Abstracts

Rationale: The analysis of interictal epileptiform discharges (IEDs) using magnetoencephalography (MEG) is utilized for the localization of seizure onset zones in the presurgical planning of epilepsy patients. Additionally, resting-state functional connectivity analyses using the IED area may provide novel insight into the underlying brain networks. In this study, we evaluate whether chronicity of seizures is related to whole-brain functional connectivity metrics using the area of IED generation (derived from MEG) as the seed region. Methods: We studied 12 adults (4 females) with intractable complex partial epilepsy, who were undergoing presurgical evaluation, including MEG. All participants were scheduled for MEG after a night of sleep deprivation to increase the frequency of interictal spikes. Each identified IED was localized using data from the 204 gradiometer-type sensors and a single equivalent-current dipole model (ECD). Phase coherence, a measure of functional connectivity that quantifies the phase relationship between two time varying signals (i.e., the seed region and any other brain area), was computed using a dense grid of regional source spaced equidistantly and the IED area as the seed region. Results: Pearson correlational analyses indicated that the duration of epilepsy was positively correlated with the amplitude of beta-band functional connectivity between the epileptogenic zone and other brain areas as measured by the PLV, r(12) = 0.61, p < 0.05). Phase-locking involving the epileptogenic zone in the delta, theta, and alpha bands was not statistically related to the duration of epilepsy. Conclusions: the significant presence of only beta band functional connectivity between regions of IEDs and other brain areas as a function of epilepsy chronicity was surprising, and raises several questions. Increases in beta activity have been seen in areas of increased GABAergic modulation (particularly with GABA-A receptor activation), thought to reflect increased inhibitory interneuron activity. Such knowledge could eventually contribute to the goal of augmenting a patient's endogenous cerebral antiepileptogenic mechanisms using targeted intracranial drug therapy and/or neurostimulation techniques, or for cellular therapy.