Neocortical gamma oscillations in idiopathic generalized epilepsy

Absence seizures in patients with idiopathic generalized epilepsy (IGE) may in part be explained by a decrease in phasic GABAA (type-A γ-aminobutyric acid) receptor function, but the mechanisms are only partly understood. Here we studied the relation between ictal and interictal spike-wave discharges (SWDs) and electroencephalography (EEG) gamma oscillatory activity (30-60 Hz) in patients with IGE.

EEG recordings were obtained of 14 children with IGE (mean age, 8.5 ± 5 years) and 14 age- and sex-matched controls. Time-frequency analysis of each seizure and seizure-free control epochs was performed and cross-coherences of neocortical gamma oscillations were calculated to describe interictal and ictal characteristics of generalized seizures.

SWDs were characterized with an abrupt increase of oscillatory activity of 3-4 and 13-60 Hz, peaking at 3-4 and 30-60 Hz, and with a simultaneous decrease in the 8-12 Hz frequency band. The rise in EEG gamma oscillations was short-lasting and decreased before activity declined at lower frequency ranges. Compared to control patients, patients with epilepsy also showed higher interictal values of mean coherence of gamma activity, but this interictal increase was not significant after post hoc analysis.

Our data support the hypothesis that gamma oscillatory activity increase concomitantly with rises in activity of lower EEG frequencies during absence seizures and that the activity starts to cease earlier than lower EEG frequencies. The data did not support a change in gamma activity preceding the 3-4 Hz SWDs. SWDs are hypothetically generated by the synchronous interaction between the thalamus and the cortex, whereas the production of gamma activity is the result of activity in local inhibitory networks. Thus, the modification of SWD by gamma activity may be understood in terms of the cellular and synaptic mechanisms involved.