Ictal time-irreversible intracranial EEG signals as markers of the epileptogenic zone.
This is the author accepted manuscript. The final version is available from Elsevier via the DOI in this record.
Reason for embargo
OBJECTIVE: To show that time-irreversible EEG signals recorded with intracranial electrodes during seizures can serve as markers of the epileptogenic zone. METHODS: We use the recently developed method of mapping time series into directed horizontal graphs (dHVG). Each node of the dHVG represents a time point in the original intracranial EEG (iEEG) signal. Statistically significant differences between the distributions of the nodes' number of input and output connections are used to detect time-irreversible iEEG signals. RESULTS: In 31 of 32 seizure recordings we found time-irreversible iEEG signals. The maximally time-irreversible signals always occurred during seizures, with highest probability in the middle of the first seizure half. These signals spanned a large range of frequencies and amplitudes but were all characterized by saw-tooth like shaped components. Brain regions removed from patients who became post-surgically seizure-free generated significantly larger time-irreversibilities than regions removed from patients who still had seizures after surgery. CONCLUSIONS: Our results corroborate that ictal time-irreversible iEEG signals can indeed serve as markers of the epileptogenic zone and can be efficiently detected and quantified in a time-resolved manner by dHVG based methods. SIGNIFICANCE: Ictal time-irreversible EEG signals can help to improve pre-surgical evaluation in patients suffering from pharmaco-resistant epilepsies.
K.S. gratefully acknowledges support by the Swiss National Science Foundation (SNF 32003B_155950). H.G. gratefully acknowledges support by a Research Grant of the Inselspital Bern. R.G.A. acknowledges funding from the Volkswagen foundation and was supported by the Spanish Ministry of Economy and Competitiveness (Grant FIS2014-54177- R). This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No 642563 (R.G.A.). MG gratefully acknowledges the financial support of the EPSRC via grant EP/N014391/1, funding from Epilepsy Research UK via grant number A1007 and was generously supported by a Wellcome Trust Institutional Strategic Support Award (WT105618MA).
Clinical Neurophysiology, 2016, Vol. 127, pp. 3051 Issue 9, pp. 3051- 3058