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The Hippocampus and Cortex Together Generate the Scalp EEG Ictal Discharge in Temporal Lobe Epilepsy

Vossler, David G.*,†; Kraemer, Diana L.; Bell, Anthony J.

Journal of Clinical Neurophysiology: September 2017 - Volume 34 - Issue 5 - p 448–455
doi: 10.1097/WNP.0000000000000394
Original Research

Purpose: The scalp EEG ictal discharge in temporal lobe epilepsy is reportedly visible only after the intracranial discharge becomes well synchronized and present over 10 to 30 cm2 of cortex. We investigated the role of the hippocampal formation in the generation of the scalp EEG ictal discharge.

Methods: Intracranial EEG video monitors were recorded using simultaneous scalp, stereotaxic depth, and subdural strip electrodes in 19 subjects with temporal lobe epilepsy. The location, frequency, morphology, and timing of the initial ictal discharge, and subsequent ictal patterns, were examined in hippocampal formation, medial paleocortex, and lateral temporal neocortex electrocorticographic and scalp temporal EEG recordings.

Results: In every subject, a scalp ictal discharge was visible only after the intracranial ictal discharge had spread to involve the whole temporal lobe (hippocampal formation, medial paleocortex, and lateral temporal neocortex). Beta/gamma frequency and decremental electrocorticographic ictal discharges were never visualized in the EEG. The scalp EEG ictal discharge frequency was 2.4 to 10 Hz and appeared a median of 18 seconds after a faster frequency electrocorticographic initial ictal discharge, once the intracranial discharge slowed to an alpha, theta, or delta frequency.

Conclusions: In temporal lobe epilepsy, an ictal pattern is not readily visible in the scalp EEG until the intracranial ictal discharge is ≤10 Hz and has propagated from its site of onset to involve the hippocampus, medial paleocortex, and lateral temporal neocortex.

*Department of Neurology, University of Washington School of Medicine, Seattle, Washington, U.S.A.;

Neuroscience Institute, UW Medicine|Valley Medical Center, Renton, Washington, U.S.A.; and

Department of Neurosurgery, University of Washington School of Medicine, Seattle, Washington, U.S.A.

Address correspondence and reprint requests to David G. Vossler, MD, Neuroscience Institute, UW Medicine|Valley Medical Center, 400 South 43rd St, M/S NWP 100, Renton, WA 98058, U.S.A.; e-mail: david_vossler@valleymed.org.

The authors have no funding or conflicts of interest to disclose.

Presented at the 68th Annual Meeting of the American Epilepsy Society, Seattle, Washington, December 7, 2014. Originally submitted October 16, 2016.

© 2017 by the American Clinical Neurophysiology Society