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The Journal of Neuroscience, December 5, 2007, 27(49):13513-13519; doi:10.1523/JNEUROSCI.3005-07.2007

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Neurobiology of Disease
The Source of Afterdischarge Activity in Neocortical Tonic–Clonic Epilepsy

Andrew J. Trevelyan,^1,5 Torsten Baldeweg,^2,3 Wim van Drongelen,⁴ Rafael Yuste,⁵ and Miles Whittington¹

¹School of Neurology, Neurobiology and Psychiatry, Medical School, University of Newcastle, Newcastle upon Tyne NE2 4HH, United Kingdom, ²Institute of Child Health, University College London, London WC1N 1EH, United Kingdom, ³Great Ormond Street Hospital, London WC1N 3JH, United Kingdom, ⁴Department of Pediatrics, The University of Chicago, Chicago, Illinois 60637-1470, and ⁵Department of Biological Sciences, Howard Hughes Medical Institute, Columbia University, New York, New York 10027

Correspondence should be addressed to Andrew J. Trevelyan, School of Neurology, Neurobiology and Psychiatry, Medical School, University of Newcastle, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK. Email: andytrev{at}gmail.com

Tonic–clonic seizures represent a common pattern of epileptic discharges, yet the relationship between the various phases of the seizure remains obscure. Here we contrast propagation of the ictal wavefront with the propagation of individual discharges in the clonic phase of the event. In an in vitro model of tonic–clonic epilepsy, the afterdischarges (clonic phase) propagate with relative uniform speed and are independent of the speed of the ictal wavefront (tonic phase). For slowly propagating ictal wavefronts, the source of the afterdischarges, relative to a given recording electrode, switched as the wavefront passed by, indicating that afterdischarges are seeded from wavefront itself. In tissue that has experienced repeated ictal events, the wavefront generalizes rapidly, and the afterdischarges in this case show a different "flip–flop" pattern, with frequent switches in their direction of propagation. This same flip–flop pattern is also seen in subdural EEG recordings in patients suffering intractable focal seizures caused by cortical dysplasias. Thus, in both slowly and rapidly generalizing ictal events, there is not a single source of afterdischarge activity: rather, the source is continuously changing. Our data suggest a complex view of seizures in which the ictal event and its constituent discharges originate from distinct locations.

Key words: epilepsy; seizure; tonic–clonic discharge; afterdischarge; pyramidal cell; cortex

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Received July 2, 2007; revised Oct. 4, 2007; accepted Oct. 8, 2007.

Correspondence should be addressed to Andrew J. Trevelyan, School of Neurology, Neurobiology and Psychiatry, Medical School, University of Newcastle, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK. Email: andytrev{at}gmail.com

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