With further advances in the understanding of the neurophysiology and neurogenetics of epileptogenic networks, the traditional view of epilepsy syndromes today becomes rather obsolete and gives way to more complex views and treatments for epilepsies, based on the underlying pathomechanism, intrinsic neuronal excitability, network architectonics, interaction of excitatory and inhibitory components, structural and functional connectivity and transient local-to-global cortical states.

In this context, the role of Electroencephalography has also changed, from basically a means of rough epilepsy classification to pushing earlier the diagnostics of epilepsy, encephalopathy and neurodegenerative conditions, directing early pharmacological management and neurosurgical interventions or monitoring of the condition and effectiveness of applied treatments. Thanks to the use of smart phones as well, epilepsy is diagnosed and treated much earlier these days, while nonepileptic attacks are also recognised earlier and managed more effectively.

On the other hand, newer pharmacological antiepileptic treatments have become more refined in their mode of action, targeting more complex pathways with fewer side-effects, while the use of neurostimulation and neurosurgical treatments has become far more widespread. Current antiseizure medications though are mostly effective at preventing initiation, propagation, spreading or generalization of epileptic seizures.

This presentation highlights recent advancements in the clinical neurophysiology of epileptogenic networks drawing from the theory of local field potentials and neuronal spiking models and uses them to explore the effect of channelopathies, receptors and neurotransmitters, intrinsic synaptic and extrasynaptic membrane properties, ionic conductances and excessive/deficient excitatory or inhibitory and neuromodulatory neurotransmitter release and receptor function.

Epileptogenic depolarising and afterhyperpolarizing currents can emerge from a combination of abnormal, insufficient or excessive ionic conductances and/or abnormal, insufficient or excessive neurotransmitter release and receptor function. Critical synchronisation, stochastic and driven resonant oscillations and massive depolarisation of excitatory and inhibitory neurons result in a sustained paroxysmal depolarisation shift (PDS) of principal/pyramidal neurons which we detect electrophysiologically as huge baseline (DC) shifts and very high amplitude pathological high-frequency oscillations (pHFOs) known as pathological beta/gamma oscillations, (fast) ripples and (ultra)fast ripples.

Modelling epileptogenic mechanisms across all scales of neuronal organization will further our understanding of the processes of epileptogenesis, leading to more efficacious pharmacological or neurosurgical and neurostimulation treatment strategies and the development of new antiepileptic and epileptogenesis-modifying medications.