Epilepsy is a paroxysmal condition characterized by repeated transient seizures separated by longer interictal periods. Ictogenesis describes the processes of transition from the interictal state to a seizure. The processes include a preictal state, with specific clinical signs and a distinct electrophysiology which may provide opportunities to anticipate, or even prevent, seizures. Biological mechanisms of ictogenesis remain poorly understood and may vary between conditions/syndromes. We review here ictogenic processes including the involvement of pyramidal cells, interneurons and astrocytes, GABAergic and glutamatergic signaling, and ionic perturbations. Our review suggests that specific excitatory influences at the transition to an ictal event include (1) GABA receptor activation with a neuronal Cl(-) load and (2) a transient increase in external K(+).

Department of Developmental Epileptology Institute of Physiology Academy of Sciences of Czech Republic Prague Czech Republic; Department of Neurology 2nd Faculty of Medicine Charles University Prague Motol University Hospital Prague Czech Republic

INSERM U1129 Infantile Epilepsies and Brain Plasticity Paris France; University Paris Descartes PRES Sorbonne Paris Cité Paris France; CEA Gif sur Yvette France; Clinical Neurophysiology Department CHU Pitié Salpêtrière APHP Paris France; Université Pierre et Marie Curie Paris France

Neurosurgery Unit Hopital Necker Enfants Malades APHP Paris France; Université Paris Descartes Paris France; INSERM U1129 Infantile Epilepsies and Brain Plasticity Paris France; University Paris Descartes PRES Sorbonne Paris Cité Paris France; CEA Gif sur Yvette France

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