Abnormally enhanced excitation is commonly believed to mark the onset of a focal seizure. This notion, however, is not supported by any firm evidence and it will be challenged here. We know in fact that a marked reduction of unit firing occurs at the onset of seizures recorded during presurgical intracranial monitoring in patients with focal, drug‑resistant epilepsies. Moreover, seizures in animal models of focal epilepsy start with an increased activity of inhibitory interneurons that silences principal neurons. This key, yet paradoxical, role of inhibition in seizure onset has been confirmed in in vitro studies where the synchronous activation of GABAA receptors at seizure onset causes sizeable elevations in extracellular potassium via post-synaptic potassium-chloride co-transport, thus facilitating neuronal recruitment and seizure progression. The proposed role played by inhibition in focal seizure onset should profoundly transform our interpretation of focal ictogenesis thus leading to new antiepileptic strategies.
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