[The familial incidence of epilepsy in the group of epileptic patients examined after their first seizure--pilot study]. / Az epilepszia családi elofordulása az elso roham után vizsgált betegek csoportjában.

INTRODUCTION: It is essential to identify the genetic factors of epilepsy in the every day clinical practice for several reasons. The proof of the genetically defined sub-clusters existing inside the epileptic disease group is significant in diagnoses and therapy. The risk of inheriting epilepsy could influence the patient's family planning which has a great impact on their quality of life. THE AIM OF THE STUDY: To analyse clinical data obtained from patients examined after their first provoked or unprovoked seizure and the observation of the recurrence of seizures. To compare the data obtained with the familial occurrence of epilepsy. POPULATION AND METHODS: Data was obtained from a questionnaire developed by the authors. The epileptic patients with positive familial data underwent to an analysis of their family tree. RESULTS: Of 120 persons who were examined the prevalence of epilepsy in their family was 20.4%. This corresponds to the familial prevalence of generalised epilepsy according to the published clinical data. The recurrence of seizures was experienced by 32% of the patients with a family background affected by epilepsy. The risk of recurring seizures was the highest if the familial epilepsy manifested itself in the same generation (among brothers or sisters) and if we were able to register epileptiform activity on the interictal EEG. According to our clinical data the genetic set up can play a role also in the provoked first epileptic seizure. The incidence of familial epilepsy was found high (12.72%) in the presence of incidental epileptic seizures when the EEG was free of epileptiform alterations. CONCLUSION: 1. The genetic basis for the first epileptic seizure in the population of young adults approaches the data known in idiopathic generalised epilepsy irrespective of the fact whether it was related to the seizure provoking factors or not. 2. The risk of seizure reactivation was higher in non-provoked seizures then at .the incidental epileptic symptoms. Seizure reactivation had to be taken into consideration when epileptiform patterns appeared on the patient's EEG and/or epileptic symptoms were experienced by the patient's brother or sister. The probability of recurring seizures was lower if the epileptic seizures manifested in parents or earlier generations.

Quantitative EEG effects of carbamazepine, oxcarbazepine, valproate, lamotrigine, and possible clinical relevance of the findings.

UNLABELLED: Quantitative EEG (QEEG) effects of therapeutic doses of carbamazepine (CBZ), oxcarbazepine (OXC), valproate (VA) and lamotrigine (LA) monotherapy were investigated in patients with beginning epilepsy. Baseline waking EEG (EEG1) was recorded in the untreated state, the second EEG (EEG2) was done after 8 weeks of reaching the therapeutic dose. Left occipital data were used for analysis. QEEG target parameters were absolute band-power (delta: AD, theta: AT, alpha: AA, beta: AB), and alpha mean frequency (AMF). Group effects (untreated versus treated condition in the CBZ, VA, OXC, LA groups) were computed for each target parameter. One group with benign rolandic epilepsy remained untreated for clinical reasons and served to estimate the QEEG test-retest differences. In addition, the individual QEEG response to each drug was calculated as (EEG2-EEG1). RESULTS: statistically significant (p<0.05) group differences indicated the QEEG domain systematically affected by the drugs. CBZ caused AT increase and AMF decrease. OXC caused AMF decrease. VA and LA did not decrease AMF (LA even increased it), but reduced broad-band power. Individual power and AMF changes showed considerable variability in each group. >0.5 Hz AMF decrease (that was reported to predict cognitive impairment in prior studies) occurred in 10/41 patients in the CBZ group but never in the OXC, VA, LA groups. The results may be utilized in planning further studies addressing the relationship between antiepileptic drugs and their CNS effects. In addition, the relationship of AED-related cognitive impairment and AMF changes was discussed.