Abstract
Objective: The FEBSTAT (Consequences of Prolonged Febrile Seizures) study is prospectively addressing the relationships among serial EEG, MRI, and clinical follow-up in a cohort of children followed from the time of presentation with febrile status epilepticus (FSE). Methods: We recruited 199 children with FSE within 72 hours of presentation. Children underwent a detailed history, physical examination, MRI, and EEG within 72 hours. All EEGs were read by 2 teams and then conferenced. Associations with abnormal EEG were determined using logistic regression. Interrater reliability was assessed using the k statistic. Results: Of the 199 EEGs, 90 (45.2%) were abnormal with the most common abnormality being focal slowing (n = 47) or attenuation (n = 25); these were maximal over the temporal areas in almost all cases. Epileptiform abnormalities were present in 13 EEGs (6.5%). In adjusted analysis, the odds of focal slowing were significantly increased by focal FSE (odds ratio [OR] = 5.08) and hippocampal T2 signal abnormality (OR = 3.50) and significantly decreased with high peak temperature (OR = 0.18). Focal EEG attenuation was also associated with hippocampal T2 signal abnormality (OR = 3.3). Conclusions: Focal EEG slowing or attenuation are present in EEGs obtainedwithin 72 hours of FSE in a substantial proportion of children and are highly associated with MRI evidence of acute hippocampal injury. These findings may be a sensitive and readily obtainable marker of acute injury associated with FSE.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2180-2186 |
| Number of pages | 7 |
| Journal | Neurology |
| Volume | 79 |
| Issue number | 22 |
| DOIs | |
| State | Published - Nov 27 2012 |
Funding
D. Nordli is funded by the NIH. S. Moshé is funded by the NIH and the Heffer and Segal Family Foundations and received a consultant fee from Eisai and a speaker's fee and travel expenses from GSK. S. Shinnar is funded by the NIH, served on a DSMB for King Pharmaceuticals, has received personal compensation for serving on Scientific Advisory Boards for Questcor and Sunovion, for consulting for Eisai, Questcor, and Neuronex, and speaker honoraria from Eisai, Questcor, and UCB. D. Hesdorffer is funded by the NIH, the CDC, AUCD, Maternal and Child Health Bureau, and grants from the Epilepsy Study Consortium and Epilepsy Foundation of America. She has served on the UCB advisory board. She is a consultant to Mt. Sinai Medical Center, New York, and has a received a travel grant award from GlaxoSmithKline. Y. Sogawa has received support in the form of the Susan Spencer Young Clinical Investigator Award from the American Epilepsy Society. She was an NSADA trainee under K12 NS-48856. J. Pellock is funded by the NIH and the CDC. He has also received research support from Eisai, Marinus, Lundbeck, Pfizer, Questcor, and UCB. He has received compensation for serving on Scientific Advisory Boards for Eisai, Lundbeck, Questcor, Sepracor, and UCB. He has been a consultant for Catalyst, Eisai, GlaxoSmithKline, King, KV Pharmaceuticals, Lundbeck, Marinus, Neuropace, Pfizer, Questcor, Sepracor, Sunovion, UCB, Upsher Smith, and Valeant. All grants, research support, consultant fees, and honoraria are paid to Virginia Commonwealth University or the physician practice plan (MCV Physicians). D. Lewis is funded by the NIH. L.M. Frank is funded by the NIH and has received grant support from Schwarz-UCB, Ovation-Lundbeck, Eisai, Supernus, and AVI BioPharma. He holds or has held stock in AVI Biopharma, Oncothyreon, Neurologix, Peregrine, Positiveid, and Nanoviricides. R. Shinnar is funded by the NIH. She has received compensation for serving on advisory panels for Questcor Pharmaceuticals, Eisai, and Lundbeck and speaker honoraria from Cyberonics and Questcor. S. Sun is funded by the NIH and serves as a consultant for Nestle. Go to Neurology.org for full disclosures.
ASJC Scopus subject areas
- Clinical Neurology