilepsy (TLE) has long been debated. Our objective is to determine whether FSE produces acute hippocampal injury that evolves to HS. Methods FEBSTAT and 2 affiliated studies prospectively recruited 226 children aged 1 month to 6 years with FSE and controls with simple febrile seizures. All had acute magnetic resonance imaging (MRI), and follow-up MRI was obtained approximately 1 year later in the majority. Visual interpretation by 2 neuroradiologists informed only of subject age was augmented by hippocampal volumetrics, analysis of the intrahippocampal distribution of T2 signal, and apparent diffusion coefficients. Results Hippocampal T2 hyperintensity, maximum in Sommer's sector, occurred acutely after FSE in 22 of 226 children in association with increased volume. Follow-up MRI obtained on 14 of the 22 with acute T2 hyperintensity showed HS in 10 and reduced hippocampal volume in 12. In contrast, follow-up of 116 children without acute hyperintensity showed abnormal T2 signal in only 1 (following another episode of FSE). Furthermore, compared to controls with simple febrile seizures, FSE subjects with normal acute MRI had abnormally low right to left hippocampal volume ratios, smaller hippocampi initially, and reduced hippocampal growth. Interpretation Hippocampal T2 hyperintensity after FSE represents acute injury often evolving to a radiological appearance of HS after 1 year. Furthermore, impaired growth of normal-appearing hippocampi after FSE suggests subtle injury even in the absence of T2 hyperintensity. Longer follow-up is needed to determine the relationship of these findings to TLE.

Original languageEnglish (US)
Pages (from-to)178-185
Number of pages8
JournalAnnals of Neurology
Volume75
Issue number2
DOIs
StatePublished - 2014

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Status Epilepticus
Sclerosis
Fever
Febrile Seizures
Magnetic Resonance Imaging
Temporal Lobe Epilepsy
Hippocampus
Wounds and Injuries
Growth

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

Hippocampal sclerosis after febrile status epilepticus : The FEBSTAT study. / Lewis, Darrell V.; Shinnar, Shlomo; Hesdorffer, Dale C.; Bagiella, Emilia; Bello, Jacqueline A.; Chan, Stephen; Xu, Yuan; MacFall, James; Gomes, William A.; Moshe, Solomon L.; Mathern, Gary W.; Pellock, John M.; Nordli, Douglas R.; Frank, L. Matthew; Provenzale, James; Shinnar, Ruth C.; Epstein, Leon G.; Masur, David; Litherland, Claire; Sun, Shumei.

In: Annals of Neurology, Vol. 75, No. 2, 2014, p. 178-185.

Research output: Contribution to journalArticle

Lewis, DV, Shinnar, S, Hesdorffer, DC, Bagiella, E, Bello, JA, Chan, S, Xu, Y, MacFall, J, Gomes, WA, Moshe, SL, Mathern, GW, Pellock, JM, Nordli, DR, Frank, LM, Provenzale, J, Shinnar, RC, Epstein, LG, Masur, D, Litherland, C & Sun, S 2014, 'Hippocampal sclerosis after febrile status epilepticus: The FEBSTAT study', Annals of Neurology, vol. 75, no. 2, pp. 178-185. https://doi.org/10.1002/ana.24081
Lewis, Darrell V. ; Shinnar, Shlomo ; Hesdorffer, Dale C. ; Bagiella, Emilia ; Bello, Jacqueline A. ; Chan, Stephen ; Xu, Yuan ; MacFall, James ; Gomes, William A. ; Moshe, Solomon L. ; Mathern, Gary W. ; Pellock, John M. ; Nordli, Douglas R. ; Frank, L. Matthew ; Provenzale, James ; Shinnar, Ruth C. ; Epstein, Leon G. ; Masur, David ; Litherland, Claire ; Sun, Shumei. / Hippocampal sclerosis after febrile status epilepticus : The FEBSTAT study. In: Annals of Neurology. 2014 ; Vol. 75, No. 2. pp. 178-185.
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abstract = "Objective Whether febrile status epilepticus (FSE) produces hippocampal sclerosis (HS) and temporal lobe epilepsy (TLE) has long been debated. Our objective is to determine whether FSE produces acute hippocampal injury that evolves to HS. Methods FEBSTAT and 2 affiliated studies prospectively recruited 226 children aged 1 month to 6 years with FSE and controls with simple febrile seizures. All had acute magnetic resonance imaging (MRI), and follow-up MRI was obtained approximately 1 year later in the majority. Visual interpretation by 2 neuroradiologists informed only of subject age was augmented by hippocampal volumetrics, analysis of the intrahippocampal distribution of T2 signal, and apparent diffusion coefficients. Results Hippocampal T2 hyperintensity, maximum in Sommer's sector, occurred acutely after FSE in 22 of 226 children in association with increased volume. Follow-up MRI obtained on 14 of the 22 with acute T2 hyperintensity showed HS in 10 and reduced hippocampal volume in 12. In contrast, follow-up of 116 children without acute hyperintensity showed abnormal T2 signal in only 1 (following another episode of FSE). Furthermore, compared to controls with simple febrile seizures, FSE subjects with normal acute MRI had abnormally low right to left hippocampal volume ratios, smaller hippocampi initially, and reduced hippocampal growth. Interpretation Hippocampal T2 hyperintensity after FSE represents acute injury often evolving to a radiological appearance of HS after 1 year. Furthermore, impaired growth of normal-appearing hippocampi after FSE suggests subtle injury even in the absence of T2 hyperintensity. Longer follow-up is needed to determine the relationship of these findings to TLE.",
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T1 - Hippocampal sclerosis after febrile status epilepticus

T2 - The FEBSTAT study

AU - Lewis, Darrell V.

AU - Shinnar, Shlomo

AU - Hesdorffer, Dale C.

AU - Bagiella, Emilia

AU - Bello, Jacqueline A.

AU - Chan, Stephen

AU - Xu, Yuan

AU - MacFall, James

AU - Gomes, William A.

AU - Moshe, Solomon L.

AU - Mathern, Gary W.

AU - Pellock, John M.

AU - Nordli, Douglas R.

AU - Frank, L. Matthew

AU - Provenzale, James

AU - Shinnar, Ruth C.

AU - Epstein, Leon G.

AU - Masur, David

AU - Litherland, Claire

AU - Sun, Shumei

PY - 2014

Y1 - 2014

N2 - Objective Whether febrile status epilepticus (FSE) produces hippocampal sclerosis (HS) and temporal lobe epilepsy (TLE) has long been debated. Our objective is to determine whether FSE produces acute hippocampal injury that evolves to HS. Methods FEBSTAT and 2 affiliated studies prospectively recruited 226 children aged 1 month to 6 years with FSE and controls with simple febrile seizures. All had acute magnetic resonance imaging (MRI), and follow-up MRI was obtained approximately 1 year later in the majority. Visual interpretation by 2 neuroradiologists informed only of subject age was augmented by hippocampal volumetrics, analysis of the intrahippocampal distribution of T2 signal, and apparent diffusion coefficients. Results Hippocampal T2 hyperintensity, maximum in Sommer's sector, occurred acutely after FSE in 22 of 226 children in association with increased volume. Follow-up MRI obtained on 14 of the 22 with acute T2 hyperintensity showed HS in 10 and reduced hippocampal volume in 12. In contrast, follow-up of 116 children without acute hyperintensity showed abnormal T2 signal in only 1 (following another episode of FSE). Furthermore, compared to controls with simple febrile seizures, FSE subjects with normal acute MRI had abnormally low right to left hippocampal volume ratios, smaller hippocampi initially, and reduced hippocampal growth. Interpretation Hippocampal T2 hyperintensity after FSE represents acute injury often evolving to a radiological appearance of HS after 1 year. Furthermore, impaired growth of normal-appearing hippocampi after FSE suggests subtle injury even in the absence of T2 hyperintensity. Longer follow-up is needed to determine the relationship of these findings to TLE.

AB - Objective Whether febrile status epilepticus (FSE) produces hippocampal sclerosis (HS) and temporal lobe epilepsy (TLE) has long been debated. Our objective is to determine whether FSE produces acute hippocampal injury that evolves to HS. Methods FEBSTAT and 2 affiliated studies prospectively recruited 226 children aged 1 month to 6 years with FSE and controls with simple febrile seizures. All had acute magnetic resonance imaging (MRI), and follow-up MRI was obtained approximately 1 year later in the majority. Visual interpretation by 2 neuroradiologists informed only of subject age was augmented by hippocampal volumetrics, analysis of the intrahippocampal distribution of T2 signal, and apparent diffusion coefficients. Results Hippocampal T2 hyperintensity, maximum in Sommer's sector, occurred acutely after FSE in 22 of 226 children in association with increased volume. Follow-up MRI obtained on 14 of the 22 with acute T2 hyperintensity showed HS in 10 and reduced hippocampal volume in 12. In contrast, follow-up of 116 children without acute hyperintensity showed abnormal T2 signal in only 1 (following another episode of FSE). Furthermore, compared to controls with simple febrile seizures, FSE subjects with normal acute MRI had abnormally low right to left hippocampal volume ratios, smaller hippocampi initially, and reduced hippocampal growth. Interpretation Hippocampal T2 hyperintensity after FSE represents acute injury often evolving to a radiological appearance of HS after 1 year. Furthermore, impaired growth of normal-appearing hippocampi after FSE suggests subtle injury even in the absence of T2 hyperintensity. Longer follow-up is needed to determine the relationship of these findings to TLE.

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