Brain Advance Access originally published online on April 8, 2003
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Brain, Vol. 126, No. 6, 1449-1459,
June 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg144
Epileptic fast intracerebral EEG activity: evidence for spatial decorrelation at seizure onset
1 Laboratoire Traitement du Signal et de L’Image, INSERM, Université de Rennes 1, Campus de Beaulieu, Rennes and 2 Laboratoire de Neurophysiologie et Neuropsychologie, INSERM, Université de la Méditerranée, Marseille, France
Correspondence to: F. Wendling, Laboratoire Traitement du Signal et de L’Image, Université de Rennes 1, INSERM, Campus de Beaulieu, Bat. 22, 35042 Rennes Cedex, France E-mail: fabrice.wendling{at}univ-rennes1.fr
Low-voltage rapid discharges (or fast EEG ictal activity) constitute a characteristic electrophysiological pattern in focal seizures of human epilepsy. They are characterized by a decrease of signal voltage with a marked increase of signal frequency (typically beyond 25 Hz). They have long been observed in stereoelectroencephalographic (SEEG) signals recorded with intra-cerebral electrodes, generally occurring at seizure onset and simultaneously involving distinct brain regions. Spectral properties of rapid ictal discharges as well as spatial correlations measured between SEEG signals generated from distant sites before, during and after these discharges were studied. Cross-correlation estimates within typical EEG sub-bands and statistical tests performed in 10 patients suffering from partial epilepsy (frontal, temporal or fronto-temporal) reveal that SEEG signals are significantly de-correlated during the discharge period compared with periods that precede and follow this discharge. These results can be interpreted as a functional decoupling of distant brain sites at seizure onset followed by an abnormally high re-coupling when the seizure develops. They lead to the concept of ‘disruption’ that is complementary of that of ‘activation’ (revealed by significantly high correlations between signals recorded during seizures), both giving insights into our understanding of pathophysiological processes involved in human partial epilepsies as well as in the interpretation of clinical semiology.
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