Christoffer Hatlestad-Hall1, Ricardo Bruña2, Marte Roa Syvertsen3, Aksel Erichsen4, Vebjørn Andersson5, Fabrizio Vecchio6, Francesca Miraglia7, Paolo M Rossini8, Hanna Renvall9, Erik Taubøll10, Fernando Maestú11, Ira H Haraldsen12. 1. Department of Neurology, Oslo University Hospital, Oslo, Norway. Electronic address: chr.hh@pm.me. 2. Center for Biomedical Technology, Technical University of Madrid, Pozuelo de Alarcón, Spain; Department of Experimental Psychology, Complutense University of Madrid, Pozuelo de Alarcón, Spain; Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Madrid, Spain. Electronic address: ricardo.bruna@ctb.upm.es. 3. Department of Neurology, Drammen Hospital, Vestre Viken Health Care Trust, Drammen, Norway. Electronic address: marsyv@vestreviken.no. 4. Department of Neurology, Oslo University Hospital, Oslo, Norway; Department of Nuclear Medicine, Oslo University Hospital, Oslo, Norway. Electronic address: akseri@ous-hf.no. 5. Department of Neurology, Oslo University Hospital, Oslo, Norway. Electronic address: vebjoran@uio.no. 6. Brain Connectivity Laboratory, Department of Neuroscience and Neurorehabilitation, IRCCS San Raffaele Pisana, Rome, Italy. Electronic address: fabrizio.vecchio@sanraffaele.it. 7. Brain Connectivity Laboratory, Department of Neuroscience and Neurorehabilitation, IRCCS San Raffaele Pisana, Rome, Italy. Electronic address: fra.miraglia@gmail.com. 8. Brain Connectivity Laboratory, Department of Neuroscience and Neurorehabilitation, IRCCS San Raffaele Pisana, Rome, Italy. Electronic address: paolomaria.rossini@sanraffaele.it. 9. Department of Neuroscience and Biomedical Engineering, Aalto University, Espoo, Finland; BioMag Laboratory, HUS Diagnostic Center, Helsinki University Hospital, University of Helsinki and Aalto University School of Science, Helsinki, Finland. Electronic address: hanna.renvall@aalto.fi. 10. Department of Neurology, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: erik.tauboll@medisin.uio.no. 11. Center for Biomedical Technology, Technical University of Madrid, Pozuelo de Alarcón, Spain; Department of Experimental Psychology, Complutense University of Madrid, Pozuelo de Alarcón, Spain; Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Madrid, Spain. Electronic address: fernando.maestu@ctb.upm.es. 12. Department of Neurology, Oslo University Hospital, Oslo, Norway. Electronic address: i.h.haraldsen@medisin.uio.no.
Abstract
OBJECTIVE: The hypersynchronous neuronal activity associated with epilepsy causes widespread functional network disruptions extending beyond the epileptogenic zone. This altered network topology is considered a mediator for non-seizure symptoms, such as cognitive impairment. The aim of this study was to investigate functional network alterations in focal epilepsy patients with good seizure control and high quality of life. METHODS: We compared twenty-two focal epilepsy patients and sixteen healthy controls on graph metrics derived from functional connectivity of source-level resting-state EEG. Graph metrics were calculated over a range of network densities in five frequency bands. RESULTS: We observed a significantly increased small world index in patients relative to controls. On the local level, two left-hemisphere regions displayed a shift towards greater alpha band "hubness". The findings were not mediated by age, sex or education, nor by age of epilepsy onset, duration or focus lateralisation. CONCLUSIONS: Widespread functional network alterations are evident in focal epilepsy, even in a cohort characterised by successful anti-seizure medication therapy and high quality of life. These findings might support the position that functional network analysis could hold clinical relevance for epilepsy. SIGNIFICANCE: Focal epilepsy is accompanied by global and local functional network aberrancies which might be implied in the sustenance of non-seizure symptoms.
OBJECTIVE: The hypersynchronous neuronal activity associated with epilepsy causes widespread functional network disruptions extending beyond the epileptogenic zone. This altered network topology is considered a mediator for non-seizure symptoms, such as cognitive impairment. The aim of this study was to investigate functional network alterations in focal epilepsypatients with good seizure control and high quality of life. METHODS: We compared twenty-two focal epilepsypatients and sixteen healthy controls on graph metrics derived from functional connectivity of source-level resting-state EEG. Graph metrics were calculated over a range of network densities in five frequency bands. RESULTS: We observed a significantly increased small world index in patients relative to controls. On the local level, two left-hemisphere regions displayed a shift towards greater alpha band "hubness". The findings were not mediated by age, sex or education, nor by age of epilepsy onset, duration or focus lateralisation. CONCLUSIONS: Widespread functional network alterations are evident in focal epilepsy, even in a cohort characterised by successful anti-seizure medication therapy and high quality of life. These findings might support the position that functional network analysis could hold clinical relevance for epilepsy. SIGNIFICANCE: Focal epilepsy is accompanied by global and local functional network aberrancies which might be implied in the sustenance of non-seizure symptoms.