BACKGROUND
Recent theories and models of brain rhythm generation and ictogenesis have emphasized: (1) the dynamic interplay of excitatory and inhibitory neuronal networks, (2) the importance of transient global states, (3) the enhanced or deficient local connectivity of excitatory and/or inhibitory neuronal networks. These result in activity overdrive or attenuation and critical-level synchronisation that would entrain large-scale neuronal ensembles into excessive and/or hypersynchronous activity.
METHODS
We developed a biological neuronal network spiking model consisting of 1000 excitatory and inhibitory neurons and simulated the activity of the network by altering critical parameters, such as the external input, the intrinsic connectivity patterns and synaptic strengths, the effects of excessive vs. deficient inhibition and other key inherent cell properties.
ANALYSIS
Systemic simulations gave rise to dynamic resonance phenomena resembling a range of activities from physiologically observed EEG oscillations to epileptiform sharp wave ripples, sharp or rhythmical slower waves and suppression responses underlying different mechanisms of epileptogenesis.
We attempt the translation of features and properties of our network model into the interpretation of epileptiform phenomena that we have observed with in-depth hippocampal or cortical grid intracranial EEG recordings, as well as with surface EEG recordings from different epilepsy types.
DISCUSSION
Sharp wave ripples in the beta/gamma and higher frequency range (fast oscillations), paroxysmal depolarisation and DC shifts (very slow oscillations) and transient rhythm attenuations (electrodecremental responses) may encapsulate the fundamental epileptogenic mechanisms at microscopic and mesoscopic levels.
The morphology of spikes+/- slow-wave complexes and sharp waves or rhythmical oscillatory activity and cortical spreading depression, their spatiotemporal distribution and amplitude/spectral characteristics observed at mesoscopic and macroscopic scales of neuronal organisation possibly reflect individual differences in the underlying cellular properties, structural and functional connectivity patterns, epilepsy types and epileptogenic network dynamics.
