John Libbey Eurotext

Interictal epileptiform discharges in sleep and the role of the thalamus in Encephalopathy related to Status Epilepticus during slow Sleep Volume 21, supplément 1, June 2019

Illustrations

  • Figure 1
  • Figure 2

Tableaux

Auteurs
1 Centre for Epilepsy Surgery “C. Munari”, Centre of Sleep Medicine, Department of Neuroscience, Niguarda Hospital, Milan, Italy
2 Centre for Advanced Studies in Sleep Medicine, Dept. of Neurosciences, Hôpital du Sacré-Coeur de Montréal, Université de Montréal, Montréal, Canada
3 Child Neuropsychiatry, IRCCS, G. Gaslini Institute, Dept. of Neuroscience (DINOGMI), University of Genoa, Italy
4 National Institute of Clinical Neuroscience, Budapest, Hungary
* Correspondence: Péter Halász National Institute of Clinical Neuroscience, Lotz K.U.18, Budapest, 1026 Hungary

EEG activation of interictal epileptiform discharges (IEDs) during NREM sleep is a well-described phenomenon that occurs in the majority of epileptic syndromes. In drug-resistant focal epilepsy, IED activation seems to be related to slow wave activity (SWA), especially during arousal fluctuations, namely phase A of the cyclic alternating pattern (CAP). Conversely, in childhood focal epileptic syndromes, including Encephalopathy related to Status Epilepticus during slow Sleep (ESES), IED activation seems primarily modulated by sleep-inducing and maintaining mechanisms as reflected by the dynamics of spindle frequency activity (SFA) rather than SWA. In this article, we will review the effect of sleep on IEDs with a particular attention on the activation and modulation of IEDs in ESES. Finally, we will discuss the role of the thalamus and cortico-thalamic circuitry in this syndrome.