ABNORMAL EEG IN FEBRILE SEIZURES - STUDY OF 17 CASES
Abstract number :
1.152
Submission category :
Year :
2003
Submission ID :
1052
Source :
www.aesnet.org
Presentation date :
12/6/2003 12:00:00 AM
Published date :
Dec 1, 2003, 06:00 AM
Authors :
Laura M.F.F. Guilhoto, Rodrigo M. Felgueira, Rosana S.C. Alves Neurophysiology, University Hospital of the University of Sao Paulo, Sao Paulo, SP, Brazil; Pediatrics, University Hospital of the University of Sao Paulo, Sao Paulo, SP, Brazil
Febrile seizure (FS) is a benign condition and it does not imply great degree of difficulty in diagnosis and outcome. Subsidiary exams are usually of no help. Familial cases have been reported as well as the recently described syndrome of generalized epilepsy with FS plus (Scheffer IE, Berkovic SF. Brain 1997; 120:479-490). Genetic studies have stressed the polygenic nature of the process, thus phenotypic manifestations are important in this context in order to conduct genetic researches (ILAE Genetics Commission. Epilepsia 2002; 43: 1262-1267; Pal DK [italic]et al.[/italic] Neurology 2003; 60: 410-414). EEG patterns in FS as studied by H. Doose since the 1970[rsquo]s may constitute phenotypic markers in this heterogeneous genetic group.
We analyzed retrospectively the EEG from 17 patients (10 boys and 7 girls) with FS referred from the pediatric emergency unit of the University Hospital of the University of Sao Paulo who had abnormal initial tracings from the period from January 1997 trough April 2003 in order to review the clinical aspects from these patients.
The age of the first seizure ranged from 7 to 32 months (mean 15.5). Five patients had partial seizures and the remaining ones only generalized fits. Family history for epilepsy was positive in 7 out of 17 patients. Neurological examination was normal in all, except for one child that had a nonspecific mild global delay. The EEG showed generalized epileptiform activity in 7 and focal in 10 patients, who had familial antecedents for epilepsy in 4 and 3, respectively. Three patients received no medication and the following drugs were used: PB (n=10), VPA (n=2) and PB+VPA (n=2). The patients were followed for a period that varied from 1 to 84 months (mean 30.3). Febrile seizure recurrence ranged from 1 to 7 episodes/patient (mean 3.4). These findings are similar to other studies of FS, but we had a great number of positive family history for epilepsy, especially in those with generalized discharges. As this is a retrospective study, perhaps when we use a direct interview focused on familial history, this number may be even higher.
In this study of FS 7 out of 17 patients with abnormal initial EEG had positive family history for epilepsy. In an individual with FS an EEG tracing may be of little useful value. Nevertheless, when we use an abnormal EEG as an epidemiological marker of the cortical hyper excitability in FS, it can help to select people for genetic studies and thus, aggregate similar genotypic presentation.