Authors :
Presenting Author: Nico Poppert, MD – Christian Doppler University Hospital, Paracelsus Medical University and Centre for Cognitive Neuroscience, Member of the European Reference Network EpiCARE
Aljoscha Thomschewski, PhD – Christian Doppler University Hospital, Paracelsus Medical University and Centre for Cognitive Neuroscience, Member of the European Reference Network EpiCARE
Sandra Lafenthaler, PhD – Christian Doppler University Hospital, Paracelsus Medical University and Centre for Cognitive Neuroscience, Member of the European Reference Network EpiCARE
Detlev Boison, PhD – Ruttgers University
Pavel Klein, MD, M.B., B.Chir. – Mid-Atlantic Epilepsy and Sleep Center
Matthias Koepp, MD PhD – UCL Queen Square Institute of Neurology/NHNN
Christine Lemke, PhD – PrevEp, Inc.
Wolfgang Löscher, PhD – 1Translational Epilepsy Research Group, Department of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine, Hannover, Germany
Alexander Rotenberg, MD, PhD – Boston Children’s Hospital, Harvard Medical School
Chris Rundfeldt, PhD – PreVep Inc.
Eugen Trinka, MD, MSc, FRCP – Christian Doppler University Hospital, Member of the European Reference Network EpiCARE, and Centre for Cognitive Neuroscience, Paracelsus Medical University, Salzburg, Austria
Rationale:
Reading epilepsy (RE), a reflex epilepsy with seizures triggered by reading, offers a valuable model to study seizure-generating networks. In a previous study using EEG and MEG, we identified the dominant premotor cortex (Brodmann Area 6) as the core of the epileptogenic network in a patient with RE.[1] Here, we re-examined the same patient using pharmacological intervention—intranasal seletracetam (SEL)—to explore how seizure activity and network dynamics change with suppression of spikes and seizures.
Methods:
A 42-year-old man with RE, on levetiracetam, participated in an individual healing attempt using intranasal SEL. Simultaneous MEG and EEG recordings were acquired under three conditions: (1) after intranasal saline (placebo), (2) after 30 mg SEL, and (3) after a second 30 mg SEL dose. A text reliably triggering seizures (a mathematics textbook) was read aloud until the third self-reported seizure, prompting SEL administration. MEG was recorded using a multi-channel sensor system in a magnetically shielded room, and surface EEG was simultaneously collected. Dipole modeling and source analysis were performed using equivalent current dipole (ECD) modeling implemented in Brainstorm [2]
Results:
At baseline (placebo), seizures began at 1:56 minutes with 3.1 spikes/min. After 30 mg SEL, seizure onset was delayed to 4:17 minutes with 1.9 spikes/min. Following a second 30 mg dose, the patient read for 25 minutes without seizures, with spike frequency reduced to 1.6 spikes/min. Ictal activity (six seizures total) was only recorded during reading aloud. MEG dipole analysis replicated earlier findings, localizing activity to the left precentral region, overlapping the motor representation of the upper mouth. Spike frequency as well as spike propagation was reduced after intranasal seletracetam application. (figure 1)
Conclusions:
MEG/EEG analysis confirmed that spike propagation reduced in keeping with the clinical finding that spikes still occurred albeit at reduced frequency, but no seizures were observed following repeat seletracetam administration. These results reinforce the potential of SEL as a fast-acting, non-sedating intervention and provide deeper insights into cortical seizure propagation dynamics.
References:
VVaudano AE , et al. Neurology. 2012;79(3):249-53
< !Tadel F et al. Computational Intelligence and Neuroscience, 2011, 879716. https://doi.org/10.1155/2011/879716
Funding: none