Abstracts

Rationale: Dysregulation of autonomic nervous system (ANS) has been associated with long-term morbidity and mortality in epileptic patients. Previous studies of ANS in epilepsy were mostly confined to temporal lobe epilepsy (TLE) and involved mainly sympathetic dysregulation. We tried to study changes in sympathetic and parasympathetic activities in patients with frontal lobe epilepsy (FLE). Methods: The study included 14 males and 11 females (age 5-34 years; mean age: 16.16 years) with FLE and healthy control subjects (mean age: 16.20 years) (Con). Brain magnetic resonance imaging was used to detect possible structural lesions and EEG was used to detect epileptogenic zones. Lead I electrocardiograms were taken in 5 minutes during an interictal period in the daytime. Using a nonparametric method of fast Fourier transformation (FFT), frequency-domain analysis of heart rate variability was performed and the data were subsequently converted to heart rate interval, high frequency (0.15-0.45 Hz) power which represented vagal (parasympathetic) regulation, low frequency (0.04-0.15 Hz) power, and LF/(HF+LF) expressed in normalized units (LF%) which was considered to mirror sympathetic regulation. Data were presented as mean ± standard error (S.E.) and differences in the data between the groups were compared using t-test. Results: All 25 patients were assumed to have idiopathic or cryptogenic epilepsies lasting 2-31 years (9.94 ± 1.57 years). In interictal EEG, epileptogenic foci were found with left frontal origin in 16 patients, with right frontal origin in 6 patients and with bilateral frontal origin in 3 patients. Between-group differences in RR and HF power (p < 0.05) but not age, height, weight, BMI, LF and LF% were significant (p > 0.05). Patients in FLE group had a significantly lower mean heart rate interval (687.76 ms vs. 780.15 ms; p = 0.008) and HF power (5.22 ln[ms2] vs. 5.96 ln[ms2]; p = 0.043). Conclusions: Our data indicate that patients with FLE have shorter interictal heart rate intervals and faster heart rates, which we postulate are due to lower parasympathetic or vagal regulation of autonomic cardiac activity. This suggests that the mechanism of ANS dysregulation in patients with FLE is different than patients with TLE.